Teva Pharmaceutical Industries Ltd. (Nasdaq: TEVA) announced that the U.S. Food and Drug Administration has granted tentative approval for the Company's Abbreviated New Drug Application (ANDA) to market its generic version of Eisai's Alzheimer's treatment Aricept® (Donepezil Hydrochloride) Tablets, 5 mg and 10 mg. The brand product had annual sales of approximately $1.6 billion in the United States for the twelve months ended September 30, 2007, based on IMS sales data.
Teva is currently in patent litigation concerning this product in the U.S. District Court for the District of New Jersey involving Teva's paragraph IV certification to U.S. Patent No. 4,895,841. Although a trial date has not been set, the Court has set a briefing schedule for a preliminary injunction motion under which Eisai must file its request no later than February 15, 2008. Final approval of this ANDA is anticipated on or about April 26, 2008, upon expiry of the mandatory stay of approval associated with the patent litigation.
Teva Pharmaceutical Industries Ltd., headquartered in Israel, is among the top 20 pharmaceutical companies in the world and is the leading generic pharmaceutical company. The company develops, manufactures and markets generic and innovative human pharmaceuticals and active pharmaceutical ingredients. Over 80 percent of Teva's sales are in North America and Europe.
Teva Pharmaceutical Industries Ltd.
View drug information on ARICEPT.
вторник, 31 мая 2011 г.
понедельник, 30 мая 2011 г.
The Molecular Power Behind Memory
Neuroscientists have long wondered how individual connections between brain cells remain diverse and "fit" enough for storing new memories. Reported in the prestigious science journal Neuron, a new study led by Dr. Inna Slutsky of the Sackler School of Medicine at Tel Aviv University describes what makes some memories stick.
The key is GABA (??-Aminobutyric acid), a natural molecule that occurs in the brain, which could be the main factor in regulating how many new memories we can generate, the new study has found. The understanding of these mechanisms might lead to the development of new memory enhancers and new treatments for neurodegenerative diseases such as Alzheimer's.
Memories, Dr. Slutsky says, are stored in synaptic connections between neurons in our brain. In the past, other teams, including her own, have demonstrated that the strength of individual synapses is highly variable, even at the single neuron level. This variability ultimately determines if and how new memories are stored, and the key to this variability is GABA, a naturally-occurring chemical found in the brain.
Tight connections and lone rangers
Dr. Slutsky's graduate student Tal Laviv and postdoctoral fellow Inbal Riven, the lead authors in the study, applied advanced nanotechnology methods in optical imaging to track how proteins engineered by Prof. Paul Slesinger and his team at The Salk Institute interact with GABA at the single-synapse level.
In the hippocampus, one of the main areas of the brain involved in learning and memory, the strength of neuronal connections is known to be highly variable. Some neurons are tightly connected to others, while some appear to be "lone rangers."
The new paper, which examines individual synapses in the hippocampus, demonstrates that this process is regulated by GABA, the main inhibitory neurotransmitter in our brain. "We determined that variations in the local level of GABA in the vicinity of individual synapses are responsible for the differences or 'heterogeneity' of synaptic strength. And this heterogeneity may facilitate the formation of new memories," Dr. Slutsky explains.
Looking at the brain at rest
While looking at the brain in its basal state - when the activity was "at rest" before attempting to memorize a list of items or after a memory had been stored - Dr. Slutsky's team could actually "see" where synapses differ at different dendritic branches in the neuronal network. Those branches of neurons close to a cell body displayed a larger number of weak synapses, while the most distant branches were composed of a smaller number of strong synapses.
"Why the difference?" they asked. GABA was the answer. Higher concentrations of GABA near a synapse induced a stronger activation of its receptors, weakening basal synapse strength. As a result, GABA makes this synapse more liable to the formation of new memories, the researchers propose.
Dr. Slutsky, who previously discovered a basal-state regulator molecule, says that the research may also have implications for treating diseases of the mind. "We found that amyloid-beta, a well-known hallmark of Alzheimer's disease, regulates basal synapse strength in an opposite way to GABA," she notes, suggesting that an increase in the basal activity of synapses may initiate memory decline in Alzheimer's and other neurodegenerative disorders.
Experiments in the study were done using neuronal cultures and brain slices of rats subjected to molecular biology, optical imaging and electrophysiological techniques. The study also constituted a technical achievement, since it used advanced imaging techniques such as fluorescence resonance energy transfer (FRET) spectroscopy that looked at protein-to-protein interactions in the brain at the 10 nanometer scale. In the past, such fine resolution was impossible - brain scientists could only investigate interactions at the level of entire tissues, not between molecules at individual synapses.
Source:
George Hunka
American Friends of Tel Aviv University
The key is GABA (??-Aminobutyric acid), a natural molecule that occurs in the brain, which could be the main factor in regulating how many new memories we can generate, the new study has found. The understanding of these mechanisms might lead to the development of new memory enhancers and new treatments for neurodegenerative diseases such as Alzheimer's.
Memories, Dr. Slutsky says, are stored in synaptic connections between neurons in our brain. In the past, other teams, including her own, have demonstrated that the strength of individual synapses is highly variable, even at the single neuron level. This variability ultimately determines if and how new memories are stored, and the key to this variability is GABA, a naturally-occurring chemical found in the brain.
Tight connections and lone rangers
Dr. Slutsky's graduate student Tal Laviv and postdoctoral fellow Inbal Riven, the lead authors in the study, applied advanced nanotechnology methods in optical imaging to track how proteins engineered by Prof. Paul Slesinger and his team at The Salk Institute interact with GABA at the single-synapse level.
In the hippocampus, one of the main areas of the brain involved in learning and memory, the strength of neuronal connections is known to be highly variable. Some neurons are tightly connected to others, while some appear to be "lone rangers."
The new paper, which examines individual synapses in the hippocampus, demonstrates that this process is regulated by GABA, the main inhibitory neurotransmitter in our brain. "We determined that variations in the local level of GABA in the vicinity of individual synapses are responsible for the differences or 'heterogeneity' of synaptic strength. And this heterogeneity may facilitate the formation of new memories," Dr. Slutsky explains.
Looking at the brain at rest
While looking at the brain in its basal state - when the activity was "at rest" before attempting to memorize a list of items or after a memory had been stored - Dr. Slutsky's team could actually "see" where synapses differ at different dendritic branches in the neuronal network. Those branches of neurons close to a cell body displayed a larger number of weak synapses, while the most distant branches were composed of a smaller number of strong synapses.
"Why the difference?" they asked. GABA was the answer. Higher concentrations of GABA near a synapse induced a stronger activation of its receptors, weakening basal synapse strength. As a result, GABA makes this synapse more liable to the formation of new memories, the researchers propose.
Dr. Slutsky, who previously discovered a basal-state regulator molecule, says that the research may also have implications for treating diseases of the mind. "We found that amyloid-beta, a well-known hallmark of Alzheimer's disease, regulates basal synapse strength in an opposite way to GABA," she notes, suggesting that an increase in the basal activity of synapses may initiate memory decline in Alzheimer's and other neurodegenerative disorders.
Experiments in the study were done using neuronal cultures and brain slices of rats subjected to molecular biology, optical imaging and electrophysiological techniques. The study also constituted a technical achievement, since it used advanced imaging techniques such as fluorescence resonance energy transfer (FRET) spectroscopy that looked at protein-to-protein interactions in the brain at the 10 nanometer scale. In the past, such fine resolution was impossible - brain scientists could only investigate interactions at the level of entire tissues, not between molecules at individual synapses.
Source:
George Hunka
American Friends of Tel Aviv University
воскресенье, 29 мая 2011 г.
New Diagnostic Criteria For Alzheimer's Disease
An international group of Alzheimer's disease (AD) experts have proposed new criteria for the reasearch diagnosis of the condition, as they argue the existing criteria are out of date due to unprecedented growth of scientific knowledge in the field. The proposal is put forward in a Position Paper published early Online and in the August edition of The Lancet Neurology.
AD is a neurodegenerative disease characterised by progressive cognitive deterioration, together with declining activities of daily living and by neuropsychiatric symptoms or behavioural changes. It is the most common form of dementia.
The existing criteria were published in 1984 by the National Institute of Neurological Disorders and Stroke-Alzheimer Disease and Related Disorders (NINCDS-ADRDA) working group.
Dr Bruno Dubois, Salp??tri??re Hosptial, Paris, France, and colleagues, say: "[These existing criteria] are the prevailing diagnostic standards in research; however they have now fallen behind the unprecedented growth of scientific knowledge. Distinctive and reliable biomarkers of AD are now available through structural MRI, molecular neuroimaging with PET*, and cerebrospinal fluid analyses."
To meet the new criteria for probable AD, patients must show progressive memory loss over more than six months, plus at least one or more of the supportive biomarker criteria. These include: atrophy in a particular part of the brain shown by MRI, abnormal biomarker proteins in the cerebrospinal fluid, a specific pattern on PET of the brain, and a genetic mutation for AD within the immediate family. The authors say: "These new criteria are centred on a clinical core of early and significant episodic memory impairment??¦the timeliness of these criteria is highlighted by the many drugs in development that are directed at changing pathogenesis."
The researchers add that validation studies are required to advance the new criteria and optimise their sensitivity, specificity and accuracy.
They conclude: "When effective disease-modifying medications are available, the argument for such biologically based studies will be even more compelling.
"These proposed criteria move away from the traditional two-step approach of first identifying dementia according to degree of functional disability, and then specifying its cause. Rather, they aim to define the clinical, biochemical, structural, and metabolic presence of AD."
In an accompanying Comment, Dr Norman Foster, Center for Alzheimer's Care, Department of Neurology, University of Utah, USA says: "We should seize this opportunity to reopen the discussion of Alzheimer's disease diagnosis. The time is right to use the advanced technology at our disposal to improve the early, accurate diagnosis of dementia and develop more effective treatments."
PET*= Positron Emission Topography
The Lancet Neurology
AD is a neurodegenerative disease characterised by progressive cognitive deterioration, together with declining activities of daily living and by neuropsychiatric symptoms or behavioural changes. It is the most common form of dementia.
The existing criteria were published in 1984 by the National Institute of Neurological Disorders and Stroke-Alzheimer Disease and Related Disorders (NINCDS-ADRDA) working group.
Dr Bruno Dubois, Salp??tri??re Hosptial, Paris, France, and colleagues, say: "[These existing criteria] are the prevailing diagnostic standards in research; however they have now fallen behind the unprecedented growth of scientific knowledge. Distinctive and reliable biomarkers of AD are now available through structural MRI, molecular neuroimaging with PET*, and cerebrospinal fluid analyses."
To meet the new criteria for probable AD, patients must show progressive memory loss over more than six months, plus at least one or more of the supportive biomarker criteria. These include: atrophy in a particular part of the brain shown by MRI, abnormal biomarker proteins in the cerebrospinal fluid, a specific pattern on PET of the brain, and a genetic mutation for AD within the immediate family. The authors say: "These new criteria are centred on a clinical core of early and significant episodic memory impairment??¦the timeliness of these criteria is highlighted by the many drugs in development that are directed at changing pathogenesis."
The researchers add that validation studies are required to advance the new criteria and optimise their sensitivity, specificity and accuracy.
They conclude: "When effective disease-modifying medications are available, the argument for such biologically based studies will be even more compelling.
"These proposed criteria move away from the traditional two-step approach of first identifying dementia according to degree of functional disability, and then specifying its cause. Rather, they aim to define the clinical, biochemical, structural, and metabolic presence of AD."
In an accompanying Comment, Dr Norman Foster, Center for Alzheimer's Care, Department of Neurology, University of Utah, USA says: "We should seize this opportunity to reopen the discussion of Alzheimer's disease diagnosis. The time is right to use the advanced technology at our disposal to improve the early, accurate diagnosis of dementia and develop more effective treatments."
PET*= Positron Emission Topography
The Lancet Neurology
Senate Special Committee On Aging Examines Alzheimer's Study Group Report, Hears Testimony From High-Profile Advocates
During a Senate Special Committee on Aging hearing on Wednesday, high-profile Alzheimer's disease funding advocates called for a public-private effort to garner more research money and support for caregivers, CQ HealthBeat reports (Reichard, CQ HealthBeat, 3/25). A recent Alzheimer's Study Group report suggested that the disease "could very easily surpass even the current economic crisis in the damage it inflicts on individuals and our economy" and cost Medicare and Medicaid more than $1 trillion annually by 2050 (Clark, Miami Herald, 3/26).
According to former House Speaker Newt Gingrich (R-Ga.), co-chair of the study group with former Sen. Bob Kerrey (D-Neb.), "There is no single breakthrough that would do more to lower the cost of entitlements than preventing the onset of Alzheimer's disease," because, "Given the present trends, Alzheimer's will cost Medicare and Medicaid a projected $19.89 trillion between 2010 and 2050."
The study group called for the creation of the Alzheimer's Solutions Project that would focus national efforts to first delay the onset of the disease and then to prevent it. Gingrich noted, "A five-year delay of onset would save $8.51 trillion over that same period." The project would change the payment system by 2012 to reward providers based on the coordinated services provided to patients and their families, and would establish a government-run Alzheimer's Solutions Project Office to work with the private sector for new research funding (CQ HealthBeat, 3/25). Gingrich said, "The human pain and financial burden of Alzheimer's is so great and the potential breakthroughs in science are so encouraging that a 'Manhattan Project' ... approach to ending Alzheimer's is more than justified," adding, "The choice for our generation is not whether or not to spend the money on Alzheimer's. The choice for our generation is to invest the money early and save a lot of lives, pain and money later or to be foolishly cheap" (Miami Herald, 3/26).
Gingrich suggested an "off-budget funding" strategy that would sell Alzheimer's bonds that would be repaid with savings on Alzheimer's outlays after a medical breakthrough. Scientists predict a breakthrough could occur by 2020 or 2025. Senate Appropriations Labor-HHS-Education Subcommittee ranking member Arlen Specter (R-Pa.) told the audience that a possible funding approach would be to use some of the additional $10 billion NIH is to receive as part of the recently enacted economic stimulus package.
Kerrey told the committee that the disease creates huge dependency on caregivers, whose needs also must be addressed by lawmakers, as they are often forced to stop working.
Other speakers at the hearing included California first lady Maria Shriver, whose father -- Sargent Shriver, founder of Peace Corps, Head Start and AmeriCorps -- has Alzheimer's; and retired Supreme Court Justice and member of the study group Sandra Day O'Connor, whose husband has Alzheimer's (CQ HealthBeat, 3/25).
The group's strategic plan is available online (.pdf).
NPR's "Talk of The Nation" on Wednesday featured a discussion with Gingrich, O'Connor and former Surgeon General David Satcher on the recommendations in the Alzheimer's Study Group report (Conan, "Talk of the Nation," NPR, 3/25).
Reprinted with kind permission from kaisernetwork. You can view the entire Kaiser Daily Health Policy Report, search the archives, or sign up for email delivery at kaisernetwork/dailyreports/healthpolicy. The Kaiser Daily Health Policy Report is published for kaisernetwork, a free service of The Henry J. Kaiser Family Foundation.
© 2009 Advisory Board Company and Kaiser Family Foundation. All rights reserved.
According to former House Speaker Newt Gingrich (R-Ga.), co-chair of the study group with former Sen. Bob Kerrey (D-Neb.), "There is no single breakthrough that would do more to lower the cost of entitlements than preventing the onset of Alzheimer's disease," because, "Given the present trends, Alzheimer's will cost Medicare and Medicaid a projected $19.89 trillion between 2010 and 2050."
The study group called for the creation of the Alzheimer's Solutions Project that would focus national efforts to first delay the onset of the disease and then to prevent it. Gingrich noted, "A five-year delay of onset would save $8.51 trillion over that same period." The project would change the payment system by 2012 to reward providers based on the coordinated services provided to patients and their families, and would establish a government-run Alzheimer's Solutions Project Office to work with the private sector for new research funding (CQ HealthBeat, 3/25). Gingrich said, "The human pain and financial burden of Alzheimer's is so great and the potential breakthroughs in science are so encouraging that a 'Manhattan Project' ... approach to ending Alzheimer's is more than justified," adding, "The choice for our generation is not whether or not to spend the money on Alzheimer's. The choice for our generation is to invest the money early and save a lot of lives, pain and money later or to be foolishly cheap" (Miami Herald, 3/26).
Gingrich suggested an "off-budget funding" strategy that would sell Alzheimer's bonds that would be repaid with savings on Alzheimer's outlays after a medical breakthrough. Scientists predict a breakthrough could occur by 2020 or 2025. Senate Appropriations Labor-HHS-Education Subcommittee ranking member Arlen Specter (R-Pa.) told the audience that a possible funding approach would be to use some of the additional $10 billion NIH is to receive as part of the recently enacted economic stimulus package.
Kerrey told the committee that the disease creates huge dependency on caregivers, whose needs also must be addressed by lawmakers, as they are often forced to stop working.
Other speakers at the hearing included California first lady Maria Shriver, whose father -- Sargent Shriver, founder of Peace Corps, Head Start and AmeriCorps -- has Alzheimer's; and retired Supreme Court Justice and member of the study group Sandra Day O'Connor, whose husband has Alzheimer's (CQ HealthBeat, 3/25).
The group's strategic plan is available online (.pdf).
NPR's "Talk of The Nation" on Wednesday featured a discussion with Gingrich, O'Connor and former Surgeon General David Satcher on the recommendations in the Alzheimer's Study Group report (Conan, "Talk of the Nation," NPR, 3/25).
Reprinted with kind permission from kaisernetwork. You can view the entire Kaiser Daily Health Policy Report, search the archives, or sign up for email delivery at kaisernetwork/dailyreports/healthpolicy. The Kaiser Daily Health Policy Report is published for kaisernetwork, a free service of The Henry J. Kaiser Family Foundation.
© 2009 Advisory Board Company and Kaiser Family Foundation. All rights reserved.
суббота, 28 мая 2011 г.
Project Lifesaver Touches Communities Nationwide
This week marks the 1,666th find nationally for the search and rescue of a Project
Lifesaver client.
You may ask why this is important; the answer in itself is simple. One life saved, is one less tragedy a family must endure and one less sad story featured on the news leaving citizens wondering what could be done to help prevent such events.
Gene Saunders, Chief Executive Officer of Project Lifesaver International stated, "Without the Project Lifesaver Program, so many searches could have resulted with tragic endings. The amount of money, resources, and time spent searching for clients on this program are drastically reduced and most importantly lives are saved."
One of the many goals of Project Lifesaver is to provide awareness that this program exist and works. As awareness increases regarding Alzheimer's, Autism and other related medical conditions that cause people to wander away from the safety of their homes, more citizens search for programs like Project Lifesaver that would assist them in safeguarding their loved ones.
Project Lifesaver International was founded in Chesapeake, Virginia in April of 1999, as an initiative of the 43rd Search and Rescue Company of the Chesapeake Sheriff's Office.
People who are enrolled in the Project Lifesaver Program wear a personalized wristband that emits a tracking signal. When caregivers notify the local Project Lifesaver agency that the person is missing, a search and rescue team responds to the wanderer's area and starts searching with a mobile locater tracking system. Search times have been reduced from hours and days to just minutes, the average rescue time if notified is less than 30-minutes.
Currently, there are over 653 agencies in 42 states and Canada participating in the Project Lifesaver® program Bringing Loved Ones Home®. Since Project Lifesaver International is a non-profit (501 (c) (3)) organization, funding is a result of private and corporate donations and grants. Donations are used directly for programs, rescues and educational expenses.
Before Project Lifesaver, searches across the country were averaging 9 hours
and costing taxpayers approximately $1,500 per hour. Many searches actually
took days, with hundreds of responders, resulting in much higher costs and many
with tragic endings. One search in Chesapeake in 1979 cost the city $342,000
and was unsuccessful. The basic cost to start this program in an agency is less
than $8,000, finding someone alive is priceless.
