An expansion of health insurance to more U.S. residents -- with "business, patients and government sharing the cost" -- is important, but unless "we find cures, American families will continue to be plagued by costly and debilitating fatal diseases such as cancer, diabetes and Alzheimer's" disease, former Rep. Harold Ford (D-Tenn.), chair of the Democratic Leadership Council, and Al From, founder and CEO of the council, write in a Memphis Commercial Appeal opinion piece.
According to the authors, although "we're delighted" that both Democratic presidential candidates Sens. Hillary Rodham Clinton (N.Y.) and Barack Obama (Ill.) have "offered constructive plans" to expand health insurance, with "interesting ideas for keeping costs down and increasing the efficiency of the system as a whole," the next president also should establish an American Center for Cures -- a "Cabinet-level authority charged with fighting life-threatening" diseases. The center would "pay for high-risk, high-reward research, fund small businesses that have created possible cures but lack the money necessary to test drugs in clinical trials, and work to streamline the clinical trial process," according to the authors.
They write that "every illness that we cure or eradicate will reduce suffering, save American lives and cut the nation's health care bill by billions and billions of dollars," which would "make it far easier to ensure that everyone has access to health care." The authors conclude, "For that reason alone, the center should be a central element of the next president's health care agenda" (Ford/From, Memphis Commercial Appeal, 5/8).
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.
© 2008 Advisory Board Company and Kaiser Family Foundation. All rights reserved.
четверг, 20 октября 2011 г.
понедельник, 17 октября 2011 г.
Competitive Technologies Announces Publication Of Positive Test Results For Memory Improvement Technology
Competitive Technologies, Inc. (AMEX: CTT) announced the publication in August of an article in the Vol. 3, No. 2, 2007 issue of the International Journal of Learning Technology (IJLT) citing the positive results in the double-blind testing of the efficacy of the MC Square device for improving verbal memory, learning and attention. Test results showed statistically reliable improvement in the measure of attention/concentration following training with the MC Square. CTT has U.S. distribution rights for the patent-pending technology licensed by Thomas Jefferson University of Philadelphia (Jefferson), to Seoul, Korea-based Daeyang E&C, Inc. (KOSDAQ: 033030).
The original device, created in Korea, designed to provide stress relief, improved concentration and relaxation, and as a learning aid, has sold over 1.2 million units. Researchers at Jefferson, under the direction of Neuropsychologist Joseph I. Tracy, Ph.D, associate professor of Neurology and Radiology, Jefferson Medical College of Thomas Jefferson University, and Director, Cognitive Neuroscience and Brain Imaging Laboratory Thomas Jefferson University Hospital, tested the Jefferson-modified device for improvement of attention and concentration.
The MC Square uses Audio-Visual Stimulation through synchronized sound and light rhythms to influence brain activity. Based upon the results of rigorous testing, as detailed in the IJLT article, A test of the efficacy of the MC Square device for improving verbal memory, learning and attention, Jefferson's researchers and Daeyang E&C jointly filed a patent to utilize the improved MC Square device as a method of treatment for age-related memory loss. Under the licensing agreement, Daeyang is granted exclusive commercial rights to the technology.
IJLT, published by Inderscience (inderscience/ijlt), is an international, refereed journal providing a peer-reviewed interdisciplinary forum for the presentation of articles regarding the role of learning technologies in learning and instruction. Articles focus on the study of knowledge and learning vis-? -vis instruction and the technologies and tools that support the process.
Based on the patent-pending treatment method, the MC Square target market has been expanded from students to include normal, healthy individuals that report, or are at risk of, mild memory loss. CTT is targeting this large growing segment of the US population with marketing and distribution plans for MC Square that focus on user experience with the device.
The Alzheimer's Association (alz) estimates that risk and costs associated with age-related memory loss contribute to the estimated costs for Alzheimer's and other dementias of $148 billion annually. Alzheimer's is a progressive, degenerative disease that alters the brain, causing impaired memory, thinking and behavior. It is estimated that nearly 13% or 4.9 million people age 65 and over have Alzheimer's, and that by 2050 the number of Americans with this disease could range from 11 to 16 million unless a way is found to prevent or effectively treat this disease.