The bottom line is that this program works in saving lives, providing training to
interested agencies and saving the taxpayers money. Project Lifesaver International has received no Federal Government Funding!
In the meantime, go to the following link and you will be able to view our
most recent video about Project Lifesaver. Our web site also has more information on the cost and benefits projectlifesaver.
Project Lifesaver
Lifesaver client.
You may ask why this is important; the answer in itself is simple. One life saved, is one less tragedy a family must endure and one less sad story featured on the news leaving citizens wondering what could be done to help prevent such events.
Gene Saunders, Chief Executive Officer of Project Lifesaver International stated, "Without the Project Lifesaver Program, so many searches could have resulted with tragic endings. The amount of money, resources, and time spent searching for clients on this program are drastically reduced and most importantly lives are saved."
One of the many goals of Project Lifesaver is to provide awareness that this program exist and works. As awareness increases regarding Alzheimer's, Autism and other related medical conditions that cause people to wander away from the safety of their homes, more citizens search for programs like Project Lifesaver that would assist them in safeguarding their loved ones.
Project Lifesaver International was founded in Chesapeake, Virginia in April of 1999, as an initiative of the 43rd Search and Rescue Company of the Chesapeake Sheriff's Office.
People who are enrolled in the Project Lifesaver Program wear a personalized wristband that emits a tracking signal. When caregivers notify the local Project Lifesaver agency that the person is missing, a search and rescue team responds to the wanderer's area and starts searching with a mobile locater tracking system. Search times have been reduced from hours and days to just minutes, the average rescue time if notified is less than 30-minutes.
Currently, there are over 653 agencies in 42 states and Canada participating in the Project Lifesaver® program Bringing Loved Ones Home®. Since Project Lifesaver International is a non-profit (501 (c) (3)) organization, funding is a result of private and corporate donations and grants. Donations are used directly for programs, rescues and educational expenses.
Before Project Lifesaver, searches across the country were averaging 9 hours
and costing taxpayers approximately $1,500 per hour. Many searches actually
took days, with hundreds of responders, resulting in much higher costs and many
with tragic endings. One search in Chesapeake in 1979 cost the city $342,000
and was unsuccessful. The basic cost to start this program in an agency is less
than $8,000, finding someone alive is priceless.
The bottom line is that this program works in saving lives, providing training to
interested agencies and saving the taxpayers money. Project Lifesaver International has received no Federal Government Funding!
In the meantime, go to the following link and you will be able to view our
most recent video about Project Lifesaver. Our web site also has more information on the cost and benefits projectlifesaver.
Project Lifesaver
пятница, 27 мая 2011 г.
Hormone Therapy Use May Increase Or Decrease Dementia Risk Depending Upon Timing
Compared to women never on hormone therapy, those taking hormone therapy only at midlife had a 26 percent decreased risk of dementia; while women taking HT only in late life had a 48 percent increased risk of dementia, according to Kaiser Permanente researchers.
Women taking HT at both midlife (mean age 48.7 years) and late life had a similar risk of dementia as women not on HT, according to the study which appears in the Annals of Neurology. The study was funded in part by the National Institutes of Health.
Although previous research has shown that initiation of postmenopausal estrogen hormone therapy in late life increases the risk of dementia, animal studies and some observational studies have suggested that midlife use of HT may be beneficial. This is the first observational, long-term study to directly compare the effect of hormone therapy status in both midlife and late life on risk of dementia.
"This study is unique because we had a group of women who were on HT in midlife only and could look at their dementia risk over time, and we found a modest, protective association. We also found that if you start HT late in life, you have a 50 percent increased risk of dementia, which is consistent with other studies," said study lead author Rachel Whitmer, PhD, a research scientist with the Kaiser Permanente Division of Research in Oakland, Calif. "Women should speak with their doctor about what's best for their individual situation, however it appears from this study that women who are on short-term HT in midlife may benefit from a modest protective association, while initiation in late-life can cause harm."
Researchers conducted an observational cohort study of long-term female members of Kaiser Permanente in Northern California who participated in periodic multiphasic health check-ups that were part of routine medical care in San Francisco and Oakland between 1964 and 1973, when they were 40-55 years old.
HT use was determined at midlife (mean age 48.7 years) from a survey in 1964 and in late life (mean age 76) using pharmacy databases from 1994 to 1998. Risk of dementia diagnosis was evaluated with inpatient and outpatient diagnoses made in neurology, neuropsychology and internal medicine from 1999 to 2008. A total of 1,524 women were diagnosed with dementia during the follow-up period.
Adjustment for high cholesterol, hypertension and stroke did not reduce the magnitude of the effect of late life HT on increased risk of dementia, according to the researchers. It's also possible that in the group of women who used HT both in midlife and late life; the potential modest benefit of midlife use was counteracted by a negative effect of late life use, they explained.
This study is part of an ongoing body of research at Kaiser Permanente to better understand the modifiable risk factors for dementia. Dr. Whitmer has led several dementia-related studies that utilize multiphasic health data collected in the 1960s and 1970s by Kaiser Permanente Health Information Technology pioneer Dr. Morris Collen on thousands of Kaiser Permanente Northern California men and women during routine health check-ups. That multiphasic data used for research studies decades later has revealed these key findings: heavy smoking in midlife is associated with a 157 percent increased risk of developing Alzheimer's disease and a 172 percent increased risk of developing vascular dementia; a larger abdomen in midlife increases risk of late-life dementia; and elevated cholesterol levels in midlife significantly increase the risk of Alzheimer's disease and vascular dementia later in life. Another study by Dr. Whitmer showed that low blood sugar events in elderly patients with type 2 diabetes increase their risk for dementia. A study led by Valerie Crooks of Kaiser Permanente in Southern California found that having a strong social network of friends and family appears to decrease the risk of dementia.
Limitations of this most recent study include the fact that HT information in midlife was self-reported and therefore researchers do not know the dose or type of HT involved. Also, because the pharmacy database was initiated in 1994, researchers do not have information on the duration of midlife HT.
Co-authors of the paper include Charles P. Quesenberry, PhD, and Jufen Zhou, MS, both with the Kaiser Permanente Division of Research, and Kristin Yaffe, MD, with the UC San Francisco department of psychiatry and the San Francisco VA Medical Center.
Source: Kaiser Permanente
Women taking HT at both midlife (mean age 48.7 years) and late life had a similar risk of dementia as women not on HT, according to the study which appears in the Annals of Neurology. The study was funded in part by the National Institutes of Health.
Although previous research has shown that initiation of postmenopausal estrogen hormone therapy in late life increases the risk of dementia, animal studies and some observational studies have suggested that midlife use of HT may be beneficial. This is the first observational, long-term study to directly compare the effect of hormone therapy status in both midlife and late life on risk of dementia.
"This study is unique because we had a group of women who were on HT in midlife only and could look at their dementia risk over time, and we found a modest, protective association. We also found that if you start HT late in life, you have a 50 percent increased risk of dementia, which is consistent with other studies," said study lead author Rachel Whitmer, PhD, a research scientist with the Kaiser Permanente Division of Research in Oakland, Calif. "Women should speak with their doctor about what's best for their individual situation, however it appears from this study that women who are on short-term HT in midlife may benefit from a modest protective association, while initiation in late-life can cause harm."
Researchers conducted an observational cohort study of long-term female members of Kaiser Permanente in Northern California who participated in periodic multiphasic health check-ups that were part of routine medical care in San Francisco and Oakland between 1964 and 1973, when they were 40-55 years old.
HT use was determined at midlife (mean age 48.7 years) from a survey in 1964 and in late life (mean age 76) using pharmacy databases from 1994 to 1998. Risk of dementia diagnosis was evaluated with inpatient and outpatient diagnoses made in neurology, neuropsychology and internal medicine from 1999 to 2008. A total of 1,524 women were diagnosed with dementia during the follow-up period.
Adjustment for high cholesterol, hypertension and stroke did not reduce the magnitude of the effect of late life HT on increased risk of dementia, according to the researchers. It's also possible that in the group of women who used HT both in midlife and late life; the potential modest benefit of midlife use was counteracted by a negative effect of late life use, they explained.
This study is part of an ongoing body of research at Kaiser Permanente to better understand the modifiable risk factors for dementia. Dr. Whitmer has led several dementia-related studies that utilize multiphasic health data collected in the 1960s and 1970s by Kaiser Permanente Health Information Technology pioneer Dr. Morris Collen on thousands of Kaiser Permanente Northern California men and women during routine health check-ups. That multiphasic data used for research studies decades later has revealed these key findings: heavy smoking in midlife is associated with a 157 percent increased risk of developing Alzheimer's disease and a 172 percent increased risk of developing vascular dementia; a larger abdomen in midlife increases risk of late-life dementia; and elevated cholesterol levels in midlife significantly increase the risk of Alzheimer's disease and vascular dementia later in life. Another study by Dr. Whitmer showed that low blood sugar events in elderly patients with type 2 diabetes increase their risk for dementia. A study led by Valerie Crooks of Kaiser Permanente in Southern California found that having a strong social network of friends and family appears to decrease the risk of dementia.
Limitations of this most recent study include the fact that HT information in midlife was self-reported and therefore researchers do not know the dose or type of HT involved. Also, because the pharmacy database was initiated in 1994, researchers do not have information on the duration of midlife HT.
Co-authors of the paper include Charles P. Quesenberry, PhD, and Jufen Zhou, MS, both with the Kaiser Permanente Division of Research, and Kristin Yaffe, MD, with the UC San Francisco department of psychiatry and the San Francisco VA Medical Center.
Source: Kaiser Permanente
четверг, 26 мая 2011 г.
Affiris Uses Definiens Technology In Fight Against Alzheimer's Disease
Affiris GmbH
announced today that it will integrate the Definiens Enterprise Image
Intelligence (TM) Suite in the company's Alzheimer's disease vaccination
program. The decision was based on the company's outstanding experience with
Definiens software. Affiris' business strategy focuses on rapid
identification of drug candidates and accelerated preclinical and clinical
development. Matching Affiris requirements comprehensively, Definiens
provides automated image analysis solutions with reliable, fast and
consistent results.
DEFINIENS ?¬ UNPARALLELED IMAGE ANALYSIS COUPLED WITH TIME AND COST SAVING
In order to launch its new AFFITOPETM vaccines, which facilitate the
induction of a desired antibody immune response, Affiris wants to streamline
its processes and control timelines more aggressively. One bottleneck common
in preclinical stages is the detailed analysis of a large amount of high
content images. In the project the challenge was automating high content
image analysis of histological slides of mouse brains. Crucial factors were
the batch processing and job scheduling capabilities of the Definiens
software which enable efficient processing of files larger than 1 GB.
Definiens' automated image analysis will not only help Affiris to reduce
costs and save its scientific personnel time, but the results will also be
more objective compared to a manual approach.
PEPTIDE-BASED VACCINES AGAINST ALZHEIMER'S DISEASE
In November 2007 Affiris attracted public attention, when it was granted a
European-wide patent for key elements of its Alzheimer's disease vaccination
strategy. The hallmark of Alzheimer's disease are deposits of aggregated
beta-amyloid peptide in the brain. Beta-amyloid is removed from larger
precursor protein by the body's own enzymes, in healthy as well as afflicted
persons. It is generally believed however, that in Alzheimer's disease the
regulation of this removal is disturbed, leading to higher amounts and/or
more aggregation-prone species of beta-amyloid. AFFITOPETM vaccines,
invented and produced by Affiris, are modified beta-amyloid-like peptides
which elicit an immune response against the aggregation-prone beta-amyloid,
but not against the physiological precursor protein. One such vaccine is
currently undergoing clinical tests, while others are still in the
preclinical stage.
Dr. Markus Mandler, Head of Neurodegeneration Department at Affiris, said
"The Definiens Enterprise Image Intelligence Suite is an open platform that
can be easily integrated with the existing hardware as well as image
acquisition devices and software. It enables even untrained users to
calibrate and execute versatile image analysis workflows. Thanks to the
user-friendliness of the platform and the excellent support provided by
Definiens, the implementation process will be very short and the technology
is expected to become part of our work routine as early as February 2008."
About AFFiRiS
AFFiRiS GmbH develops peptide-based vaccines for the treatment of
Alzheimer's disease, atherosclerosis and other serious diseases. The company
has established its AFFITOME platform technologies. It employs 30 highly
qualified members of staff on 600 sqm of rented laboratory facilities at the
Campus Vienna Biocenter (affiris).
AFFITOPE and AFFITOME are registered trademarks of Affiris GmbH.
Definiens in Life Sciences
By automating image analysis on an enterprise level, Definiens supports Life
Science organizations to analyze and interpret vast numbers of images
accurately and consistently. Definiens improves the measurement of cell
assays, the examination of tissue samples and the interpretation of
non-invasive imaging, enabling high-content screening, digital pathology and
translational medicine.
About Definiens
Definiens is the number one Enterprise Image Intelligence company for
analyzing and interpreting images on every scale, from microscopic cell
structures to satellite images. The Definiens Cognition Network Technology®,
developed by Nobel laureate Prof. Gerd Binnig and his team, is an advanced
and robust context-based technology designed to fulfill the image analysis
requirements of the Life and Earth sciences markets. The technology is
modeled on the powerful human cognitive perception processes to extract
intelligence from images. Definiens provides organizations with faster image
analysis results, allowing deeper insights enabling better business
decisions. The company is headquartered in Munich, Germany and has offices
throughout the United States. Further information is available at
definiens
Definiens, Definiens Cellenger, Definiens Cognition Network Technology,
Definiens eCognition, Enterprise Image Intelligence and Understanding Images
are trademarks or registered trademarks of Definiens.
announced today that it will integrate the Definiens Enterprise Image
Intelligence (TM) Suite in the company's Alzheimer's disease vaccination
program. The decision was based on the company's outstanding experience with
Definiens software. Affiris' business strategy focuses on rapid
identification of drug candidates and accelerated preclinical and clinical
development. Matching Affiris requirements comprehensively, Definiens
provides automated image analysis solutions with reliable, fast and
consistent results.
DEFINIENS ?¬ UNPARALLELED IMAGE ANALYSIS COUPLED WITH TIME AND COST SAVING
In order to launch its new AFFITOPETM vaccines, which facilitate the
induction of a desired antibody immune response, Affiris wants to streamline
its processes and control timelines more aggressively. One bottleneck common
in preclinical stages is the detailed analysis of a large amount of high
content images. In the project the challenge was automating high content
image analysis of histological slides of mouse brains. Crucial factors were
the batch processing and job scheduling capabilities of the Definiens
software which enable efficient processing of files larger than 1 GB.
Definiens' automated image analysis will not only help Affiris to reduce
costs and save its scientific personnel time, but the results will also be
more objective compared to a manual approach.
PEPTIDE-BASED VACCINES AGAINST ALZHEIMER'S DISEASE
In November 2007 Affiris attracted public attention, when it was granted a
European-wide patent for key elements of its Alzheimer's disease vaccination
strategy. The hallmark of Alzheimer's disease are deposits of aggregated
beta-amyloid peptide in the brain. Beta-amyloid is removed from larger
precursor protein by the body's own enzymes, in healthy as well as afflicted
persons. It is generally believed however, that in Alzheimer's disease the
regulation of this removal is disturbed, leading to higher amounts and/or
more aggregation-prone species of beta-amyloid. AFFITOPETM vaccines,
invented and produced by Affiris, are modified beta-amyloid-like peptides
which elicit an immune response against the aggregation-prone beta-amyloid,
but not against the physiological precursor protein. One such vaccine is
currently undergoing clinical tests, while others are still in the
preclinical stage.
Dr. Markus Mandler, Head of Neurodegeneration Department at Affiris, said
"The Definiens Enterprise Image Intelligence Suite is an open platform that
can be easily integrated with the existing hardware as well as image
acquisition devices and software. It enables even untrained users to
calibrate and execute versatile image analysis workflows. Thanks to the
user-friendliness of the platform and the excellent support provided by
Definiens, the implementation process will be very short and the technology
is expected to become part of our work routine as early as February 2008."
About AFFiRiS
AFFiRiS GmbH develops peptide-based vaccines for the treatment of
Alzheimer's disease, atherosclerosis and other serious diseases. The company
has established its AFFITOME platform technologies. It employs 30 highly
qualified members of staff on 600 sqm of rented laboratory facilities at the
Campus Vienna Biocenter (affiris).
AFFITOPE and AFFITOME are registered trademarks of Affiris GmbH.
Definiens in Life Sciences
By automating image analysis on an enterprise level, Definiens supports Life
Science organizations to analyze and interpret vast numbers of images
accurately and consistently. Definiens improves the measurement of cell
assays, the examination of tissue samples and the interpretation of
non-invasive imaging, enabling high-content screening, digital pathology and
translational medicine.
About Definiens
Definiens is the number one Enterprise Image Intelligence company for
analyzing and interpreting images on every scale, from microscopic cell
structures to satellite images. The Definiens Cognition Network Technology®,
developed by Nobel laureate Prof. Gerd Binnig and his team, is an advanced
and robust context-based technology designed to fulfill the image analysis
requirements of the Life and Earth sciences markets. The technology is
modeled on the powerful human cognitive perception processes to extract
intelligence from images. Definiens provides organizations with faster image
analysis results, allowing deeper insights enabling better business
decisions. The company is headquartered in Munich, Germany and has offices
throughout the United States. Further information is available at
definiens
Definiens, Definiens Cellenger, Definiens Cognition Network Technology,
Definiens eCognition, Enterprise Image Intelligence and Understanding Images
are trademarks or registered trademarks of Definiens.
New Imaging Tool Could Eventually Lead To Earlier Detection Of Alzheimer's Disease Among Pre-Symptomatic Individuals
A family history of Alzheimer's is one of the biggest risk factors for developing the memory-robbing disease, which affects more than 5 million Americans and is the most common form of senile dementia. Now an international collaboration led by NYU Langone Medical Center researchers has found the likely basis for this heightened familial risk - especially from the maternal side.
Aided by a new version of a brain scanning technique, the researchers discovered a far greater number of protein clumps linked to the disease among healthy adult children of parents with Alzheimer's compared to counterparts with no family history of dementia. The average increase in these clumps, called amyloid-beta plaques, was particularly striking among study volunteers whose mothers had been diagnosed with the disease. The plaques appeared throughout most regions of the brain.
The study examined 42 healthy individuals, including 14 whose mothers had Alzheimer's, 14 whose fathers had Alzheimer's, and 14 counterparts with no family history of the disease. On average, the first group of volunteers showed a 15 percent higher burden of amyloid-beta deposits than those with a paternal family history, and a 20 percent higher burden of the protein clumps than those with no familial risk factors.
The new findings, published in the March 15, 2010, online early edition of Proceedings of the National Academy of Sciences, may help explain why a family history is such a big risk factor for the brain disease - individuals with an affected parent have a four- to ten-fold greater risk than those with no family history.
The study was led by Lisa Mosconi, PhD, research assistant professor of psychiatry at NYU Langone, and colleagues at NYU Langone who collaborated with researchers at the University of Turku in Finland and Weill Cornell Medical Center in New York.
"Given that brain pathology begins to accumulate years ahead of memory problems in Alzheimer's disease, our findings are intriguing," says Dr. Mosconi. "There is a great effort underway to find early markers of disease, before symptoms appear, so that therapeutic approaches will one day delay or ultimately prevent this disease."
Amyloid plaques are one of the hallmarks of Alzheimer's disease, although not everyone with plaques develops the disease. For many years, amyloid-beta plaques could only be measured in autopsied brains, but methods have recently emerged that allow the plaques to be observed in living brains.
The new study combines positron emission tomography (PET) with a fluorescent dye called Pittsburgh Compound B (PiB) that highlights brain amyloid plaques, enabling researchers to actually see the deposits. The dye attaches to plaques and acts like a temporary beacon to highlight their presence during a PET scan. Dr. Mosconi cautions that her team's imaging technique is a potentially powerful research tool and is not ready for use as a diagnostic tool in the clinic.
Plaques begin forming in the brain when, for unknown reasons, normal amyloid-beta proteins change their shape and structure and begin sticking together. The presence of plaques, however, does not necessarily mean an individual will develop Alzheimer's, and much of the harm may arrive well before the plaques appear - no one can yet say whether they are a cause or a consequence of the disease.
It isn't known why the deposits were more common among children of parents with the disease in the study, but Dr. Mosconi suspects that a genetic mechanism is involved. "At this point, we can only speculate that genes that are transmitted from parents, particularly mothers, to their children lead to amyloid depositions, which increase risk for developing dementia," she says.
Dr. Mosconi and her colleagues hope to follow the study's 42 volunteers and more subjects over time to analyze the link between plaque formation and Alzheimer's. For those who never develop dementia, she likewise hopes to determine what preventive factors may be neutralizing the bad effects of amyloid on the brain.
The scanning technique used in the new study also provides more evidence supporting a maternal family link to Alzheimer's, notes Dr. Mosconi, whose previous studies have shown such an association based on reduced glucose metabolism in the brains of healthy adults whose mothers had the disease.
"This imaging study further anchors the risk for Alzheimer's disease associated with having a mother affected by the disease," says Mony J. de Leon, EdD, professor of psychiatry and Director of the Center for Brain Health at NYU Langone Medical Center, and one of the study's authors.
The study's co-authors include Yi Li, Huiyu Wang, John Murray, Schantel Williams, Lidia Glodzik, Wai Tsui and Susan De Santi from NYU Langone Medical Center; Juha Rinne and Noora Scheinin from the University of Turku; Kjell N??gren from Turku and Odense University Hospital, Denmark; and Shankar Vallabhajosula from Weill Cornell Medical College.
The study was supported by grants from the National Institutes of Health's National Institute on Aging and National Center for Research Resources, the Alzheimer's Association, the Academy of Finland, the Sigrid Juselius Foundation, and Turku University Hospital. New York.
Source:
Lorinda Klein
NYU Langone Medical Center / New York University School of Medicine
Aided by a new version of a brain scanning technique, the researchers discovered a far greater number of protein clumps linked to the disease among healthy adult children of parents with Alzheimer's compared to counterparts with no family history of dementia. The average increase in these clumps, called amyloid-beta plaques, was particularly striking among study volunteers whose mothers had been diagnosed with the disease. The plaques appeared throughout most regions of the brain.
The study examined 42 healthy individuals, including 14 whose mothers had Alzheimer's, 14 whose fathers had Alzheimer's, and 14 counterparts with no family history of the disease. On average, the first group of volunteers showed a 15 percent higher burden of amyloid-beta deposits than those with a paternal family history, and a 20 percent higher burden of the protein clumps than those with no familial risk factors.
The new findings, published in the March 15, 2010, online early edition of Proceedings of the National Academy of Sciences, may help explain why a family history is such a big risk factor for the brain disease - individuals with an affected parent have a four- to ten-fold greater risk than those with no family history.
The study was led by Lisa Mosconi, PhD, research assistant professor of psychiatry at NYU Langone, and colleagues at NYU Langone who collaborated with researchers at the University of Turku in Finland and Weill Cornell Medical Center in New York.
"Given that brain pathology begins to accumulate years ahead of memory problems in Alzheimer's disease, our findings are intriguing," says Dr. Mosconi. "There is a great effort underway to find early markers of disease, before symptoms appear, so that therapeutic approaches will one day delay or ultimately prevent this disease."
Amyloid plaques are one of the hallmarks of Alzheimer's disease, although not everyone with plaques develops the disease. For many years, amyloid-beta plaques could only be measured in autopsied brains, but methods have recently emerged that allow the plaques to be observed in living brains.
The new study combines positron emission tomography (PET) with a fluorescent dye called Pittsburgh Compound B (PiB) that highlights brain amyloid plaques, enabling researchers to actually see the deposits. The dye attaches to plaques and acts like a temporary beacon to highlight their presence during a PET scan. Dr. Mosconi cautions that her team's imaging technique is a potentially powerful research tool and is not ready for use as a diagnostic tool in the clinic.
Plaques begin forming in the brain when, for unknown reasons, normal amyloid-beta proteins change their shape and structure and begin sticking together. The presence of plaques, however, does not necessarily mean an individual will develop Alzheimer's, and much of the harm may arrive well before the plaques appear - no one can yet say whether they are a cause or a consequence of the disease.
It isn't known why the deposits were more common among children of parents with the disease in the study, but Dr. Mosconi suspects that a genetic mechanism is involved. "At this point, we can only speculate that genes that are transmitted from parents, particularly mothers, to their children lead to amyloid depositions, which increase risk for developing dementia," she says.
Dr. Mosconi and her colleagues hope to follow the study's 42 volunteers and more subjects over time to analyze the link between plaque formation and Alzheimer's. For those who never develop dementia, she likewise hopes to determine what preventive factors may be neutralizing the bad effects of amyloid on the brain.
The scanning technique used in the new study also provides more evidence supporting a maternal family link to Alzheimer's, notes Dr. Mosconi, whose previous studies have shown such an association based on reduced glucose metabolism in the brains of healthy adults whose mothers had the disease.
"This imaging study further anchors the risk for Alzheimer's disease associated with having a mother affected by the disease," says Mony J. de Leon, EdD, professor of psychiatry and Director of the Center for Brain Health at NYU Langone Medical Center, and one of the study's authors.
The study's co-authors include Yi Li, Huiyu Wang, John Murray, Schantel Williams, Lidia Glodzik, Wai Tsui and Susan De Santi from NYU Langone Medical Center; Juha Rinne and Noora Scheinin from the University of Turku; Kjell N??gren from Turku and Odense University Hospital, Denmark; and Shankar Vallabhajosula from Weill Cornell Medical College.
The study was supported by grants from the National Institutes of Health's National Institute on Aging and National Center for Research Resources, the Alzheimer's Association, the Academy of Finland, the Sigrid Juselius Foundation, and Turku University Hospital. New York.
Source:
Lorinda Klein
NYU Langone Medical Center / New York University School of Medicine
среда, 25 мая 2011 г.
Amyloid Aggregations And Tau Pathology Reflected By Cortical Thickness In The Default Network Of MCI And AD
Alzheimer's disease patients show a relentless decline in memory over the course of the disease, which is accompanied by both brain atrophy and by characteristic deposits in the brain tissue called amyloid plaques and neurofibrillary tangles. Researchers from the Chinese Academy of Sciences studied a large database, collected in the US, of patients with Alzheimer's or memory complaints who had MRI scans and had spinal taps to collect cerebrospinal fluid, which is in the brain and spinal chord. By examining the CFS they could measure the amounts of the substances that make p plaques and tangles, and related this to brain atrophy. They found that the amount of plaque and tangle-producing chemicals in the cerebrospinal fluid correlated with brain tissue loss in selective regions of the brain which are typically affected in Alzheimer's disease. The brains in these regions had thinned out suggesting that brain cells had died. These regions are important for memory and are typically active when the brain is at rest. Using these techniques may ultimately help identify early markers of disease in Alzheimer's, potentially indicating who is likely to develop Alzheimer's before memory loss is critical.
Authors: J Jiang, S Wang, X Zhen, Z Yao, C Xu, T Jiang, AD NI3 LIAMA Center for Computational Medicine, National Laboratory of Pattern Recognition, Institute of Automation, Chinese Academy of Sciences, 100190, Beijing, China
Source: Organization for Human Brain Mapping
Authors: J Jiang, S Wang, X Zhen, Z Yao, C Xu, T Jiang, AD NI3 LIAMA Center for Computational Medicine, National Laboratory of Pattern Recognition, Institute of Automation, Chinese Academy of Sciences, 100190, Beijing, China
Source: Organization for Human Brain Mapping
вторник, 24 мая 2011 г.
Moderate Drinking May Boost Memory, Study Suggests
In the long run, a drink or two a day may be good for the brain.
Researchers found that moderate amounts of alcohol - amounts equivalent to a couple of drinks a day for a human - improved the memories of laboratory rats.
Such a finding may have implications for serious neurodegenerative diseases like Alzheimer's, said Matthew During, the study's senior author and a professor of molecular virology, immunology and cancer genetics at Ohio State University .
"There is some evidence suggesting that mild to moderate alcohol consumption can protect against diseases like Alzheimer's in humans," said During. "But it's not apparent how this happens."
He and his colleague, Margaret Kalev-Zylinska, a postdoctoral researcher at the University of Auckland, in New Zealand, uncovered a neuronal mechanism that may help explain the link between alcohol and improved memory.
"We saw a noticeable change on the surface of certain neurons in rats that were given alcohol," During said. "This change may have something to do with the positive effects of alcohol on memory."
The researchers presented their findings at the annual Society for Neuroscience conference in Atlanta.
During and Kalev-Zylinska designed a special liquid diet for the rats. One formulation included a low dose of alcohol, comparable to two or three drinks a day for a human, while the other diet included a much higher dose of alcohol, comparable to six or seven drinks a day for a human. A third group of rats was given a liquid diet without alcohol. All animals were given their respective diets daily for about four weeks.
The researchers measured the rats' blood-alcohol levels three times throughout the study. Toward the end of the study, they subjected the rats to two different memory tasks.
For the first task, the rats were given several minutes to examine two identical, square plastic objects. After a certain amount of time, a researcher replaced one of the objects with a new, round object made of glass. The researchers measured the amount of time that each rat spent checking out the new object - an indication that the animal recognizes it as a new object.
Rats given low doses of alcohol spent about three times longer examining the new object than did rats on the alcohol-free diet. Rats given the high dose of alcohol spent equivalent amounts of time checking out both objects, suggesting that they were unable to differentiate the old object from the new one.
For the second task rats were placed in a box with two chambers separated by a door. One chamber was well-lit, while the adjacent chamber was dark. After placing a rat in the well-lit chamber and then lifting the door, the researchers timed how quickly the rats entered the dark chamber (rats are nocturnal, and naturally prefer dark spaces.) Once inside the dark chamber, the rat received a mild electric shock to its feet.
The researchers repeated this same experiment 24 hours later, and kept track of how long it took the animal to enter the dark chamber. Many of the animals re-entered the dark area, yet the rats given alcohol waited anywhere from 2.5 to 4.5 times longer to enter the dark chamber than did the animals given the alcohol-free diet.
"The results suggest that both doses of alcohol moderately improved the animals' ability to remember this negative event, since they seemed hesitant to go into the dark area," During said. "It also suggests that high levels of alcohol can reinforce bad memories.
"People who drink to forget bad memories may actually be doing the opposite by reinforcing the neural circuits that control negative emotional memory," he continued.
At the end of the study, the researchers analyzed brain and liver tissue from each animal.
They found that low levels of alcohol increased the expression of a particular receptor, NR1, on the surface of neurons in a region of the brain, the hippocampus, that plays a role in memory. Researchers think that NR1 plays a role in memory and learning.
In a separate set of experiments, During and Kalev-Zylinska increased the number of NR1 receptors in another group of rats, and found that this boost improved the animals' memories to an extent similar to the improvement seen in the rats given low doses of alcohol. They also they used a new gene transfer technique to knock down the NR1 receptors in a group of rats given alcohol - alcohol had no memory-enhancing effects on these animals.
"These experiments suggest that the effect of alcohol works through the NR1 receptor, at least where memory and learning are concerned," During said.
"We didn't see any toxic effects of low-level alcohol consumption on the brain or the liver," During said. "It didn't damage neurons nor did it cause liver damage during the short study. But the higher dose of alcohol damaged both."
Written by Holly Wagner
Contact: Matthew During
Ohio State University
Researchers found that moderate amounts of alcohol - amounts equivalent to a couple of drinks a day for a human - improved the memories of laboratory rats.
Such a finding may have implications for serious neurodegenerative diseases like Alzheimer's, said Matthew During, the study's senior author and a professor of molecular virology, immunology and cancer genetics at Ohio State University .
"There is some evidence suggesting that mild to moderate alcohol consumption can protect against diseases like Alzheimer's in humans," said During. "But it's not apparent how this happens."
He and his colleague, Margaret Kalev-Zylinska, a postdoctoral researcher at the University of Auckland, in New Zealand, uncovered a neuronal mechanism that may help explain the link between alcohol and improved memory.
"We saw a noticeable change on the surface of certain neurons in rats that were given alcohol," During said. "This change may have something to do with the positive effects of alcohol on memory."
The researchers presented their findings at the annual Society for Neuroscience conference in Atlanta.
During and Kalev-Zylinska designed a special liquid diet for the rats. One formulation included a low dose of alcohol, comparable to two or three drinks a day for a human, while the other diet included a much higher dose of alcohol, comparable to six or seven drinks a day for a human. A third group of rats was given a liquid diet without alcohol. All animals were given their respective diets daily for about four weeks.
The researchers measured the rats' blood-alcohol levels three times throughout the study. Toward the end of the study, they subjected the rats to two different memory tasks.
For the first task, the rats were given several minutes to examine two identical, square plastic objects. After a certain amount of time, a researcher replaced one of the objects with a new, round object made of glass. The researchers measured the amount of time that each rat spent checking out the new object - an indication that the animal recognizes it as a new object.
Rats given low doses of alcohol spent about three times longer examining the new object than did rats on the alcohol-free diet. Rats given the high dose of alcohol spent equivalent amounts of time checking out both objects, suggesting that they were unable to differentiate the old object from the new one.
For the second task rats were placed in a box with two chambers separated by a door. One chamber was well-lit, while the adjacent chamber was dark. After placing a rat in the well-lit chamber and then lifting the door, the researchers timed how quickly the rats entered the dark chamber (rats are nocturnal, and naturally prefer dark spaces.) Once inside the dark chamber, the rat received a mild electric shock to its feet.
The researchers repeated this same experiment 24 hours later, and kept track of how long it took the animal to enter the dark chamber. Many of the animals re-entered the dark area, yet the rats given alcohol waited anywhere from 2.5 to 4.5 times longer to enter the dark chamber than did the animals given the alcohol-free diet.
"The results suggest that both doses of alcohol moderately improved the animals' ability to remember this negative event, since they seemed hesitant to go into the dark area," During said. "It also suggests that high levels of alcohol can reinforce bad memories.
"People who drink to forget bad memories may actually be doing the opposite by reinforcing the neural circuits that control negative emotional memory," he continued.
At the end of the study, the researchers analyzed brain and liver tissue from each animal.
They found that low levels of alcohol increased the expression of a particular receptor, NR1, on the surface of neurons in a region of the brain, the hippocampus, that plays a role in memory. Researchers think that NR1 plays a role in memory and learning.
In a separate set of experiments, During and Kalev-Zylinska increased the number of NR1 receptors in another group of rats, and found that this boost improved the animals' memories to an extent similar to the improvement seen in the rats given low doses of alcohol. They also they used a new gene transfer technique to knock down the NR1 receptors in a group of rats given alcohol - alcohol had no memory-enhancing effects on these animals.
"These experiments suggest that the effect of alcohol works through the NR1 receptor, at least where memory and learning are concerned," During said.
"We didn't see any toxic effects of low-level alcohol consumption on the brain or the liver," During said. "It didn't damage neurons nor did it cause liver damage during the short study. But the higher dose of alcohol damaged both."
Written by Holly Wagner
Contact: Matthew During
Ohio State University
понедельник, 23 мая 2011 г.
Dementia Research Funding To Be Prioritised, UK
Dementia research is being prioritised from March, Paul Burstow, the Care Services Minister, will announce.
The Minister will say that he wants more of the billion pound research budget to be spent on dementia research. He is speaking at an event of more than 350 researchers and professionals. The announcement is the first action to come out of the Ministerial Advisory Group on Dementia Research.
Alzheimer's Society comment:
'Dementia research is desperately underfunded so it is encouraging to hear that bids for dementia researchers will be prioritised. We now need to see these promises become a reality. 750,000 people in the UK have a form of dementia. In just 15 years a million people will be living with the condition. The dementia research budget must rise if we are to move forward in our understanding of this devastating condition.'
Dr Susanne Sorensen
Head of Research
Source:
Alzheimer's Society
The Minister will say that he wants more of the billion pound research budget to be spent on dementia research. He is speaking at an event of more than 350 researchers and professionals. The announcement is the first action to come out of the Ministerial Advisory Group on Dementia Research.
Alzheimer's Society comment:
'Dementia research is desperately underfunded so it is encouraging to hear that bids for dementia researchers will be prioritised. We now need to see these promises become a reality. 750,000 people in the UK have a form of dementia. In just 15 years a million people will be living with the condition. The dementia research budget must rise if we are to move forward in our understanding of this devastating condition.'
Dr Susanne Sorensen
Head of Research
Source:
Alzheimer's Society
воскресенье, 22 мая 2011 г.
Typing This Headline Could Be Difficult If You Have Rheumatoid Arthritis
Joint damage caused by rheumatoid arthritis can lead to difficulties in typing and can force people to seek alternative but potentially more destructive ways of putting their fingers to the keyboard, according to research presented this week at the American College of Rheumatology Annual Scientific Meeting in Atlanta.
Rheumatoid arthritis is a chronic disease that causes pain, stiffness, swelling, and limitation in the motion and function of multiple joints. Though joints are the principal body parts affected by RA, inflammation can develop in other organs as well. An estimated 1.3 million Americans have RA, and the disease typically affects women twice as often as men.
People who suffer from RA often experience work limitations. In fact, without adequate treatment, 60 percent of people with RA are unable to work 10 years after the onset of their disease. The U.S. Census Bureau reports that nearly 215,000 professionals are employed as typists. For those with RA whose work depends on touch typing typing based on knowing the location of keys on a keyboard, rather than using sight to find the keys understanding the mechanism of hand motions during touch typing may provide insight into how people with RA can safely and efficiently type.
In a study funded in part by the ACR Research and Education Foundation, researchers recently set out to determine the effects of structural deformities on the postures and motions of the hands and wrists during touch typing. They hypothesized that touch typists with structural deformities caused by RA would have significantly different typing postures, motions and speeds than those without structural deformities. They studied 33 participants with RA to determine if their hypothesis would hold true.
Researchers videotaped each participant and studied their postures and motions while typing. Additionally, each participant's video was rated by a certified hand therapist for the presence of visual structural deformities damage to varying joints, which causes a visible change in the shape of the hand. Finally, typing postures and motions were rated by two raters trained in the use of the Keyboard-Personal Computer Style Instrument an observational instrument that documents postures and actions of keyboard users.
The 22 participants with structural deformities were compared to those without. Researchers found that participants with structural deformities due to RA showed more whole hand and wrist motion commonly called the 'hunt-and-peck' method of typing than those without (64 percent) structural deformities. These participants used this style of typing to activate the keys rather than individual finger motions. Finally, researchers found that significantly fewer participants with structural deformities used a wrist support, and there was no significant difference in typing speed between the two groups of participants.
Based on these findings, researchers concluded that structural deformities can affect the typing styles of touch typists with RA. Moreover, biomechanical research that examines the degree to which different postures and actions increase or reduce mechanical stress on joints suggests that alternative typing strategies such as the hunt and-peck style, floating the wrists, using fewer fingers, and keeping fingers straight rather than curved may increase existing problems by putting additional stress on already affected joints.