About Thomas Jefferson University
Thomas Jefferson University, based in Philadelphia, PA, is an academic health center consisting of Jefferson Medical College, Jefferson College of Graduate Studies, Jefferson College of Health Professions and associated university services. Dedicated to the health sciences, Jefferson educates professionals in a variety of disciplines to form and lead the integrated healthcare delivery and research teams of tomorrow; discovers new knowledge that will define the future of clinical care through investigation from the laboratory to the bedside, and into the community; and sets the standard for quality, compassionate and efficient patient care for their community and for the nation. Jefferson accomplishes its mission in partnership with Thomas Jefferson University Hospital, its education and clinical care affiliate. Visit Jefferson's website: jefferson
About Daeyang E&C
Daeyang E&C, founded in 1979, is a publicly traded company in Korea (KOSDAQ: 03303) with a market capitalization of $200 million. With a stated corporate philosophy of "Customer success is equivalent to corporate success," Daeyang is the market leader in its unique product segments. To fulfill the company's principle of returning profit to its customers, Daeyang created the MC Square Scholarship in 1993 with over 1,600 scholarships granted to date. Daeyang manufactures and markets a neuroscience device for increasing study efficiency called MC Square that has been established as a strong consumer brand name in Korea. Daeyang E&C accesses multiple business fields, especially in the IT and biotechnology industries, through the resources available from its affiliate Daeyang Venture Capital Ltd., also of Korea. Daeyang develops these VC business lines in health-related fields based on neuroscience technologies. Visit Daeyang's website: daeyangenc
About Competitive Technologies, Inc.
Competitive Technologies, established in 1968, is a full service technology transfer and licensing provider focused on the technology needs of its customers and transforming those requirements into commercially viable solutions. CTT is a global leader in identifying, developing and commercializing innovative technologies in life, electronic, nano, and physical sciences developed by universities, companies and inventors. CTT maximizes the value of intellectual assets for the benefit of its customers, clients and shareholders. Visit CTT's website: competitivetech
Statements about our future expectations are "forward-looking statements" within the meaning of applicable Federal Securities Laws, and are not guarantees of future performance. When used herein, the words "may," "will," "should," "anticipate," "believe," "appear," "intend," "plan," "expect," "estimate," "approximate," and similar expressions are intended to identify such forward-looking statements. These statements involve risks and uncertainties inherent in our business, including those set forth in Item 1A under the caption "Risk Factors," in our most recent Annual Report on Form 10-K for the year ended July 31, 2006, filed with the SEC on October 30, 2006, and other filings with the SEC, and are subject to change at any time. Our actual results could differ materially from these forward-looking statements. We undertake no obligation to update publicly any forward-looking statement.
competitivetech
The original device, created in Korea, designed to provide stress relief, improved concentration and relaxation, and as a learning aid, has sold over 1.2 million units. Researchers at Jefferson, under the direction of Neuropsychologist Joseph I. Tracy, Ph.D, associate professor of Neurology and Radiology, Jefferson Medical College of Thomas Jefferson University, and Director, Cognitive Neuroscience and Brain Imaging Laboratory Thomas Jefferson University Hospital, tested the Jefferson-modified device for improvement of attention and concentration.
The MC Square uses Audio-Visual Stimulation through synchronized sound and light rhythms to influence brain activity. Based upon the results of rigorous testing, as detailed in the IJLT article, A test of the efficacy of the MC Square device for improving verbal memory, learning and attention, Jefferson's researchers and Daeyang E&C jointly filed a patent to utilize the improved MC Square device as a method of treatment for age-related memory loss. Under the licensing agreement, Daeyang is granted exclusive commercial rights to the technology.
IJLT, published by Inderscience (inderscience/ijlt), is an international, refereed journal providing a peer-reviewed interdisciplinary forum for the presentation of articles regarding the role of learning technologies in learning and instruction. Articles focus on the study of knowledge and learning vis-? -vis instruction and the technologies and tools that support the process.
Based on the patent-pending treatment method, the MC Square target market has been expanded from students to include normal, healthy individuals that report, or are at risk of, mild memory loss. CTT is targeting this large growing segment of the US population with marketing and distribution plans for MC Square that focus on user experience with the device.