"This research suggests that as people develop changes in the structures of their joints, they may find alternative ways to accomplish tasks," says Nancy Baker, ScD, MPH, OTR/L; associate professor at the University of Pittsburgh and lead investigator in the study. "The alternative methods are often to change their physical performance; for example they may slow down, change their postures, or move differently. While changing their performance may allow the continuance of doing the task, it may place them at risk for other problems. Thus, touch typists with joint damage may shift to techniques that place biomechanical stress on their already weakened joints."
For touch typists with RA, researchers offer alternative suggestions to ensure proper working hand and wrist posture including using an ergonomic keyboard and moveable wrist support and/or redesigning your computer workstation to better suit your individual typing needs.
"While altering tasks is almost certainly necessary in any disease or injury that causes physical changes, there are ways to make changes that are less likely to place a person at risk," says Dr. Baker. "It is often better to change the environment to support the person doing the task than it is to change the performance itself.
Occupational therapists are experts in the identification of safe and effective alternative methods to perform daily tasks and can help people with limitations to develop the method that best suits their needs. Providing access to occupational therapists may allow people with diseases like RA to identify and implement strategies that can keep them at work and at play and living life to the fullest."
Source: American College of Rheumatology (ACR)
Rheumatoid arthritis is a chronic disease that causes pain, stiffness, swelling, and limitation in the motion and function of multiple joints. Though joints are the principal body parts affected by RA, inflammation can develop in other organs as well. An estimated 1.3 million Americans have RA, and the disease typically affects women twice as often as men.
People who suffer from RA often experience work limitations. In fact, without adequate treatment, 60 percent of people with RA are unable to work 10 years after the onset of their disease. The U.S. Census Bureau reports that nearly 215,000 professionals are employed as typists. For those with RA whose work depends on touch typing typing based on knowing the location of keys on a keyboard, rather than using sight to find the keys understanding the mechanism of hand motions during touch typing may provide insight into how people with RA can safely and efficiently type.
In a study funded in part by the ACR Research and Education Foundation, researchers recently set out to determine the effects of structural deformities on the postures and motions of the hands and wrists during touch typing. They hypothesized that touch typists with structural deformities caused by RA would have significantly different typing postures, motions and speeds than those without structural deformities. They studied 33 participants with RA to determine if their hypothesis would hold true.
Researchers videotaped each participant and studied their postures and motions while typing. Additionally, each participant's video was rated by a certified hand therapist for the presence of visual structural deformities damage to varying joints, which causes a visible change in the shape of the hand. Finally, typing postures and motions were rated by two raters trained in the use of the Keyboard-Personal Computer Style Instrument an observational instrument that documents postures and actions of keyboard users.
The 22 participants with structural deformities were compared to those without. Researchers found that participants with structural deformities due to RA showed more whole hand and wrist motion commonly called the 'hunt-and-peck' method of typing than those without (64 percent) structural deformities. These participants used this style of typing to activate the keys rather than individual finger motions. Finally, researchers found that significantly fewer participants with structural deformities used a wrist support, and there was no significant difference in typing speed between the two groups of participants.
Based on these findings, researchers concluded that structural deformities can affect the typing styles of touch typists with RA. Moreover, biomechanical research that examines the degree to which different postures and actions increase or reduce mechanical stress on joints suggests that alternative typing strategies such as the hunt and-peck style, floating the wrists, using fewer fingers, and keeping fingers straight rather than curved may increase existing problems by putting additional stress on already affected joints.
"This research suggests that as people develop changes in the structures of their joints, they may find alternative ways to accomplish tasks," says Nancy Baker, ScD, MPH, OTR/L; associate professor at the University of Pittsburgh and lead investigator in the study. "The alternative methods are often to change their physical performance; for example they may slow down, change their postures, or move differently. While changing their performance may allow the continuance of doing the task, it may place them at risk for other problems. Thus, touch typists with joint damage may shift to techniques that place biomechanical stress on their already weakened joints."
For touch typists with RA, researchers offer alternative suggestions to ensure proper working hand and wrist posture including using an ergonomic keyboard and moveable wrist support and/or redesigning your computer workstation to better suit your individual typing needs.
"While altering tasks is almost certainly necessary in any disease or injury that causes physical changes, there are ways to make changes that are less likely to place a person at risk," says Dr. Baker. "It is often better to change the environment to support the person doing the task than it is to change the performance itself.
Occupational therapists are experts in the identification of safe and effective alternative methods to perform daily tasks and can help people with limitations to develop the method that best suits their needs. Providing access to occupational therapists may allow people with diseases like RA to identify and implement strategies that can keep them at work and at play and living life to the fullest."
Source: American College of Rheumatology (ACR)
суббота, 21 мая 2011 г.
Possible Alzheimer's Disease Marker Discovered In Rare Genotype
Researchers at Banner Health's Sun Health Research Institute have uncovered evidence that Alzheimer's disease (AD) may be clinically confirmed in patients with apolipoprotein E2 homozygote. The results of their study are published in the January 2009 issue of the Journal of Alzheimer's Disease.
Apolipoprotein E2 homozygote has been associated with a protective effect against AD and contributes to delaying the onset of symptoms. However previously, no significant data had pointed to clinically confirmed AD in persons with apolipoprotein E2 homozygote. The reverse is true of apolipoprotein E4. Previous studies have confirmed that apolipoprotein E4 is a predictive risk factor for AD and indicates an increased genetic risk of AD.
Clinical confirmation of the apolipoprotein E2 homozygote Alzheimer's disease finding in this study was confirmed by MRI, PET and neuropsychological evaluation and testing. AD pathology is yet to be determined and will occur at post mortem.
"Clinical diagnosis of possible AD has now become extremely accurate and is especially helpful to physicians looking for the best outcomes in treating patients," says Marwan Sabbagh, MD, Sun Health Research Institute's chief medical/scientific officer and lead investigator of the study.
"This study may hold many clues to the nature of how Alzheimer's genetics work. Although clinically rare, the information gleaned in this study allows us to ask new questions and possibly answer others," says Sabbagh.
The article is "Possible Alzheimer's Disease in an Apolipoprotein E2 Homozygote" by Ignat Ignatov, Christine Belden, Sandra Jacobson, Donald Connor and Marwan N. Sabbagh. It is published in the Journal of Alzheimer's Disease 16:1 (January 2008).
Source: Astrid Engelen
IOS Press
Apolipoprotein E2 homozygote has been associated with a protective effect against AD and contributes to delaying the onset of symptoms. However previously, no significant data had pointed to clinically confirmed AD in persons with apolipoprotein E2 homozygote. The reverse is true of apolipoprotein E4. Previous studies have confirmed that apolipoprotein E4 is a predictive risk factor for AD and indicates an increased genetic risk of AD.
Clinical confirmation of the apolipoprotein E2 homozygote Alzheimer's disease finding in this study was confirmed by MRI, PET and neuropsychological evaluation and testing. AD pathology is yet to be determined and will occur at post mortem.
"Clinical diagnosis of possible AD has now become extremely accurate and is especially helpful to physicians looking for the best outcomes in treating patients," says Marwan Sabbagh, MD, Sun Health Research Institute's chief medical/scientific officer and lead investigator of the study.
"This study may hold many clues to the nature of how Alzheimer's genetics work. Although clinically rare, the information gleaned in this study allows us to ask new questions and possibly answer others," says Sabbagh.
The article is "Possible Alzheimer's Disease in an Apolipoprotein E2 Homozygote" by Ignat Ignatov, Christine Belden, Sandra Jacobson, Donald Connor and Marwan N. Sabbagh. It is published in the Journal of Alzheimer's Disease 16:1 (January 2008).
Source: Astrid Engelen
IOS Press
пятница, 20 мая 2011 г.
Interactions Of Three Proteins Might Disrupt Neural Network In Alzheimer's
Though the cause of Alzheimer's disease still is unknown, recent studies have implicated three proteins strongly in its onset. New research from the University of Alabama at Birmingham, the Gladstone Institutes and the Baylor College of Medicine indicates that interactions between those three proteins might lead to brain dysfunction and AD in a mouse model of the disease.
"There has been growing interest in 'network dysfunction' as a cause of AD," said Erik Roberson, M.D., Ph.D., assistant professor in the Departments of Neurology and Neurobiology at UAB and lead author of the study. "Rather than thinking about individual cells dying, we are thinking about abnormalities in the way groups of neurons fire together as a cause of cognitive impairment in AD.
"Currently, we only have a few drugs to treat Alzheimer's disease, and those do not have dramatic effects in most patients," said Roberson. "It is exciting to me that our results might point to a new direction for developing drugs to treat this dreaded disease."
The three proteins are amyloid beta (A??), tau, and Fyn. A?? collects into aggregates in the brains of AD patients. These A?? plaques are a pathologic hallmark of AD and smaller complexes of A?? are considered a primary cause of memory dysfunction in the disease. Fyn is an enzyme that regulates other proteins by adding small phosphate chemical groups to them. Fyn cooperates with A?? to increase cognitive deficits in mice. The protein tau makes up part of the "skeleton" of the cell and aggregates into tangles in the brains of AD patients.
The research team used mice that were engineered genetically to produce large amounts of A?? or A?? plus Fyn in the brain. These mouse models replicate many symptoms of AD. They then used genetics to determine whether or not reducing tau levels might have beneficial effects in the mice. The results of the study were published in the Jan. 12, 2011, issue of the Journal of Neuroscience.
Previous studies have shown that AD mice have abnormal, seizure-like discharges during which many neurons fire at the same time. The findings indicate that tau reduction blocks this network dysfunction.
"We show, by putting an electrode into individual cells in the network, that neurons affected by A?? have an imbalance between the excitatory and inhibitory input onto the cells they are still getting excitatory input, but the inhibitory input is greatly reduced," said Roberson. "This may be why the neurons are all firing together abnormally. Tau reduction blocked this excitation/inhibition imbalance, which probably is how it corrects the network dysfunction."
"These results show how three proteins work together to disrupt signaling that occurs between brain cells to form our memories," said Lennart Mucke M.D., director of the Gladstone Institute of Neurological Disease and senior author on the study. "We might be able to develop therapies to disrupt this problematic relationship and benefit patients."
Previous studies by the authors showed that reducing levels of tau prevents the cognitive deficits in AD mice. In the present study, the scientists showed that reducing tau levels also prevented cognitive deficits due to the combined effects of A?? and Fyn. They also found that reducing tau prevented the disruption of connections between neurons in the brain that allow us to store memories and normalized the firing patterns of neurons, and that the frequent epileptic-like events in AD mice did not occur when tau levels were reduced.
Also contributing to the study were Brian Halabisky, Jinghua Yao, Jeannie Chin, Fengrong Yan, Tiffany Wu, Patricia Hamto, Nino Devidze, Gui-Qui Yu, and Jorge J. Palop of Gladstone Institutes, and Jong W. Yoo and Jeffrey L. Noebels of Baylor College of Medicine.
The study was supported by the Stephen Bechtel Fund and the National Institutes of Health.
Source: University of Alabama at Birmingham
"There has been growing interest in 'network dysfunction' as a cause of AD," said Erik Roberson, M.D., Ph.D., assistant professor in the Departments of Neurology and Neurobiology at UAB and lead author of the study. "Rather than thinking about individual cells dying, we are thinking about abnormalities in the way groups of neurons fire together as a cause of cognitive impairment in AD.
"Currently, we only have a few drugs to treat Alzheimer's disease, and those do not have dramatic effects in most patients," said Roberson. "It is exciting to me that our results might point to a new direction for developing drugs to treat this dreaded disease."
The three proteins are amyloid beta (A??), tau, and Fyn. A?? collects into aggregates in the brains of AD patients. These A?? plaques are a pathologic hallmark of AD and smaller complexes of A?? are considered a primary cause of memory dysfunction in the disease. Fyn is an enzyme that regulates other proteins by adding small phosphate chemical groups to them. Fyn cooperates with A?? to increase cognitive deficits in mice. The protein tau makes up part of the "skeleton" of the cell and aggregates into tangles in the brains of AD patients.
The research team used mice that were engineered genetically to produce large amounts of A?? or A?? plus Fyn in the brain. These mouse models replicate many symptoms of AD. They then used genetics to determine whether or not reducing tau levels might have beneficial effects in the mice. The results of the study were published in the Jan. 12, 2011, issue of the Journal of Neuroscience.
Previous studies have shown that AD mice have abnormal, seizure-like discharges during which many neurons fire at the same time. The findings indicate that tau reduction blocks this network dysfunction.
"We show, by putting an electrode into individual cells in the network, that neurons affected by A?? have an imbalance between the excitatory and inhibitory input onto the cells they are still getting excitatory input, but the inhibitory input is greatly reduced," said Roberson. "This may be why the neurons are all firing together abnormally. Tau reduction blocked this excitation/inhibition imbalance, which probably is how it corrects the network dysfunction."
"These results show how three proteins work together to disrupt signaling that occurs between brain cells to form our memories," said Lennart Mucke M.D., director of the Gladstone Institute of Neurological Disease and senior author on the study. "We might be able to develop therapies to disrupt this problematic relationship and benefit patients."
Previous studies by the authors showed that reducing levels of tau prevents the cognitive deficits in AD mice. In the present study, the scientists showed that reducing tau levels also prevented cognitive deficits due to the combined effects of A?? and Fyn. They also found that reducing tau prevented the disruption of connections between neurons in the brain that allow us to store memories and normalized the firing patterns of neurons, and that the frequent epileptic-like events in AD mice did not occur when tau levels were reduced.
Also contributing to the study were Brian Halabisky, Jinghua Yao, Jeannie Chin, Fengrong Yan, Tiffany Wu, Patricia Hamto, Nino Devidze, Gui-Qui Yu, and Jorge J. Palop of Gladstone Institutes, and Jong W. Yoo and Jeffrey L. Noebels of Baylor College of Medicine.
The study was supported by the Stephen Bechtel Fund and the National Institutes of Health.
Source: University of Alabama at Birmingham
четверг, 19 мая 2011 г.
Families Say Healthsense's ENeighbor(R) Remote Monitoring System Helps Keep Relatives With Alzheimer's Safe At Home And Out Of Memory Care
Families in Ohio and Pennsylvania who use Healthsense's state-of-the-art eNeighbor® remote monitoring to help care for elderly relatives with Alzheimer's disease or dementia say the technology has enabled them to keep their loved ones safe at home for longer and delay placing them permanently in secured memory care units. They also credit the Healthsense technology with improving their own quality of life by helping relieve the stress and strain of tending to seniors with Alzheimer's or dementia.
"Without the eNeighbor system, I honestly don't think my mother would still be able to live at home with us," said Mary White, who has used the Healthsense technology for about a year in her Toledo, Ohio residence to help care for her 88-year-old mother, who has Alzheimer's. "She does so much better here with me than in a nursing home. She eats better. She exercises more. She has more company here. It also gives me peace of mind. Before, I couldn't even go out to the mailbox to get the mail without worrying that she might open a door and wander off."
An estimated 5.3 million Americans have Alzheimer's disease, the most frequent cause of dementia and the seventh leading cause of death, according to the Alzheimer's Association. As the baby boomer population ages, the number of people aged 65 and older with Alzheimer's is expected to reach 7.7 million in 2030 and between 11 million and 16 million by 2050. The Alzheimer's Association estimates that as many as 10 million people, including family members, currently provide unpaid care for individuals with Alzheimer's.
Developed with grants from the National Institutes of Aging (NIA) and the Defense Advanced Research Projects Agency (DARPA), the eNeighbor system is built around a set of battery-operated Wi-Fi sensors placed in private homes or senior living residences to monitor residents' daily living activities and wellness. These sensors include pressure sensors in beds to detect when a resident gets in or out of bed; motion detectors on walls to detect movement or inactivity; toilet sensors to monitor toilet usage; contact sensors on kitchen cupboards and refrigerator doors to monitor whether the resident is eating regularly; and door sensors that alert when the resident tries to leave the residence or enter potentially hazardous areas, such as stairways. eNeighbor's "smart" operating system uses algorithms to analyze the sensor data and determine whether the resident requires assistance. The system automatically issues assistive prompts or alerts via any phone when the data indicate help is needed. Information and reports can also be accessed from a secure web portal.
White has several sensors installed in the upstairs portion of her home where her mother lives. A motion sensor by the stairs alerts her via a call to her cordless home phone if her mother attempts to come downstairs at any time between 9 p.m. and 9 a.m. And if her mother gets up at night to go to the bathroom, the system (including a bed sensor and motion sensors) alerts White if she has not returned to her bed within 10 minutes. Downstairs, the side, front and back doors are all installed with sensors that alert if they're opened between the hours of 9 a.m. and 9 p.m. A pressure sensor on her mother's chair also notifies White whenever her mother gets out of the chair during daylight hours.
"I'm able to get a lot more sleep now," said White. "Before I had the Healthsense technology installed, I'd always have to sleep with one ear open. It was the same in the daytime. I had to make sure my house was locked at all times. I couldn't even go out into the yard. I was running back and forth all the time, exhausting myself, worrying that she'd get out into the street. Now, it's a lot safer for her and it's such a relief to me. I feel good that I'm able to take care of her here in my own home."
Eleanor Watts, also a Toledo, Ohio resident, has used the eNeighbor technology in her home for more than a year to help care for her 66-year-old husband, who has Alzheimer's. The sensor in his bed alerts her via the home phone whenever he gets up. "It has freed me up so much, especially in summer," she said. "I can take my phone now and go and do some gardening in the back yard. Before, I was trapped in the living room. I had to be close enough to hear him, because I never knew when he would get up. The technology has really opened up my world. I feel it will definitely help keep him at home with me for longer. It's a great boon for the caregiver."
Adrienne Briggs, a Philadelphia resident whose 70-year-old mother came to live with her two years ago after she was diagnosed with dementia, began using the eNeighbor system 20 months ago. In addition to bed, motion and door sensors, her system is also set up to alert her if her mother does not return to bed at night within 10 minutes after getting up to use the bathroom. "The eNeighbor technology has definitely helped keep my mom out of a nursing home, and it has given me peace of mind, knowing that she is being monitored at night when I'm asleep," said Briggs. "Before, I was never really able to go into a deep sleep, because I would always be listening out for her."
"More and more families are telling us that the eNeighbor system has helped prolong the time that their loved ones with Alzheimer's or dementia are able to live at home with them," said Brian Bischoff, President and CEO of Healthsense. "This is a significant quality-of-life benefit not only for the caregivers but also for the patients, because once they are admitted to memory care, they permanently give up whatever remaining level of independence they may still enjoy. There are also important financial implications. The longer a patient's passage to higher acuity care can be postponed, the less costly it is for families, patients, providers and payors."
White and Watts are participants in a NIA-funded two-year research project titled "Impact of Monitoring Technology on Family Caregivers" currently underway at Miami University in Oxford, Ohio. The project is directed by Jennifer M. Kinney, Ph.D., professor of gerontology and research fellow of the Scripps Gerontology Center (SGC) and Cary S. Kart, Ph.D., senior researcher with the SGC. Briggs's mother receives her eNeighbor system through NewCourtland, a leading non-profit provider of community services, housing and nursing homes in Philadelphia. Mary White and Eleanor Watts are pseudonyms, used to protect the privacy of the research study participants.
Source
Healthsense
"Without the eNeighbor system, I honestly don't think my mother would still be able to live at home with us," said Mary White, who has used the Healthsense technology for about a year in her Toledo, Ohio residence to help care for her 88-year-old mother, who has Alzheimer's. "She does so much better here with me than in a nursing home. She eats better. She exercises more. She has more company here. It also gives me peace of mind. Before, I couldn't even go out to the mailbox to get the mail without worrying that she might open a door and wander off."
An estimated 5.3 million Americans have Alzheimer's disease, the most frequent cause of dementia and the seventh leading cause of death, according to the Alzheimer's Association. As the baby boomer population ages, the number of people aged 65 and older with Alzheimer's is expected to reach 7.7 million in 2030 and between 11 million and 16 million by 2050. The Alzheimer's Association estimates that as many as 10 million people, including family members, currently provide unpaid care for individuals with Alzheimer's.
Developed with grants from the National Institutes of Aging (NIA) and the Defense Advanced Research Projects Agency (DARPA), the eNeighbor system is built around a set of battery-operated Wi-Fi sensors placed in private homes or senior living residences to monitor residents' daily living activities and wellness. These sensors include pressure sensors in beds to detect when a resident gets in or out of bed; motion detectors on walls to detect movement or inactivity; toilet sensors to monitor toilet usage; contact sensors on kitchen cupboards and refrigerator doors to monitor whether the resident is eating regularly; and door sensors that alert when the resident tries to leave the residence or enter potentially hazardous areas, such as stairways. eNeighbor's "smart" operating system uses algorithms to analyze the sensor data and determine whether the resident requires assistance. The system automatically issues assistive prompts or alerts via any phone when the data indicate help is needed. Information and reports can also be accessed from a secure web portal.
White has several sensors installed in the upstairs portion of her home where her mother lives. A motion sensor by the stairs alerts her via a call to her cordless home phone if her mother attempts to come downstairs at any time between 9 p.m. and 9 a.m. And if her mother gets up at night to go to the bathroom, the system (including a bed sensor and motion sensors) alerts White if she has not returned to her bed within 10 minutes. Downstairs, the side, front and back doors are all installed with sensors that alert if they're opened between the hours of 9 a.m. and 9 p.m. A pressure sensor on her mother's chair also notifies White whenever her mother gets out of the chair during daylight hours.
"I'm able to get a lot more sleep now," said White. "Before I had the Healthsense technology installed, I'd always have to sleep with one ear open. It was the same in the daytime. I had to make sure my house was locked at all times. I couldn't even go out into the yard. I was running back and forth all the time, exhausting myself, worrying that she'd get out into the street. Now, it's a lot safer for her and it's such a relief to me. I feel good that I'm able to take care of her here in my own home."
Eleanor Watts, also a Toledo, Ohio resident, has used the eNeighbor technology in her home for more than a year to help care for her 66-year-old husband, who has Alzheimer's. The sensor in his bed alerts her via the home phone whenever he gets up. "It has freed me up so much, especially in summer," she said. "I can take my phone now and go and do some gardening in the back yard. Before, I was trapped in the living room. I had to be close enough to hear him, because I never knew when he would get up. The technology has really opened up my world. I feel it will definitely help keep him at home with me for longer. It's a great boon for the caregiver."
Adrienne Briggs, a Philadelphia resident whose 70-year-old mother came to live with her two years ago after she was diagnosed with dementia, began using the eNeighbor system 20 months ago. In addition to bed, motion and door sensors, her system is also set up to alert her if her mother does not return to bed at night within 10 minutes after getting up to use the bathroom. "The eNeighbor technology has definitely helped keep my mom out of a nursing home, and it has given me peace of mind, knowing that she is being monitored at night when I'm asleep," said Briggs. "Before, I was never really able to go into a deep sleep, because I would always be listening out for her."
"More and more families are telling us that the eNeighbor system has helped prolong the time that their loved ones with Alzheimer's or dementia are able to live at home with them," said Brian Bischoff, President and CEO of Healthsense. "This is a significant quality-of-life benefit not only for the caregivers but also for the patients, because once they are admitted to memory care, they permanently give up whatever remaining level of independence they may still enjoy. There are also important financial implications. The longer a patient's passage to higher acuity care can be postponed, the less costly it is for families, patients, providers and payors."
White and Watts are participants in a NIA-funded two-year research project titled "Impact of Monitoring Technology on Family Caregivers" currently underway at Miami University in Oxford, Ohio. The project is directed by Jennifer M. Kinney, Ph.D., professor of gerontology and research fellow of the Scripps Gerontology Center (SGC) and Cary S. Kart, Ph.D., senior researcher with the SGC. Briggs's mother receives her eNeighbor system through NewCourtland, a leading non-profit provider of community services, housing and nursing homes in Philadelphia. Mary White and Eleanor Watts are pseudonyms, used to protect the privacy of the research study participants.
Source
Healthsense
среда, 18 мая 2011 г.
Dementia Mysteries Unveiled By Largest Ever Alzheimer's Gene Study
The results, from the largest ever Alzheimer's genome-wide association study (GWAS) involving 16,000 individuals, are published in Nature Genetics. They are the first new genes found to be associated with the common form of Alzheimer's disease since 1993.
The Alzheimer's Research Trust spoke of "a leap forward for dementia research", the MRC's Sir Leszek Borysiewicz praised "a huge step towards achieving an earlier diagnosis of Alzheimer's", and the Welsh First Minister Rhodri Morgan hailed the Cardiff-led study as "a real feather in the cap of Welsh science".
The study was funded by the Wellcome Trust, Medical Research Council, Alzheimer's Research Trust and Welsh Assembly Government among others. The UK-led research involved scientists from universities in Cardiff, London, Cambridge, Nottingham, Southampton, Manchester, Oxford, Bristol and Belfast, who collaborated with Irish, German, Belgian, Greek and American institutions.
Previously only one gene, APOE4, had been associated with Alzheimer's disease. This study reveals two further genes, CLU and PICALM, are related to the disease. This is expected to provide scientists with a much clearer route to developing new treatments.
The paper's lead-author, Prof Julie Williams, Chief Scientific Adviser to the Alzheimer's Research Trust, said: "Both CLU and PICALM highlight new pathways that lead to Alzheimer's disease. The CLU gene produces clusterin which normally acts to protect the brain in a variety of ways. Variation in this gene could remove this protection and contribute to Alzheimer's development. PICALM is important at synapses - connections between brain cells - and is involved in the transport of molecules into and inside of nerve cells, helping form memories and other brain functions. We know that the health of synapses is closely related to memory performance in Alzheimer's disease, thus changes in genes which affect synapses are likely to have a direct effect on disease development."
"This research is changing our understanding of what causes the common form of Alzheimer's disease and provides valuable new leads in the race to find treatments and possibly cures."
"It also shows that other genes can be identified using this method, and the group are already planning a larger study involving 60,000 people, which can be achieved within the next year."
Rebecca Wood, Chief Executive of the Alzheimer's Research Trust, which part-funded the study, said: "These findings are a leap forward for dementia research. At a time when we are yet to find ways of halting this devastating condition, this development is likely to spark off numerous new ideas, collaborations and more in the race for a cure.
"The work of Professor Williams and colleagues shows how British researchers lead the world in the struggle to understand and defeat dementia. With the right support for scientists, we can offer hope to the 30 million people worldwide who live with dementia.
The First Minister for Wales, Rhodri Morgan, said: "This major breakthrough in the battle to understand and develop treatments for Alzheimer's is good news for the 37,000 people in Wales and their carers who are affected by Alzheimer's or other forms of dementia. It is a real feather in the cap of Welsh science that this important global study has been led by a Welsh scientist, Professor Julie Williams and that the Welsh Assembly Government was able to give financial support for her work. World-class research like this will help lead to improved treatment for this distressing disease, and may one day even mean we can cure dementia."
Sir Leszek Borysiewicz, Chief Executive of the Medical Research Council, said: "Funding work on neurodegenerative diseases is a priority for us and MRC investment in this kind of innovative research is crucial in piecing together the Alzheimer's puzzle. This study is a huge step towards achieving an earlier diagnosis of Alzheimer's and improving the lives of the many people affected by the disease."
The team shared their data with a further French-led study, also published in Nature Genetics, which has revealed compelling evidence for a third gene associated with Alzheimer's called CR1.
The only other genes that have been connected to Alzheimer's disease are in extremely rare cases of familial Alzheimer's disease, which is inherited in less than 1% of cases.
"It's possible that in diabetic patients, the signal to turn this gene on and off might be impaired. But we might be able to use one of the other pathways to turn it on," he said.
Source:
Andrew Scheuber
Alzheimer's Research Trust
The Alzheimer's Research Trust spoke of "a leap forward for dementia research", the MRC's Sir Leszek Borysiewicz praised "a huge step towards achieving an earlier diagnosis of Alzheimer's", and the Welsh First Minister Rhodri Morgan hailed the Cardiff-led study as "a real feather in the cap of Welsh science".
The study was funded by the Wellcome Trust, Medical Research Council, Alzheimer's Research Trust and Welsh Assembly Government among others. The UK-led research involved scientists from universities in Cardiff, London, Cambridge, Nottingham, Southampton, Manchester, Oxford, Bristol and Belfast, who collaborated with Irish, German, Belgian, Greek and American institutions.
Previously only one gene, APOE4, had been associated with Alzheimer's disease. This study reveals two further genes, CLU and PICALM, are related to the disease. This is expected to provide scientists with a much clearer route to developing new treatments.
The paper's lead-author, Prof Julie Williams, Chief Scientific Adviser to the Alzheimer's Research Trust, said: "Both CLU and PICALM highlight new pathways that lead to Alzheimer's disease. The CLU gene produces clusterin which normally acts to protect the brain in a variety of ways. Variation in this gene could remove this protection and contribute to Alzheimer's development. PICALM is important at synapses - connections between brain cells - and is involved in the transport of molecules into and inside of nerve cells, helping form memories and other brain functions. We know that the health of synapses is closely related to memory performance in Alzheimer's disease, thus changes in genes which affect synapses are likely to have a direct effect on disease development."
"This research is changing our understanding of what causes the common form of Alzheimer's disease and provides valuable new leads in the race to find treatments and possibly cures."
"It also shows that other genes can be identified using this method, and the group are already planning a larger study involving 60,000 people, which can be achieved within the next year."
Rebecca Wood, Chief Executive of the Alzheimer's Research Trust, which part-funded the study, said: "These findings are a leap forward for dementia research. At a time when we are yet to find ways of halting this devastating condition, this development is likely to spark off numerous new ideas, collaborations and more in the race for a cure.
"The work of Professor Williams and colleagues shows how British researchers lead the world in the struggle to understand and defeat dementia. With the right support for scientists, we can offer hope to the 30 million people worldwide who live with dementia.
The First Minister for Wales, Rhodri Morgan, said: "This major breakthrough in the battle to understand and develop treatments for Alzheimer's is good news for the 37,000 people in Wales and their carers who are affected by Alzheimer's or other forms of dementia. It is a real feather in the cap of Welsh science that this important global study has been led by a Welsh scientist, Professor Julie Williams and that the Welsh Assembly Government was able to give financial support for her work. World-class research like this will help lead to improved treatment for this distressing disease, and may one day even mean we can cure dementia."
Sir Leszek Borysiewicz, Chief Executive of the Medical Research Council, said: "Funding work on neurodegenerative diseases is a priority for us and MRC investment in this kind of innovative research is crucial in piecing together the Alzheimer's puzzle. This study is a huge step towards achieving an earlier diagnosis of Alzheimer's and improving the lives of the many people affected by the disease."
The team shared their data with a further French-led study, also published in Nature Genetics, which has revealed compelling evidence for a third gene associated with Alzheimer's called CR1.
The only other genes that have been connected to Alzheimer's disease are in extremely rare cases of familial Alzheimer's disease, which is inherited in less than 1% of cases.
"It's possible that in diabetic patients, the signal to turn this gene on and off might be impaired. But we might be able to use one of the other pathways to turn it on," he said.
Source:
Andrew Scheuber
Alzheimer's Research Trust
вторник, 17 мая 2011 г.
Tau-induced Memory Loss In Alzheimer's Mice Is Reversible
Amyloid-beta and tau protein deposits in the brain are characteristic features of Alzheimer disease. The effect on the hippocampus, the area of the brain that plays a central role in learning and memory, is particularly severe. However, it appears that the toxic effect of tau protein is largely eliminated when the corresponding tau gene is switched off. Researchers from the Max Planck Research Unit for Structural Molecular Biology at DESY in Hamburg have succeeded in demonstrating that once the gene is deactivated, mice with a human tau gene, which previously presented symptoms of dementia, regain their ability to learn and remember, and that the synapses of the mice also reappear in part. The scientists are now testing active substances to prevent the formation of tau deposits in mice. This may help to reverse memory loss in the early stages of Alzheimer disease in part, at least.
Whereas aggregated amyloid-beta protein forms insoluble clumps between the neurons, the tau protein accumulates inside them. Tau protein stabilises the tube-shaped fibers of the cytoskeleton, known as microtubules, which provide the "rails" for cellular transport. In Alzheimer disease, excess phosphate groups cause the tau protein to malfunction and form clumps (the 'neurofibrillary tangles'). As a result, nutrient transport breaks down and the neurons and their synapses die off. This process is accompanied by the initial stage of memory loss.
Together with colleagues from Leuven, Hamburg and Erlangen, Eva and Eckhard Mandelkow's team from the Max Planck Research Unit for Structural Molecular Biology generated regulatable transgenic mice with two different human tau gene variants that can be switched on and off again: one group was given a form of the protein that cannot become entangled (anti-aggregant), and a second was provided with the code for the strongly aggregating protein variant (pro-aggregant). The mice with the first form developed no Alzheimer symptoms; the rodents that were given the pro-aggregant tau developed the disease.
The scientists measured the mice's memory loss with the help of a swimming test: the healthy mice quickly learn how to find a life-saving platform located under the surface of the water in a water basin. In contrast, the transgenic animals, which have the additional pro-aggregant tau gene paddle aimlessly around the basin until they accidentally stumble on the platform; they require over four times more time to do this than their healthy counterparts. However, if the mutated toxic tau gene is switched off again, the mice learn to reach "dry land" with ease just a few weeks later. As a control, the mice with the anti-aggregant form of tau have no defects in learning, just as normal non-transgenic mice.
Surprising tissue results
Tissue tests showed that, as expected, no tau clumps had formed in the brains of the first group of mice expressing anti-aggregant tau. In the second group the mice suffering from Alzheimer's co-aggregates from human tau and "mouse tau" were formed against expectations, because tau protein from mice does not usually aggregate. "Even more astonishingly, weeks after the additional gene had been switched off, the aggregated human tau had dissolved again. However, the 'mouse tau' remained clumped. Despite this, the mice were able to learn and remember again," says Eckhard Mandelkow. More precise tests revealed that new synapses had actually formed in their brains.
The scientists concluded from this that mutated or pathological tau can alter healthy tau. It appears that pro-aggregant tau can act similar to a crystal nucleus once it has started to clump up, it drags neighboring "healthy" tau into the clumps as well. This is what makes the process so toxic to the neurons. "The really important discovery here, however, is that the progression of Alzheimer's disease can be reversed in principle - at least at an early stage of the illness before too many neurons have been destroyed," explains Eva Mandelkow who, together with her husband, will be awarded the Potamkin Prize 2011 for Alzheimer's disease research, which is sponsored by the American Academy of Neurology.
The aggregation of tau proteins, however, cannot simply be switched off in humans the way it can in the transgenic mice. Nevertheless, special substances exist that could dissolve the tau aggregates. By screening 200,000 substances, the Hamburg researchers have already identified several classes of active substances that could re-convert the tau aggregates into soluble tau. These are now being tested on animals.
Sources: Max-Planck-Gesellschaft, AlphaGalileo Foundation.
Whereas aggregated amyloid-beta protein forms insoluble clumps between the neurons, the tau protein accumulates inside them. Tau protein stabilises the tube-shaped fibers of the cytoskeleton, known as microtubules, which provide the "rails" for cellular transport. In Alzheimer disease, excess phosphate groups cause the tau protein to malfunction and form clumps (the 'neurofibrillary tangles'). As a result, nutrient transport breaks down and the neurons and their synapses die off. This process is accompanied by the initial stage of memory loss.
Together with colleagues from Leuven, Hamburg and Erlangen, Eva and Eckhard Mandelkow's team from the Max Planck Research Unit for Structural Molecular Biology generated regulatable transgenic mice with two different human tau gene variants that can be switched on and off again: one group was given a form of the protein that cannot become entangled (anti-aggregant), and a second was provided with the code for the strongly aggregating protein variant (pro-aggregant). The mice with the first form developed no Alzheimer symptoms; the rodents that were given the pro-aggregant tau developed the disease.
The scientists measured the mice's memory loss with the help of a swimming test: the healthy mice quickly learn how to find a life-saving platform located under the surface of the water in a water basin. In contrast, the transgenic animals, which have the additional pro-aggregant tau gene paddle aimlessly around the basin until they accidentally stumble on the platform; they require over four times more time to do this than their healthy counterparts. However, if the mutated toxic tau gene is switched off again, the mice learn to reach "dry land" with ease just a few weeks later. As a control, the mice with the anti-aggregant form of tau have no defects in learning, just as normal non-transgenic mice.
Surprising tissue results
Tissue tests showed that, as expected, no tau clumps had formed in the brains of the first group of mice expressing anti-aggregant tau. In the second group the mice suffering from Alzheimer's co-aggregates from human tau and "mouse tau" were formed against expectations, because tau protein from mice does not usually aggregate. "Even more astonishingly, weeks after the additional gene had been switched off, the aggregated human tau had dissolved again. However, the 'mouse tau' remained clumped. Despite this, the mice were able to learn and remember again," says Eckhard Mandelkow. More precise tests revealed that new synapses had actually formed in their brains.
The scientists concluded from this that mutated or pathological tau can alter healthy tau. It appears that pro-aggregant tau can act similar to a crystal nucleus once it has started to clump up, it drags neighboring "healthy" tau into the clumps as well. This is what makes the process so toxic to the neurons. "The really important discovery here, however, is that the progression of Alzheimer's disease can be reversed in principle - at least at an early stage of the illness before too many neurons have been destroyed," explains Eva Mandelkow who, together with her husband, will be awarded the Potamkin Prize 2011 for Alzheimer's disease research, which is sponsored by the American Academy of Neurology.
The aggregation of tau proteins, however, cannot simply be switched off in humans the way it can in the transgenic mice. Nevertheless, special substances exist that could dissolve the tau aggregates. By screening 200,000 substances, the Hamburg researchers have already identified several classes of active substances that could re-convert the tau aggregates into soluble tau. These are now being tested on animals.
Sources: Max-Planck-Gesellschaft, AlphaGalileo Foundation.
понедельник, 16 мая 2011 г.
New Survey Reveals Nearly Two Thirds Of People Think They Are Not Very Well Informed About The Early Signs Of Alzheimer's Disease And Dementia, UK
With an estimated 700,000 people in the UK suffering from some form of dementia and an ageing UK population, a new YouGov survey highlights a lack of public awareness regarding Alzheimer's disease and dementia.
When respondents were asked how well informed they are about the early symptoms of Alzheimer's disease or dementia, 66% were either not very well informed or not informed at all. Only 5% considered themselves very well informed1.
When asked for the most likely reasons that somebody might not encourage their relative to seek medical advice for their memory loss, 62% percent of people said that the reason would be because they think that memory loss is a natural part of ageing. Other reasons cited were2:
- They would not wish to worry their family (28%)
- They lack sufficient knowledge about memory loss (24%)
- They would not consider memory loss to be a serious medical problem (20%)
- They would not want to bother the GP (10%)
The survey also looked at what worries people most about old age. From a list of questions, respondents cited their concerns as being2.
- Not having the independence to look after oneself (30%)
- Losing a partner or loved one (29%)
- Not being financially secure (25%)
- Having to go into a nursing home (8%)
- Having to live with your children or family (1%)
To coincide with the results of this survey, the 'Worried about your MEMORY?' Alzheimer's disease awareness roadshow will be starting its tour of the UK from 2nd October until 3rd November visiting ten UK cities. The roadshow will offer materials about Alzheimer's disease to the general public and dementia-specialist nurses will be available to offer advice to anyone with concerns or queries.