The Alzheimer's Association (alz) estimates that risk and costs associated with age-related memory loss contribute to the estimated costs for Alzheimer's and other dementias of $148 billion annually. Alzheimer's is a progressive, degenerative disease that alters the brain, causing impaired memory, thinking and behavior. It is estimated that nearly 13% or 4.9 million people age 65 and over have Alzheimer's, and that by 2050 the number of Americans with this disease could range from 11 to 16 million unless a way is found to prevent or effectively treat this disease.
About Thomas Jefferson University
Thomas Jefferson University, based in Philadelphia, PA, is an academic health center consisting of Jefferson Medical College, Jefferson College of Graduate Studies, Jefferson College of Health Professions and associated university services. Dedicated to the health sciences, Jefferson educates professionals in a variety of disciplines to form and lead the integrated healthcare delivery and research teams of tomorrow; discovers new knowledge that will define the future of clinical care through investigation from the laboratory to the bedside, and into the community; and sets the standard for quality, compassionate and efficient patient care for their community and for the nation. Jefferson accomplishes its mission in partnership with Thomas Jefferson University Hospital, its education and clinical care affiliate. Visit Jefferson's website: jefferson
About Daeyang E&C
Daeyang E&C, founded in 1979, is a publicly traded company in Korea (KOSDAQ: 03303) with a market capitalization of $200 million. With a stated corporate philosophy of "Customer success is equivalent to corporate success," Daeyang is the market leader in its unique product segments. To fulfill the company's principle of returning profit to its customers, Daeyang created the MC Square Scholarship in 1993 with over 1,600 scholarships granted to date. Daeyang manufactures and markets a neuroscience device for increasing study efficiency called MC Square that has been established as a strong consumer brand name in Korea. Daeyang E&C accesses multiple business fields, especially in the IT and biotechnology industries, through the resources available from its affiliate Daeyang Venture Capital Ltd., also of Korea. Daeyang develops these VC business lines in health-related fields based on neuroscience technologies. Visit Daeyang's website: daeyangenc
About Competitive Technologies, Inc.
Competitive Technologies, established in 1968, is a full service technology transfer and licensing provider focused on the technology needs of its customers and transforming those requirements into commercially viable solutions. CTT is a global leader in identifying, developing and commercializing innovative technologies in life, electronic, nano, and physical sciences developed by universities, companies and inventors. CTT maximizes the value of intellectual assets for the benefit of its customers, clients and shareholders. Visit CTT's website: competitivetech
Statements about our future expectations are "forward-looking statements" within the meaning of applicable Federal Securities Laws, and are not guarantees of future performance. When used herein, the words "may," "will," "should," "anticipate," "believe," "appear," "intend," "plan," "expect," "estimate," "approximate," and similar expressions are intended to identify such forward-looking statements. These statements involve risks and uncertainties inherent in our business, including those set forth in Item 1A under the caption "Risk Factors," in our most recent Annual Report on Form 10-K for the year ended July 31, 2006, filed with the SEC on October 30, 2006, and other filings with the SEC, and are subject to change at any time. Our actual results could differ materially from these forward-looking statements. We undertake no obligation to update publicly any forward-looking statement.
competitivetech
пятница, 14 октября 2011 г.
Poor Dementia Care In Hospitals Costing Lives And Hundreds Of Millions, UK
People with dementia - who occupy a quarter of all hospital beds - are staying far longer in hospital than people without the condition who go in for the same treatment at a cost of hundreds of millions of pounds to the NHS, an Alzheimer's Society report found today (Tuesday, 17 November 2009). Based on research involving 2,400 people, Counting the Cost: caring for people with dementia on hospital wards reveals large, costly variations in the quality of care for people with dementia.
Poor hospital care also had a negative impact on the people's dementia and physical health. The majority of people with dementia leave hospital worse than when they arrive and a third enter a care home, unable to return home. Alzheimer's Society is calling for all hospitals to reduce the average length of stay for a person with dementia by at least a week. The charity is also supporting calls from nurses to be equipped with the right training and tools to do the job.
Nurses told Alzheimer's Society that they want more access to specialist advice and help. 97 per cent of nurses work with people with dementia yet 80 per cent do not receive any or enough dementia training. 89 per cent of nurses said they found working with people with dementia very or quite challenging.