Dr David Wilkinson, Consultant in Old Age Psychiatry at Moorgreen Hospital, Southampton said, "Whilst we all become more forgetful as we get older memory loss can be an early sign of Alzheimer's disease and if we delay getting it assessed it may mean patients only come for help when things have already deteriorated.
"There are very clear distinctions between what is normal memory loss and what isn't. Forgetting the name of a friend, politician or actor is normal. Not being able to retain new information, not being able to learn and so becoming very repetitive is not, and when that is the case people should seek help early to gain the maximum help from available treatments and support. There is a real need to raise awareness of Alzheimer's disease so that people know what signs to look out for and where they can go to seek help and advice."
About the YouGov survey
Research was conducted online by YouGov Plc between 4th and 6th September 2007. YouGov interviewed a sample of 2,178 GB adults. Results have been weighted to be representative of the GB adult population. YouGov is a member of the British Polling Council. Survey commissioned by Eisai Limited and Pfizer Limited.
Founded in May 2000, YouGov is a professional market research agency pioneering the use of the Internet and information technology to collect higher-quality in-depth data for market research and public consultation. YouGov pro-actively recruits respondents from all ages, socio economic groups and regions of Britain. The sample for each survey is carefully selected and controlled so that it is representative of the adult population as a whole - or the specific audience that the survey is designed to measure.
About the 'Worried about your MEMORY?' roadshow
This roadshow has been initiated and funded by Eisai Limited and Pfizer Limited. Both Eisai Limited and Pfizer Limited are committed to ongoing disease awareness activities across a variety of therapeutic areas. Permission to use the Worried About Your Memory branding kindly granted courtesy of the Alzheimer's Society. Alzheimer's Society materials will be available on the roadshow.
Roadshow dates and locations:
1. Tues 2 & Weds 3 October: Broadmead Podium, Bristol, BS1 3DX
2. Fri 5 & Sat 6 October: St John's Street, Cardiff town centre, CF10 1GL
3. Tues 9 & Weds 10 October: High Street, North End, Croydon, CR0 1YE
4. Fri 12 & Sat 13 October: Terminus Road, Eastbourne, BN21 3AP
5. Tues 16 & Weds 17 October: Amphitheatre Space, Norwich, NR2 1TF
6. Fri 19 & Sat 20 October: Victoria Square, Town Hall, Birmingham Town Centre, B1 1BB
7. Mon 22 & Tues 23 October: Market Square, Nottingham, NG1 2DT
8. Fri 26 & Sat 27 October: Northumberland Street, Newcastle, NE1 7AL
9. Tues 30 & Weds 31 October: Piccadilly Gardens, Manchester, M1 1LZ
10. Fri 2 & Sat 3 November: Main gates outside City Hall, Belfast, BT1 5GS
About Eisai
Eisai is a research-based human health care (hhc) company that discovers, develops and markets products throughout the world. Eisai focuses its efforts in two therapeutic areas: Integrative Neuroscience including neuroscience, neurology and psychiatric medicine and Integrative Oncology including oncotherapy and supportive-care treatment. Through a global network of research facilities, manufacturing sites and marketing subsidiaries, Eisai actively participates in all aspects of the worldwide health care system. Eisai employs more than 9,000 people worldwide. For more information please visit Eisai or Eisai.co.jp
About Pfizer
Pfizer Inc, the world's largest research-based pharmaceutical company, discovers, develops, manufactures and markets prescription medicines in 9 therapeutic areas. Pfizer is also the world's largest animal health company.
Pfizer Inc employs approximately 105,000 colleagues worldwide, all of whom are devoted to working for a healthier world. Pfizer conducts more biomedical research than any other corporation, and has 14,000 professionals working in R&D sites worldwide, including Sandwich in Kent. Pfizer's research investment in 2005 was more than $7.4 billion. In the UK, Pfizer Ltd has its UK business headquarters in Surrey and is the major supplier of medicines to the NHS.
References
Knapp et al. (2007) Dementia UK: Report to the Alzheimer's Society, King's College London and the London School of Economics and Political Science
2 YouGov survey. yougov. September 2007
pfizer/
When respondents were asked how well informed they are about the early symptoms of Alzheimer's disease or dementia, 66% were either not very well informed or not informed at all. Only 5% considered themselves very well informed1.
When asked for the most likely reasons that somebody might not encourage their relative to seek medical advice for their memory loss, 62% percent of people said that the reason would be because they think that memory loss is a natural part of ageing. Other reasons cited were2:
- They would not wish to worry their family (28%)
- They lack sufficient knowledge about memory loss (24%)
- They would not consider memory loss to be a serious medical problem (20%)
- They would not want to bother the GP (10%)
The survey also looked at what worries people most about old age. From a list of questions, respondents cited their concerns as being2.
- Not having the independence to look after oneself (30%)
- Losing a partner or loved one (29%)
- Not being financially secure (25%)
- Having to go into a nursing home (8%)
- Having to live with your children or family (1%)
To coincide with the results of this survey, the 'Worried about your MEMORY?' Alzheimer's disease awareness roadshow will be starting its tour of the UK from 2nd October until 3rd November visiting ten UK cities. The roadshow will offer materials about Alzheimer's disease to the general public and dementia-specialist nurses will be available to offer advice to anyone with concerns or queries.
Dr David Wilkinson, Consultant in Old Age Psychiatry at Moorgreen Hospital, Southampton said, "Whilst we all become more forgetful as we get older memory loss can be an early sign of Alzheimer's disease and if we delay getting it assessed it may mean patients only come for help when things have already deteriorated.
"There are very clear distinctions between what is normal memory loss and what isn't. Forgetting the name of a friend, politician or actor is normal. Not being able to retain new information, not being able to learn and so becoming very repetitive is not, and when that is the case people should seek help early to gain the maximum help from available treatments and support. There is a real need to raise awareness of Alzheimer's disease so that people know what signs to look out for and where they can go to seek help and advice."
About the YouGov survey
Research was conducted online by YouGov Plc between 4th and 6th September 2007. YouGov interviewed a sample of 2,178 GB adults. Results have been weighted to be representative of the GB adult population. YouGov is a member of the British Polling Council. Survey commissioned by Eisai Limited and Pfizer Limited.
Founded in May 2000, YouGov is a professional market research agency pioneering the use of the Internet and information technology to collect higher-quality in-depth data for market research and public consultation. YouGov pro-actively recruits respondents from all ages, socio economic groups and regions of Britain. The sample for each survey is carefully selected and controlled so that it is representative of the adult population as a whole - or the specific audience that the survey is designed to measure.
About the 'Worried about your MEMORY?' roadshow
This roadshow has been initiated and funded by Eisai Limited and Pfizer Limited. Both Eisai Limited and Pfizer Limited are committed to ongoing disease awareness activities across a variety of therapeutic areas. Permission to use the Worried About Your Memory branding kindly granted courtesy of the Alzheimer's Society. Alzheimer's Society materials will be available on the roadshow.
Roadshow dates and locations:
1. Tues 2 & Weds 3 October: Broadmead Podium, Bristol, BS1 3DX
2. Fri 5 & Sat 6 October: St John's Street, Cardiff town centre, CF10 1GL
3. Tues 9 & Weds 10 October: High Street, North End, Croydon, CR0 1YE
4. Fri 12 & Sat 13 October: Terminus Road, Eastbourne, BN21 3AP
5. Tues 16 & Weds 17 October: Amphitheatre Space, Norwich, NR2 1TF
6. Fri 19 & Sat 20 October: Victoria Square, Town Hall, Birmingham Town Centre, B1 1BB
7. Mon 22 & Tues 23 October: Market Square, Nottingham, NG1 2DT
8. Fri 26 & Sat 27 October: Northumberland Street, Newcastle, NE1 7AL
9. Tues 30 & Weds 31 October: Piccadilly Gardens, Manchester, M1 1LZ
10. Fri 2 & Sat 3 November: Main gates outside City Hall, Belfast, BT1 5GS
About Eisai
Eisai is a research-based human health care (hhc) company that discovers, develops and markets products throughout the world. Eisai focuses its efforts in two therapeutic areas: Integrative Neuroscience including neuroscience, neurology and psychiatric medicine and Integrative Oncology including oncotherapy and supportive-care treatment. Through a global network of research facilities, manufacturing sites and marketing subsidiaries, Eisai actively participates in all aspects of the worldwide health care system. Eisai employs more than 9,000 people worldwide. For more information please visit Eisai or Eisai.co.jp
About Pfizer
Pfizer Inc, the world's largest research-based pharmaceutical company, discovers, develops, manufactures and markets prescription medicines in 9 therapeutic areas. Pfizer is also the world's largest animal health company.
Pfizer Inc employs approximately 105,000 colleagues worldwide, all of whom are devoted to working for a healthier world. Pfizer conducts more biomedical research than any other corporation, and has 14,000 professionals working in R&D sites worldwide, including Sandwich in Kent. Pfizer's research investment in 2005 was more than $7.4 billion. In the UK, Pfizer Ltd has its UK business headquarters in Surrey and is the major supplier of medicines to the NHS.
References
Knapp et al. (2007) Dementia UK: Report to the Alzheimer's Society, King's College London and the London School of Economics and Political Science
2 YouGov survey. yougov. September 2007
pfizer/
воскресенье, 15 мая 2011 г.
Regulate Anti Psychotic Drugs Now, UK
Help the Aged have backed an MPs bid to regulate the prescription of anti-psychotic drugs for people with dementia in care homes.
Lizzie McLennan, Policy Officer at Help the Aged said:
"Help the Aged supports David Taylor's bid to regulate the prescription of anti-psychotic drugs for people with dementia in care homes
"With approx 700,000 people living with dementia in the UK, and a large number of people with this illness cared for in general care homes, it's vital that all care home residents should have access to GPs who can diagnose dementia.
"All care homes should have a recognised expert on dementia working in the homes, and drug therapies should be closely monitored for continued effectiveness during the development of the condition.
"More than a million people are expected to have dementia by 2025. Help the Aged believe it is vital that staff in all care homes are equipped with the necessary skills to care effectively for people with dementia.
"General care staff and nurses need to have more detailed knowledge of dementia, along with its symptoms and the effect it has on individual behaviour."
Notes
Help the Aged is the charity fighting to free disadvantaged older people in the UK and overseas from poverty, isolation, neglect and ageism. It campaigns to raise public awareness of the issues affecting older people and to bring about policy change. The Charity delivers a range of services: information and advice, home support and community living, including international development work. These are supported by its paid-for services and fundraising activities - which aim to increase funding in the future to respond to the growing unmet needs of disadvantaged older people. Help the Aged also funds vital research into the health issues and experiences of older people to improve the quality of later life.
Help the Aged urgently needs donations and support to help it in the increasingly challenging fight to free disadvantaged older people from poverty, isolation and neglect.
Help the Aged
Lizzie McLennan, Policy Officer at Help the Aged said:
"Help the Aged supports David Taylor's bid to regulate the prescription of anti-psychotic drugs for people with dementia in care homes
"With approx 700,000 people living with dementia in the UK, and a large number of people with this illness cared for in general care homes, it's vital that all care home residents should have access to GPs who can diagnose dementia.
"All care homes should have a recognised expert on dementia working in the homes, and drug therapies should be closely monitored for continued effectiveness during the development of the condition.
"More than a million people are expected to have dementia by 2025. Help the Aged believe it is vital that staff in all care homes are equipped with the necessary skills to care effectively for people with dementia.
"General care staff and nurses need to have more detailed knowledge of dementia, along with its symptoms and the effect it has on individual behaviour."
Notes
Help the Aged is the charity fighting to free disadvantaged older people in the UK and overseas from poverty, isolation, neglect and ageism. It campaigns to raise public awareness of the issues affecting older people and to bring about policy change. The Charity delivers a range of services: information and advice, home support and community living, including international development work. These are supported by its paid-for services and fundraising activities - which aim to increase funding in the future to respond to the growing unmet needs of disadvantaged older people. Help the Aged also funds vital research into the health issues and experiences of older people to improve the quality of later life.
Help the Aged urgently needs donations and support to help it in the increasingly challenging fight to free disadvantaged older people from poverty, isolation and neglect.
Help the Aged
суббота, 14 мая 2011 г.
Hallmark Alzheimer's Disease Changes Found In Retinas Of Humans And Imaged In Live Animals
The nerve cell-damaging plaque that builds up in the brain with Alzheimer's disease also builds up in the retinas of the eyes - and it shows up there earlier, leading to the prospect that noninvasive optical imaging of the eyes could lead to earlier diagnosis, intervention and monitoring of the disease, according to new research.
Scientists discovered characteristic amyloid plaques in retinas from deceased Alzheimer's disease patients and used a noninvasive optical imaging technique to detect retinal plaques in live laboratory mice genetically modified to model the human disease. The combined results suggest the possibility that noninvasive retinal imaging may be helpful in early diagnosis of the disease.
The research was conducted by a team of scientists at Cedars-Sinai Medical Center in collaboration with colleagues from the Weizmann Institute of Science in Israel and the University of Southern California. Results were published online June 13 in the journal NeuroImage, and related findings will be presented July 13 at the Alzheimer's Association International Conference on Alzheimer's Disease.
Alzheimer's disease is a devastating condition that is becoming more prevalent worldwide as the baby-boom generation advances into its senior years, but there is no conclusive, noninvasive way to diagnose it. Previous studies have suggested that changes in the brain may begin years or even decades before symptoms occur - emphasizing the need for earlier, reliable detection for early therapeutic intervention to achieve effective remedy. The new study suggests the possibility of monitoring Alzheimer's disease through a simple retinal imaging approach.
Abnormal deposits in the brain called beta-amyloid plaques, which damage cells and interrupt cell-to-cell communications, are recognized as a hallmark sign of the disease. However, because existing noninvasive brain-imaging technologies cannot provide sufficient detail about these changes, the most definitive diagnosis of Alzheimer's disease comes after an autopsy.
The research team considered the retina a better target for noninvasive imaging of Alzheimer's disease because it is readily accessible and, unlike other components of the eye, it is part of the central nervous system, having a direct connection and thus many similarities with the brain. Previous studies have documented non-specific visual disturbances, eye disorders and certain types of retinal abnormalities occurring with Alzheimer's disease and other neurodegenerative conditions, but this is the first to identify human retinal plaque deposits that could provide a specific diagnostic marker of Alzheimer's disease.
Among the new findings:
1) In lab tests, plaques in the retinas of mice genetically modified to model Alzheimer's disease could be detected at a very early, pre-symptomatic stage - before the plaque appeared in the brain.
2) A high-resolution, noninvasive optical imaging approach was developed to monitor individual beta-amyloid plaques in the retinas of live mice. The system is based on a harmless specific marker and the adaptation of an existing optical system used to examine rodent eyes.
3) The research team used a fluorescent compound called curcumin to label and detect retinal plaques. This is believed to be the first use of curcumin as an imaging agent to detect Alzheimer's disease-related plaques in the retinas of live animals. Curcumin, a natural component of the spice turmeric, binds to beta-amyloid plaques and makes them visible when viewed microscopically. In the Cedars-Sinai research, curcumin injected into the bloodstream of live mice crossed the blood-retinal barrier and specifically bound to the retinal plaques, allowing them to be viewed in high resolution with a noninvasive procedure.
4) Observations from multiple genetically engineered mouse models of Alzheimer's disease demonstrated a correlation between retinal plaques and brain plaques as disease progressed.
v
5) In the laboratory mice, a unique immune system-based therapy that reduces the amount of plaques in the brain also reduced plaque load in the retina to the same extent, suggesting that the retina could faithfully represent the brain in assessing response to therapy.
6) Beta-amyloid plaques were identified in retinal samples from human patients who had died from Alzheimer's disease, and their features correlated with the diagnosed stage of the disease. Importantly, plaques were clearly detected not only in patients who definitely had the disease, but also in the retinas of some people who were suspected of having early-stage Alzheimer's disease based on clinical diagnosis and microscopic examination of brain tissue after death.
Together, the results offer the first evidence for the existence of Alzheimer's-specific plaques in the retina of human patients and the ability to detect individual plaques in live mouse models, creating a strong basis for future research building on these findings. According to the authors, these studies establish the potential of direct retinal beta-amyloid plaque imaging in live subjects as a tool for early Alzheimer's disease diagnosis and prognosis, as well as assessment of therapies.
Specialists in neurosurgery, ophthalmology, imaging systems, neuroimmunology, pathology, neurology and biomedical engineering collaborated on these studies, which were conducted at Cedars-Sinai Medical Center by scientists from Cedars-Sinai, the Weizmann Institute of Science in Israel, and the University of Southern California.
The journal article's first authors are Maya Koronyo-Hamaoui, Ph.D., a research scientist and assistant professor of neurosurgery at Cedars-Sinai's Maxine Dunitz Neurosurgical Institute and a principal investigator in the Neuroimmunology Laboratory at Cedars-Sinai; and Yosef Koronyo, M.Sc., LL.B., a research associate in the departments of Surgery and Neurosurgery at Cedars-Sinai. Senior authors are Michal Schwartz, Ph.D., visiting professor in the Department of Neurosurgery at Cedars-Sinai, and the Ilze and Maurice Professorial Chair of Neuroimmunology at the Weizmann Institute of Science in Rehovot, Israel; and Daniel L. Farkas, Ph.D., professor of surgery and biomedical sciences and director of the Minimally Invasive Surgical Technologies Institute at Cedars-Sinai.
The work was supported by the Marciano Family Foundation, the Maxine Dunitz Neurosurgical Institute, the U.S. Navy Bureau of Medicine and Surgery, the National Eye Institute, the Winnick Family Foundation, and a National Institute on Aging grant to the University of Southern California Alzheimer's Disease Research Center.
Source:
Cedars-Sinai Medical Center
Scientists discovered characteristic amyloid plaques in retinas from deceased Alzheimer's disease patients and used a noninvasive optical imaging technique to detect retinal plaques in live laboratory mice genetically modified to model the human disease. The combined results suggest the possibility that noninvasive retinal imaging may be helpful in early diagnosis of the disease.
The research was conducted by a team of scientists at Cedars-Sinai Medical Center in collaboration with colleagues from the Weizmann Institute of Science in Israel and the University of Southern California. Results were published online June 13 in the journal NeuroImage, and related findings will be presented July 13 at the Alzheimer's Association International Conference on Alzheimer's Disease.
Alzheimer's disease is a devastating condition that is becoming more prevalent worldwide as the baby-boom generation advances into its senior years, but there is no conclusive, noninvasive way to diagnose it. Previous studies have suggested that changes in the brain may begin years or even decades before symptoms occur - emphasizing the need for earlier, reliable detection for early therapeutic intervention to achieve effective remedy. The new study suggests the possibility of monitoring Alzheimer's disease through a simple retinal imaging approach.
Abnormal deposits in the brain called beta-amyloid plaques, which damage cells and interrupt cell-to-cell communications, are recognized as a hallmark sign of the disease. However, because existing noninvasive brain-imaging technologies cannot provide sufficient detail about these changes, the most definitive diagnosis of Alzheimer's disease comes after an autopsy.
The research team considered the retina a better target for noninvasive imaging of Alzheimer's disease because it is readily accessible and, unlike other components of the eye, it is part of the central nervous system, having a direct connection and thus many similarities with the brain. Previous studies have documented non-specific visual disturbances, eye disorders and certain types of retinal abnormalities occurring with Alzheimer's disease and other neurodegenerative conditions, but this is the first to identify human retinal plaque deposits that could provide a specific diagnostic marker of Alzheimer's disease.
Among the new findings:
1) In lab tests, plaques in the retinas of mice genetically modified to model Alzheimer's disease could be detected at a very early, pre-symptomatic stage - before the plaque appeared in the brain.
2) A high-resolution, noninvasive optical imaging approach was developed to monitor individual beta-amyloid plaques in the retinas of live mice. The system is based on a harmless specific marker and the adaptation of an existing optical system used to examine rodent eyes.
3) The research team used a fluorescent compound called curcumin to label and detect retinal plaques. This is believed to be the first use of curcumin as an imaging agent to detect Alzheimer's disease-related plaques in the retinas of live animals. Curcumin, a natural component of the spice turmeric, binds to beta-amyloid plaques and makes them visible when viewed microscopically. In the Cedars-Sinai research, curcumin injected into the bloodstream of live mice crossed the blood-retinal barrier and specifically bound to the retinal plaques, allowing them to be viewed in high resolution with a noninvasive procedure.
4) Observations from multiple genetically engineered mouse models of Alzheimer's disease demonstrated a correlation between retinal plaques and brain plaques as disease progressed.
v
5) In the laboratory mice, a unique immune system-based therapy that reduces the amount of plaques in the brain also reduced plaque load in the retina to the same extent, suggesting that the retina could faithfully represent the brain in assessing response to therapy.
6) Beta-amyloid plaques were identified in retinal samples from human patients who had died from Alzheimer's disease, and their features correlated with the diagnosed stage of the disease. Importantly, plaques were clearly detected not only in patients who definitely had the disease, but also in the retinas of some people who were suspected of having early-stage Alzheimer's disease based on clinical diagnosis and microscopic examination of brain tissue after death.
Together, the results offer the first evidence for the existence of Alzheimer's-specific plaques in the retina of human patients and the ability to detect individual plaques in live mouse models, creating a strong basis for future research building on these findings. According to the authors, these studies establish the potential of direct retinal beta-amyloid plaque imaging in live subjects as a tool for early Alzheimer's disease diagnosis and prognosis, as well as assessment of therapies.
Specialists in neurosurgery, ophthalmology, imaging systems, neuroimmunology, pathology, neurology and biomedical engineering collaborated on these studies, which were conducted at Cedars-Sinai Medical Center by scientists from Cedars-Sinai, the Weizmann Institute of Science in Israel, and the University of Southern California.
The journal article's first authors are Maya Koronyo-Hamaoui, Ph.D., a research scientist and assistant professor of neurosurgery at Cedars-Sinai's Maxine Dunitz Neurosurgical Institute and a principal investigator in the Neuroimmunology Laboratory at Cedars-Sinai; and Yosef Koronyo, M.Sc., LL.B., a research associate in the departments of Surgery and Neurosurgery at Cedars-Sinai. Senior authors are Michal Schwartz, Ph.D., visiting professor in the Department of Neurosurgery at Cedars-Sinai, and the Ilze and Maurice Professorial Chair of Neuroimmunology at the Weizmann Institute of Science in Rehovot, Israel; and Daniel L. Farkas, Ph.D., professor of surgery and biomedical sciences and director of the Minimally Invasive Surgical Technologies Institute at Cedars-Sinai.
The work was supported by the Marciano Family Foundation, the Maxine Dunitz Neurosurgical Institute, the U.S. Navy Bureau of Medicine and Surgery, the National Eye Institute, the Winnick Family Foundation, and a National Institute on Aging grant to the University of Southern California Alzheimer's Disease Research Center.
Source:
Cedars-Sinai Medical Center
пятница, 13 мая 2011 г.
Penn Study Finds Inhaled Anesthetics Could Lead To Early Onset Of Alzheimer's Disease
Researchers at the University of Pennsylvania's School of Medicine have discovered that common inhaled anesthetics increase the number of amyloid plaques in the brains of animals, which might accelerate the onset of neurodegenerative diseases like Alzheimer's. Roderic Eckenhoff, MD, Vice Chair of Research in the University of Pennsylvania's Department of Anesthesia and Critical Care, and his co-authors, report their findings in the online edition of Neurobiology of Aging.
Every year over 100 million people undergo surgery worldwide, most under general anesthesia with an inhaled drug. These drugs clearly affect cognitive ability at least in the short term, but the growing concern is that inhaled anesthetics may affect a person well beyond the perioperative period, even permanently. Several factors appear to play a role in this subtle loss of cognitive ability, most notably age.
A specific effect of these drugs on dementias like Alzheimer's disease, though suspected for many years, has only been recently supported by data. In 2003, Eckenhoff's group showed that the inhaled anesthetics enhance the aggregation and cytotoxicity of the amyloid beta peptide. Just last month, a study reported that these drugs also enhance the production of amyloid beta in isolated cells. But these protein and cell culture studies are a long way from showing that an effect occurs in vivo. This new study provides the first evidence that the predicted effect occurs in animals.
"This animal study data suggests that we have to at least consider the possibility that anesthetics accelerate certain neurodegenerative disorders," said Eckenhoff. "In the field of Alzheimer's research, most effort is focused on delaying, not curing the disease. A delay in the onset of Alzheimer's disease of only three to five years would be considered a success. Therefore, if commonly used drugs, like anesthetics, are accelerating this disorder, even by a few years, then a similar success might follow even small changes in the care of the operative patient."
Mice don't naturally get Alzheimer's, so the animals in this study were genetically engineered to express the human protein responsible, called amyloid beta. "These mice develop a syndrome with many features of the human disease," explains Eckenhoff. Post-doctoral fellow and first author Shannon Bianchi, MD, exposed "middle-aged" Alzheimer mice to anesthetics at low to moderate concentrations for two hours a day over a total of five days, not unusual for a clinical scenario. The cognitive abilities of the mice were then analyzed using standard behavioral tests, and their brains were examined for plaque and cell death.
"Compared to controls, the anesthesia did not appear to worsen cognitive ability, which was already considerably compromised at this age, but it did accelerate amyloid beta aggregation and plaque appearance," said corresponding author Maryellen Eckenhoff, PhD. "We need to test whether anesthetic at earlier, presymptomatic stages, might accelerate both cognitive loss and plaque." This is the main cause of concern because a large fraction of clinical patients receiving inhaled anesthetics during surgery are older, but presymptomatic individuals.
Are there anesthetics that do not accelerate plaque? "We think so, but far more research is necessary to show this with any confidence. We have to take this one step at a time - a problem has still not been demonstrated in humans". It is important to remember that this effect is likely to be subtle, especially with brief surgical procedures, so the risk of not having needed surgery may exceed any potential risk from this still unproven effect. But this latest study adds a little urgency to the effort to find out. "If inhaled anesthetics are contributing to the rise and early onset of this devastating disease then we need to know, and soon," concludes Eckenhoff.
To access the full article click here
PENN Medicine is a $2.9 billion enterprise dedicated to the related missions of medical education, biomedical research, and high-quality patient care. PENN Medicine consists of the University of Pennsylvania School of Medicine (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System.
Penn's School of Medicine is ranked #2 in the nation for receipt of NIH research funds; and ranked #3 in the nation in U.S. News & World Report's most recent ranking of top research-oriented medical schools. Supporting 1,400 fulltime faculty and 700 students, the School of Medicine is recognized worldwide for its superior education and training of the next generation of physician-scientists and leaders of academic medicine.
The University of Pennsylvania Health System includes three hospitals, all of which have received numerous national patient-care honors [Hospital of the University of Pennsylvania; Pennsylvania Hospital, the nation's first hospital; and Penn Presbyterian Medical Center]; a faculty practice plan; a primary-care provider network; two multispecialty satellite facilities; and home care and hospice.
Contact: Rick Cushman
University of Pennsylvania School of Medicine
Every year over 100 million people undergo surgery worldwide, most under general anesthesia with an inhaled drug. These drugs clearly affect cognitive ability at least in the short term, but the growing concern is that inhaled anesthetics may affect a person well beyond the perioperative period, even permanently. Several factors appear to play a role in this subtle loss of cognitive ability, most notably age.
A specific effect of these drugs on dementias like Alzheimer's disease, though suspected for many years, has only been recently supported by data. In 2003, Eckenhoff's group showed that the inhaled anesthetics enhance the aggregation and cytotoxicity of the amyloid beta peptide. Just last month, a study reported that these drugs also enhance the production of amyloid beta in isolated cells. But these protein and cell culture studies are a long way from showing that an effect occurs in vivo. This new study provides the first evidence that the predicted effect occurs in animals.
"This animal study data suggests that we have to at least consider the possibility that anesthetics accelerate certain neurodegenerative disorders," said Eckenhoff. "In the field of Alzheimer's research, most effort is focused on delaying, not curing the disease. A delay in the onset of Alzheimer's disease of only three to five years would be considered a success. Therefore, if commonly used drugs, like anesthetics, are accelerating this disorder, even by a few years, then a similar success might follow even small changes in the care of the operative patient."
Mice don't naturally get Alzheimer's, so the animals in this study were genetically engineered to express the human protein responsible, called amyloid beta. "These mice develop a syndrome with many features of the human disease," explains Eckenhoff. Post-doctoral fellow and first author Shannon Bianchi, MD, exposed "middle-aged" Alzheimer mice to anesthetics at low to moderate concentrations for two hours a day over a total of five days, not unusual for a clinical scenario. The cognitive abilities of the mice were then analyzed using standard behavioral tests, and their brains were examined for plaque and cell death.
"Compared to controls, the anesthesia did not appear to worsen cognitive ability, which was already considerably compromised at this age, but it did accelerate amyloid beta aggregation and plaque appearance," said corresponding author Maryellen Eckenhoff, PhD. "We need to test whether anesthetic at earlier, presymptomatic stages, might accelerate both cognitive loss and plaque." This is the main cause of concern because a large fraction of clinical patients receiving inhaled anesthetics during surgery are older, but presymptomatic individuals.
Are there anesthetics that do not accelerate plaque? "We think so, but far more research is necessary to show this with any confidence. We have to take this one step at a time - a problem has still not been demonstrated in humans". It is important to remember that this effect is likely to be subtle, especially with brief surgical procedures, so the risk of not having needed surgery may exceed any potential risk from this still unproven effect. But this latest study adds a little urgency to the effort to find out. "If inhaled anesthetics are contributing to the rise and early onset of this devastating disease then we need to know, and soon," concludes Eckenhoff.
To access the full article click here
PENN Medicine is a $2.9 billion enterprise dedicated to the related missions of medical education, biomedical research, and high-quality patient care. PENN Medicine consists of the University of Pennsylvania School of Medicine (founded in 1765 as the nation's first medical school) and the University of Pennsylvania Health System.
Penn's School of Medicine is ranked #2 in the nation for receipt of NIH research funds; and ranked #3 in the nation in U.S. News & World Report's most recent ranking of top research-oriented medical schools. Supporting 1,400 fulltime faculty and 700 students, the School of Medicine is recognized worldwide for its superior education and training of the next generation of physician-scientists and leaders of academic medicine.
The University of Pennsylvania Health System includes three hospitals, all of which have received numerous national patient-care honors [Hospital of the University of Pennsylvania; Pennsylvania Hospital, the nation's first hospital; and Penn Presbyterian Medical Center]; a faculty practice plan; a primary-care provider network; two multispecialty satellite facilities; and home care and hospice.
Contact: Rick Cushman
University of Pennsylvania School of Medicine
среда, 11 мая 2011 г.
Alzheimer's Society Comment On Mark Foster Backing The Big Care Debate
Olympic swimmer Mark Forster and television presenters Phillippa Forrester and Cerri Burnell gave their backing to the Big Care Debate.
They have all added their voice to a short film that highlights four real life experiences of why care matters.
The Big Care Debate, which is looking at a series of potential options for the future of social care funding, draws to a close next week.
Alzheimer's Society comment:
'It is great news to hear that Mark Forster, Phillippa Forrester and Cerri Burnell are backing the Big Care Debate. It is vitally important that other people now follow their lead and have their say to ensure a fair and transparent social care system is created.
There are currently too many people with dementia in England being forced to pay enormous bills for substandard care. Quality provision needs to be guaranteed and available at a fair price. Only a new care system that can meet the rising challenge of dementia will succeed.'
Neil Hunt
Chief Executive
Source
Alzheimer's Society
They have all added their voice to a short film that highlights four real life experiences of why care matters.
The Big Care Debate, which is looking at a series of potential options for the future of social care funding, draws to a close next week.
Alzheimer's Society comment:
'It is great news to hear that Mark Forster, Phillippa Forrester and Cerri Burnell are backing the Big Care Debate. It is vitally important that other people now follow their lead and have their say to ensure a fair and transparent social care system is created.
There are currently too many people with dementia in England being forced to pay enormous bills for substandard care. Quality provision needs to be guaranteed and available at a fair price. Only a new care system that can meet the rising challenge of dementia will succeed.'
Neil Hunt
Chief Executive
Source
Alzheimer's Society
вторник, 10 мая 2011 г.
New Technology Used To Construct The First Map Of Structural Variation In The Human Genome
Beyond the simple stream of one-letter characters in the human genome sequence lies a complex, higher-order code. In order to decipher this level of architecture, scientists have developed powerful new experimental and algorithmic methods to detect copy number variants (CNVs)--defined as large deletions and duplications of DNA segments. These technologies--reported in the journal Genome Research--were used to create the first comprehensive map of CNVs in the human genome, concurrently published in Nature. A related article appears in Nature Genetics.
CNVs are responsible for genetic changes in Alzheimer's and Parkinson's, susceptibility to HIV-1, some forms of color blindness, and many other diseases. They lead to variation in gene expression levels and may account for a large amount of phenotypic variation among individuals and ethnic populations, including differential responses to drugs and environmental stimuli. Mechanisms underlying the formation of CNVs also provide insight into evolutionary processes and human origins.
Using microarray technology, scientists can scan for CNVs across the genome in a single experiment. While this is a cost-effective means of obtaining large amounts of data, scientists have struggled to accurately determine CNV copy number and to precisely define the boundaries of CNVs in the genome. Two papers published in Genome Research present groundbreaking approaches to address these issues.
One paper describes a new whole-genome tiling path microarray, which was constructed from the same DNA used to sequence the human genome in 2001. The array covers 93.7% of the euchromatic (gene-containing) regions of the human genome and substantially improves resolution over previous arrays. The array was employed in a process known as comparative genomic hybridization (CGH), which involves tagging genomic DNA from two individuals and then co-hybridizing it to the array. Data from the array were assessed with a new algorithmic tool, called CNVfinder, which accurately and reliably identified CNVs in the human genome.
"This method helped us to develop the first comprehensive map of structural variation in the human genome," says Dr. Nigel Carter, one of the lead investigators on the project. "We used it to help identify 1,447 CNVs, which covered 12% of the human genome."
The other paper presents a new multi-step algorithm used with the Affymetrix GeneChip® Human Mapping 500K Early Access SNP arrays. The specificity of the algorithm, coupled with the increased probe density of these arrays, permitted the identification of approximately 1,000 CNVs, many of which were below the detection size limit of alternative methodologies. Furthermore, the algorithm more accurately estimated CNV boundaries, thereby permitting a detailed comparison with other genomic features.
"This new approach will be useful in understanding the role of CNVs in disease pathology--not only copy number changes in cancer cells, but also possible association of CNVs with common diseases," explains Dr. Hiroyuki Aburatani, one of the scientists who led the development of the algorithm. "We'll be able to develop diagnostic tests with sub-microscopic resolution, and because the analysis detects SNPs--single-nucleotide polymorphisms--in addition to CNVs, it will find widespread use among researchers performing disease-association studies."
Both projects were part of the International Structural Genomic Variation Consortium's Copy Number Variation Project (sanger.ac.uk/humgen/cnv). The Principal Investigators on this project were Hiroyuki Aburatani (University of Tokyo); Nigel P. Carter, Matthew E. Hurles, and Chris Tyler-Smith (Sanger Institute); Keith W. Jones (Affymetrix); Charles Lee (Harvard Medical School); and Stephen W. Scherer (Sick Kids Hospital, Toronto, Canada).
ABOUT GENOME RESEARCH:
Genome Research (genome/) is an international, continuously published, peer-reviewed journal published by Cold Spring Harbor Laboratory Press. Launched in 1995, it is one of the five most highly cited primary research journals in genetics and genomics.
ABOUT COLD SPRING HARBOR LABORATORY PRESS:
Cold Spring Harbor Laboratory Press is an internationally renowned publisher of books, journals, and electronic media, located on Long Island, New York. It is a division of Cold Spring Harbor Laboratory, an innovator in life science research and the education of scientists, students, and the public. For more information, visit cshlpress/.
Contact: Maria A. Smit
Cold Spring Harbor Laboratory
CNVs are responsible for genetic changes in Alzheimer's and Parkinson's, susceptibility to HIV-1, some forms of color blindness, and many other diseases. They lead to variation in gene expression levels and may account for a large amount of phenotypic variation among individuals and ethnic populations, including differential responses to drugs and environmental stimuli. Mechanisms underlying the formation of CNVs also provide insight into evolutionary processes and human origins.
Using microarray technology, scientists can scan for CNVs across the genome in a single experiment. While this is a cost-effective means of obtaining large amounts of data, scientists have struggled to accurately determine CNV copy number and to precisely define the boundaries of CNVs in the genome. Two papers published in Genome Research present groundbreaking approaches to address these issues.
One paper describes a new whole-genome tiling path microarray, which was constructed from the same DNA used to sequence the human genome in 2001. The array covers 93.7% of the euchromatic (gene-containing) regions of the human genome and substantially improves resolution over previous arrays. The array was employed in a process known as comparative genomic hybridization (CGH), which involves tagging genomic DNA from two individuals and then co-hybridizing it to the array. Data from the array were assessed with a new algorithmic tool, called CNVfinder, which accurately and reliably identified CNVs in the human genome.
"This method helped us to develop the first comprehensive map of structural variation in the human genome," says Dr. Nigel Carter, one of the lead investigators on the project. "We used it to help identify 1,447 CNVs, which covered 12% of the human genome."
The other paper presents a new multi-step algorithm used with the Affymetrix GeneChip® Human Mapping 500K Early Access SNP arrays. The specificity of the algorithm, coupled with the increased probe density of these arrays, permitted the identification of approximately 1,000 CNVs, many of which were below the detection size limit of alternative methodologies. Furthermore, the algorithm more accurately estimated CNV boundaries, thereby permitting a detailed comparison with other genomic features.
"This new approach will be useful in understanding the role of CNVs in disease pathology--not only copy number changes in cancer cells, but also possible association of CNVs with common diseases," explains Dr. Hiroyuki Aburatani, one of the scientists who led the development of the algorithm. "We'll be able to develop diagnostic tests with sub-microscopic resolution, and because the analysis detects SNPs--single-nucleotide polymorphisms--in addition to CNVs, it will find widespread use among researchers performing disease-association studies."
Both projects were part of the International Structural Genomic Variation Consortium's Copy Number Variation Project (sanger.ac.uk/humgen/cnv). The Principal Investigators on this project were Hiroyuki Aburatani (University of Tokyo); Nigel P. Carter, Matthew E. Hurles, and Chris Tyler-Smith (Sanger Institute); Keith W. Jones (Affymetrix); Charles Lee (Harvard Medical School); and Stephen W. Scherer (Sick Kids Hospital, Toronto, Canada).
ABOUT GENOME RESEARCH:
Genome Research (genome/) is an international, continuously published, peer-reviewed journal published by Cold Spring Harbor Laboratory Press. Launched in 1995, it is one of the five most highly cited primary research journals in genetics and genomics.
ABOUT COLD SPRING HARBOR LABORATORY PRESS:
Cold Spring Harbor Laboratory Press is an internationally renowned publisher of books, journals, and electronic media, located on Long Island, New York. It is a division of Cold Spring Harbor Laboratory, an innovator in life science research and the education of scientists, students, and the public. For more information, visit cshlpress/.
Contact: Maria A. Smit
Cold Spring Harbor Laboratory
понедельник, 9 мая 2011 г.
Brain-Imaging Study Supports The Relevance Of A Common Genetic Risk Factor For Alzheimer's Disease In Latinos
A brain-imaging study published in the Archives of Neurology suggests that a major genetic risk factor for Alzheimer's disease in the Anglo population is also a risk factor for the disease in Latinos.
While a gene called APOE4 has been firmly established to increase an Anglo person's risk of Alzheimer's disease, its relationship to the disease in different Latino populations has been less clear. In previous studies, researchers from the Banner Alzheimer's Institute and their collaborators in the Arizona Alzheimer's Consortium used a brain-imaging technique called PET to show that cognitively healthy late-middle-aged carriers of the APOE4 gene have lower activity than non-carriers of the gene in brain regions known to be affected by Alzheimer's disease.
In the present study, they extended their findings to 27 Latinos with and without the APOE4 gene, mostly from Arizona's Mexican-American community. As predicted, cognitively healthy Latinos in their 50s and 60s with the APOE4 gene had lower activity than non-carriers of the gene in brain regions known to be affected by Alzheimer's disease.
"This study provides support for the relationship between the APOE4 gene and the risk of Alzheimer's disease in Latinos," said Dr. Jessica Langbaum, staff scientist at the Banner Alzheimer's Institute and the study's lead author. "It also shows how brain imaging techniques can be used in healthy people to evaluate genetic and non-genetic risk factors for this disorder."
Latinos are about 1.5 times more likely than Anglos to develop Alzheimer's disease, according to the Alzheimer's Association. Alzheimer disease is the most common form of dementia. Between the years 2000 and 2050, the number of affected Latinos is projected to increase by 600 percent. Latinos may be at higher risk due to higher amounts of diabetes mellitus, obesity, cardiovascular disease and hypertension, each of which is also a risk factor for Alzheimer's disease.
The researchers have proposed using the same brain imaging techniques in healthy APOE4 carriers to evaluate promising treatments to prevent Alzheimer's disease without having to wait many years to determine whether they go on to develop symptoms. Among other things, the present study supports the inclusion of APOE4 carriers from Latino community in these studies.
About the study
The study was conducted by a team of researchers at Banner Alzheimer's Institute, Translational Genomics Research Institute (TGen), Arizona State University, Mayo Clinic Arizona, University of Arizona, University of California San Diego and the Arizona Alzheimer's Consortium.
The authors include Jessica B.S. Langbaum, PhD; Kewei Chen, PhD; Richard J. Caselli, MD; Wendy Lee, MS; Cole Reschke, BS; Daniel Bandy, MS; Gene E. Alexander, PhD; Christine M. Burns, BA; Alfred W. Kaszniak, PhD; Stephanie A. Reeder, BA; Jason J. Corneveaux, BS; April N. Allen, BS; Jeremy Pruzin, BS, BA; Matthew J. Huentelman, PhD; Adam S. Fleisher, MD; and Eric M. Reiman, MD.
The authors gratefully acknowledge support from National Institute of Mental Health grant R01MH57899 (Dr. Reiman), National Institute on Aging grants R01AG031581 and P30AG19610 (Dr. Reiman), the Evelyn G. McKnight Brain Institute (Dr. Alexander), the state of Arizona (Drs. Reiman, Caselli, Alexander, and Chen), and contributions from the Banner Alzheimer's Foundation and Mayo Clinic Foundation.
About Banner Alzheimer's Institute
Banner Alzheimer's Institute (BAI) is a treatment and research facility dedicated to helping patients with memory and thinking problems. It offers clinical care for patients; provides education, referral and support services for families and caregivers; and conducts leading-edge brain-imaging, clinical trials, brain imaging and genetics studies. The Institute is devoted to finding effective Alzheimer's disease-slowing and prevention treatments in the shortest time possible. BAI is owned and operated by Phoenix-based Banner Health, a nonprofit organization.
About National Institute on Aging
The NIA leads the federal government effort conducting and supporting research on the biomedical, social and behavioral issues of older people.
Source: Banner Alzheimer's Institute
While a gene called APOE4 has been firmly established to increase an Anglo person's risk of Alzheimer's disease, its relationship to the disease in different Latino populations has been less clear. In previous studies, researchers from the Banner Alzheimer's Institute and their collaborators in the Arizona Alzheimer's Consortium used a brain-imaging technique called PET to show that cognitively healthy late-middle-aged carriers of the APOE4 gene have lower activity than non-carriers of the gene in brain regions known to be affected by Alzheimer's disease.
In the present study, they extended their findings to 27 Latinos with and without the APOE4 gene, mostly from Arizona's Mexican-American community. As predicted, cognitively healthy Latinos in their 50s and 60s with the APOE4 gene had lower activity than non-carriers of the gene in brain regions known to be affected by Alzheimer's disease.
"This study provides support for the relationship between the APOE4 gene and the risk of Alzheimer's disease in Latinos," said Dr. Jessica Langbaum, staff scientist at the Banner Alzheimer's Institute and the study's lead author. "It also shows how brain imaging techniques can be used in healthy people to evaluate genetic and non-genetic risk factors for this disorder."
Latinos are about 1.5 times more likely than Anglos to develop Alzheimer's disease, according to the Alzheimer's Association. Alzheimer disease is the most common form of dementia. Between the years 2000 and 2050, the number of affected Latinos is projected to increase by 600 percent. Latinos may be at higher risk due to higher amounts of diabetes mellitus, obesity, cardiovascular disease and hypertension, each of which is also a risk factor for Alzheimer's disease.
The researchers have proposed using the same brain imaging techniques in healthy APOE4 carriers to evaluate promising treatments to prevent Alzheimer's disease without having to wait many years to determine whether they go on to develop symptoms. Among other things, the present study supports the inclusion of APOE4 carriers from Latino community in these studies.
About the study
The study was conducted by a team of researchers at Banner Alzheimer's Institute, Translational Genomics Research Institute (TGen), Arizona State University, Mayo Clinic Arizona, University of Arizona, University of California San Diego and the Arizona Alzheimer's Consortium.
The authors include Jessica B.S. Langbaum, PhD; Kewei Chen, PhD; Richard J. Caselli, MD; Wendy Lee, MS; Cole Reschke, BS; Daniel Bandy, MS; Gene E. Alexander, PhD; Christine M. Burns, BA; Alfred W. Kaszniak, PhD; Stephanie A. Reeder, BA; Jason J. Corneveaux, BS; April N. Allen, BS; Jeremy Pruzin, BS, BA; Matthew J. Huentelman, PhD; Adam S. Fleisher, MD; and Eric M. Reiman, MD.
The authors gratefully acknowledge support from National Institute of Mental Health grant R01MH57899 (Dr. Reiman), National Institute on Aging grants R01AG031581 and P30AG19610 (Dr. Reiman), the Evelyn G. McKnight Brain Institute (Dr. Alexander), the state of Arizona (Drs. Reiman, Caselli, Alexander, and Chen), and contributions from the Banner Alzheimer's Foundation and Mayo Clinic Foundation.
About Banner Alzheimer's Institute
Banner Alzheimer's Institute (BAI) is a treatment and research facility dedicated to helping patients with memory and thinking problems. It offers clinical care for patients; provides education, referral and support services for families and caregivers; and conducts leading-edge brain-imaging, clinical trials, brain imaging and genetics studies. The Institute is devoted to finding effective Alzheimer's disease-slowing and prevention treatments in the shortest time possible. BAI is owned and operated by Phoenix-based Banner Health, a nonprofit organization.
About National Institute on Aging
The NIA leads the federal government effort conducting and supporting research on the biomedical, social and behavioral issues of older people.
Source: Banner Alzheimer's Institute
воскресенье, 8 мая 2011 г.
Researchers Find Possible Environmental Causes For Alzheimer's, Diabetes
A new study by researchers at Rhode Island Hospital have found a substantial link between increased levels of nitrates in our environment and food, with increased deaths from diseases, including Alzheimer's, diabetes mellitus and Parkinson's. The study was published in the Journal of Alzheimer's Disease (Volume 17:3 July 2009).
Led by Suzanne de la Monte, MD, MPH, of Rhode Island Hospital, researchers studied the trends in mortality rates due to diseases that are associated with aging, such as diabetes, Alzheimer's, Parkinson's, diabetes and cerebrovascular disease, as well as HIV. They found strong parallels between age adjusted increases in death rate from Alzheimer's, Parkinson's, and diabetes and the progressive increases in human exposure to nitrates, nitrites and nitrosamines through processed and preserved foods as well as fertilizers. Other diseases including HIV-AIDS, cerebrovascular disease, and leukemia did not exhibit those trends. De la Monte and the authors propose that the increase in exposure plays a critical role in the cause, development and effects of the pandemic of these insulin-resistant diseases.
De la Monte, who is also a professor of pathology and lab medicine at The Warren Alpert Medical School of Brown University, says, "We have become a 'nitrosamine generation.' In essence, we have moved to a diet that is rich in amines and nitrates, which lead to increased nitrosamine production. We receive increased exposure through the abundant use of nitrate-containing fertilizers for agriculture." She continues, "Not only do we consume them in processed foods, but they get into our food supply by leeching from the soil and contaminating water supplies used for crop irrigation, food processing and drinking."
Nitrites and nitrates belong to a class of chemical compounds that have been found to be harmful to humans and animals. More than 90 percent of these compounds that have been tested have been determined to be carcinogenic in various organs. They are found in many food products, including fried bacon, cured meats and cheese products as well as beer and water. Exposure also occurs through manufacturing and processing of rubber and latex products, as well as fertilizers, pesticides and cosmetics.
Nitrosamines are formed by a chemical reaction between nitrites or other proteins. Sodium nitrite is deliberately added to meat and fish to prevent toxin production; it is also used to preserve, color and flavor meats. Ground beef, cured meats and bacon in particular contain abundant amounts of amines due to their high protein content. Because of the significant levels of added nitrates and nitrites, nitrosamines are nearly always detectable in these foods. Nitrosamines are also easily generated under strong acid conditions, such as in the stomach, or at high temperatures associated with frying or flame broiling. Reducing sodium nitrite content reduces nitrosamine formation in foods.
Nitrosamines basically become highly reactive at the cellular level, which then alters gene expression and causes DNA damage. The researchers note that the role of nitrosamines has been well-studied, and their role as a carcinogen has been fully documented. The investigators propose that the cellular alterations that occur as a result of nitrosamine exposure are fundamentally similar to those that occur with aging, as well as Alzheimer's, Parkinson's and Type 2 diabetes mellitus.
De la Monte comments, "All of these diseases are associated with increased insulin resistance and DNA damage. Their prevalence rates have all increased radically over the past several decades and show no sign of plateau. Because there has been a relatively short time interval associated with the dramatic shift in disease incidence and prevalence rates, we believe this is due to exposure-related rather than genetic etiologies."
The researchers recognize that an increase in death rates is anticipated in higher age groups. Yet when the researchers compared mortality from Parkinson's and Alzheimer's disease among 75 to 84 year olds from 1968 to 2005, the death rates increased much more dramatically than for cerebrovascular and cardiovascular disease, which are also aging-associated. For example, in Alzheimer's patients, the death rate increased 150-fold, from 0 deaths to more than 150 deaths per 100,000. Parkinson's disease death rates also increased across all age groups. However, mortality rates from cerebrovascular disease in the same age group declined, even though this is a disease associated with aging as well.
De la Monte notes, "Because of the similar trending in nearly all age groups within each disease category, this indicates that these overall trends are not due to an aging population. This relatively short time interval for such dramatic increases in death rates associated with these diseases is more consistent with exposure-related causes rather than genetic changes." She also comments, "Moreover, the strikingly higher and climbing mortality rates in older age brackets suggest that aging and/or longer durations of exposure have greater impacts on progression and severity of these diseases."
The researchers graphed and analyzed mortality rates, and compared them with increasing age for each disease. They then studied United States population growth, annual use and consumption of nitrite-containing fertilizers, annual sales at popular fast food chains, and sales for a major meat processing company, as well as consumption of grain and consumption of watermelon and cantaloupe (the melons were used as a control since they are not typically associated with nitrate or nitrite exposure).
The findings indicate that while nitrogen-containing fertilizer consumption increased by 230 percent between 1955 and 2005, its usage doubled between 1960 and 1980, which just precedes the insulin-resistant epidemics the researchers found. They also found that sales from the fast food chain and the meat processing company increased more than 8-fold from 1970 to 2005, and grain consumption increased 5-fold.
The authors state that the time course of the increased prevalence rates of Alzheimer's, Parkinson's and diabetes cannot be explained on the basis of gene mutations. They instead mirror the classical trends of exposure-related disease. Because nitrosamines produce biochemical changes within cells and tissues, it is conceivable that chronic exposure to low levels of nitrites and nitrosamines through processed foods, water and fertilizers is responsible for the current epidemics of these diseases and the increasing mortality rates associated with them.
De la Monte states, "If this hypothesis is correct, potential solutions include eliminating the use of nitrites and nitrates in food processing, preservation and agriculture; taking steps to prevent the formation of nitrosamines and employing safe and effective measures to detoxify food and water before human consumption."
Notes:
Other researchers involved in the study with de la Monte include Alexander Neusner, Jennifer Chu and Margot Lawton, from the departments of pathology, neurology and medicine at Rhode Island Hospital and The Warren Alpert Medical School of Brown University.
The study was funded through grants from the National Institutes of Health. Two subsequent papers have been accepted for publication in the near future that demonstrate experimentally that low levels of nitrosamine exposure cause neurodegeneration, NASH and diabetes.
De la Monte, Suzanne M., Alexander Neusner, Jennifer Chu and Margot Lawton. "Epidemilogical Trends Strongly Suggest Exposures as Etiologic Agents in the Pathogenesis of Sporadic Alzheimer's Disease, Diabetes Mellitus, and Non-Alcoholic Steatohepatitis." Journal of Alzheimer's Disease, 17:3 (July 2009) pp 519-529.
Source:
Nancy Cawley Jean
Lifespan
Led by Suzanne de la Monte, MD, MPH, of Rhode Island Hospital, researchers studied the trends in mortality rates due to diseases that are associated with aging, such as diabetes, Alzheimer's, Parkinson's, diabetes and cerebrovascular disease, as well as HIV. They found strong parallels between age adjusted increases in death rate from Alzheimer's, Parkinson's, and diabetes and the progressive increases in human exposure to nitrates, nitrites and nitrosamines through processed and preserved foods as well as fertilizers. Other diseases including HIV-AIDS, cerebrovascular disease, and leukemia did not exhibit those trends. De la Monte and the authors propose that the increase in exposure plays a critical role in the cause, development and effects of the pandemic of these insulin-resistant diseases.
De la Monte, who is also a professor of pathology and lab medicine at The Warren Alpert Medical School of Brown University, says, "We have become a 'nitrosamine generation.' In essence, we have moved to a diet that is rich in amines and nitrates, which lead to increased nitrosamine production. We receive increased exposure through the abundant use of nitrate-containing fertilizers for agriculture." She continues, "Not only do we consume them in processed foods, but they get into our food supply by leeching from the soil and contaminating water supplies used for crop irrigation, food processing and drinking."
Nitrites and nitrates belong to a class of chemical compounds that have been found to be harmful to humans and animals. More than 90 percent of these compounds that have been tested have been determined to be carcinogenic in various organs. They are found in many food products, including fried bacon, cured meats and cheese products as well as beer and water. Exposure also occurs through manufacturing and processing of rubber and latex products, as well as fertilizers, pesticides and cosmetics.
Nitrosamines are formed by a chemical reaction between nitrites or other proteins. Sodium nitrite is deliberately added to meat and fish to prevent toxin production; it is also used to preserve, color and flavor meats. Ground beef, cured meats and bacon in particular contain abundant amounts of amines due to their high protein content. Because of the significant levels of added nitrates and nitrites, nitrosamines are nearly always detectable in these foods. Nitrosamines are also easily generated under strong acid conditions, such as in the stomach, or at high temperatures associated with frying or flame broiling. Reducing sodium nitrite content reduces nitrosamine formation in foods.
Nitrosamines basically become highly reactive at the cellular level, which then alters gene expression and causes DNA damage. The researchers note that the role of nitrosamines has been well-studied, and their role as a carcinogen has been fully documented. The investigators propose that the cellular alterations that occur as a result of nitrosamine exposure are fundamentally similar to those that occur with aging, as well as Alzheimer's, Parkinson's and Type 2 diabetes mellitus.
De la Monte comments, "All of these diseases are associated with increased insulin resistance and DNA damage. Their prevalence rates have all increased radically over the past several decades and show no sign of plateau. Because there has been a relatively short time interval associated with the dramatic shift in disease incidence and prevalence rates, we believe this is due to exposure-related rather than genetic etiologies."
The researchers recognize that an increase in death rates is anticipated in higher age groups. Yet when the researchers compared mortality from Parkinson's and Alzheimer's disease among 75 to 84 year olds from 1968 to 2005, the death rates increased much more dramatically than for cerebrovascular and cardiovascular disease, which are also aging-associated. For example, in Alzheimer's patients, the death rate increased 150-fold, from 0 deaths to more than 150 deaths per 100,000. Parkinson's disease death rates also increased across all age groups. However, mortality rates from cerebrovascular disease in the same age group declined, even though this is a disease associated with aging as well.
De la Monte notes, "Because of the similar trending in nearly all age groups within each disease category, this indicates that these overall trends are not due to an aging population. This relatively short time interval for such dramatic increases in death rates associated with these diseases is more consistent with exposure-related causes rather than genetic changes." She also comments, "Moreover, the strikingly higher and climbing mortality rates in older age brackets suggest that aging and/or longer durations of exposure have greater impacts on progression and severity of these diseases."
The researchers graphed and analyzed mortality rates, and compared them with increasing age for each disease. They then studied United States population growth, annual use and consumption of nitrite-containing fertilizers, annual sales at popular fast food chains, and sales for a major meat processing company, as well as consumption of grain and consumption of watermelon and cantaloupe (the melons were used as a control since they are not typically associated with nitrate or nitrite exposure).
The findings indicate that while nitrogen-containing fertilizer consumption increased by 230 percent between 1955 and 2005, its usage doubled between 1960 and 1980, which just precedes the insulin-resistant epidemics the researchers found. They also found that sales from the fast food chain and the meat processing company increased more than 8-fold from 1970 to 2005, and grain consumption increased 5-fold.
The authors state that the time course of the increased prevalence rates of Alzheimer's, Parkinson's and diabetes cannot be explained on the basis of gene mutations. They instead mirror the classical trends of exposure-related disease. Because nitrosamines produce biochemical changes within cells and tissues, it is conceivable that chronic exposure to low levels of nitrites and nitrosamines through processed foods, water and fertilizers is responsible for the current epidemics of these diseases and the increasing mortality rates associated with them.
De la Monte states, "If this hypothesis is correct, potential solutions include eliminating the use of nitrites and nitrates in food processing, preservation and agriculture; taking steps to prevent the formation of nitrosamines and employing safe and effective measures to detoxify food and water before human consumption."
Notes:
Other researchers involved in the study with de la Monte include Alexander Neusner, Jennifer Chu and Margot Lawton, from the departments of pathology, neurology and medicine at Rhode Island Hospital and The Warren Alpert Medical School of Brown University.
The study was funded through grants from the National Institutes of Health. Two subsequent papers have been accepted for publication in the near future that demonstrate experimentally that low levels of nitrosamine exposure cause neurodegeneration, NASH and diabetes.
De la Monte, Suzanne M., Alexander Neusner, Jennifer Chu and Margot Lawton. "Epidemilogical Trends Strongly Suggest Exposures as Etiologic Agents in the Pathogenesis of Sporadic Alzheimer's Disease, Diabetes Mellitus, and Non-Alcoholic Steatohepatitis." Journal of Alzheimer's Disease, 17:3 (July 2009) pp 519-529.
Source:
Nancy Cawley Jean
Lifespan
Подписаться на:
Комментарии (Atom)