Alzheimer's Society is calling for cost savings gained to be reinvested in workforce development and more appropriate care in the community.
Neil Hunt, Chief Executive of Alzheimer's Society, says,
'It is shocking that people with dementia are occupying up to a quarter of hospital beds yet there are scandalous variations in quality of dementia care in hospitals. A million more people will develop dementia in the next ten years. The NHS needs to start taking dementia seriously.
'At least ??80 million a year and probably hundreds of millions could be saved if people with dementia are enabled to leave hospital one week earlier. Hospitals must commit to reducing the length of stay if we are to stop people with dementia deteriorating in hospital and lessen the chance of people being discharged to a care home.'
Broadcaster, journalist and Alzheimer's Society Ambassador, Angela Rippon, who's supporting the campaign, says,
'I know only too well how scary it can be for a person with dementia to go into hospital. It was awful watching my mother so vulnerable and frightened in this strange, noisy environment full of people she did not know. Some people with dementia are not able to eat or drink due to a lack of appropriate dementia care and many are not being treated with dignity and respect. But good hospitals show us that with the right investment and training, quality dementia care is possible.'
Ann Reid, 63, from Eastbourne, whose mother has dementia, says,
'My mum quickly became confused and frightened in hospital. One day the staff left a sign next to her bed telling her: "you are not well, you need to stay in hospital. Just sit there, rest, relax and don't bang the table". My mum did not understand: she did not have her reading glasses with her and could not remember anything for more than two seconds.
'This was very upsetting for me - I nursed my husband through severe dementia until his death six months earlier. He too received poor care in hospital. He went in walking, and within ten days he was unable to walk and barely able to talk. I knew my mum deserved better.'
Counting the Cost: caring for people with dementia on hospital wards, based on a survey of 2,427 people with dementia, carers, nursing staff and nurse managers, found:
- 47% of carers said being in hospital had a significant negative effect on the person with dementia's health.
- 54% of carers said being in hospital had a significant negative effect on the person's dementia.
- 77% of carers dissatisfied with the quality of dementia care.
- 35% of carers complained and 38% would have liked to but didn't.
- 36% of people with dementia who go into hospital from living in their own homes are discharged to a care home.
- 34% of nurses don't receive enough dementia training.
- 54% nurses don't receive any dementia training.
- 89% nurses said people with dementia are treated with dignity and respect but 36% of carers said they were not.
(Breakdown of respondents: Carers - 1,291, Nursing Staff - 657, Nurse/Ward Managers - 479)
Notes
- Case studies, good practice examples and spokespeople available for interviews on request.
- Find out more about Alzheimer's Society's campaign to improve hospital care by visiting alzheimers.uk/countingthecost.
- People with dementia occupy one quarter of hospital beds at any one time.
- The report provides evidence on the quality of dementia care provided on general wards in hospitals across England, Wales and Northern Ireland.
- One in three people over 65 will die with dementia.
- Alzheimer's Society research shows that 700,000 people in the UK have a form of dementia, more than half have Alzheimer's disease. In less than 20 years nearly a million people will be living with dementia. This will soar to 1.7 million people by 2051.
- Alzheimer's Society champions the rights of people living with dementia and the millions of people who care for them.
Source
Alzheimer's Society
Poor hospital care also had a negative impact on the people's dementia and physical health. The majority of people with dementia leave hospital worse than when they arrive and a third enter a care home, unable to return home. Alzheimer's Society is calling for all hospitals to reduce the average length of stay for a person with dementia by at least a week. The charity is also supporting calls from nurses to be equipped with the right training and tools to do the job.
Nurses told Alzheimer's Society that they want more access to specialist advice and help. 97 per cent of nurses work with people with dementia yet 80 per cent do not receive any or enough dementia training. 89 per cent of nurses said they found working with people with dementia very or quite challenging.
Alzheimer's Society is calling for cost savings gained to be reinvested in workforce development and more appropriate care in the community.
Neil Hunt, Chief Executive of Alzheimer's Society, says,
'It is shocking that people with dementia are occupying up to a quarter of hospital beds yet there are scandalous variations in quality of dementia care in hospitals. A million more people will develop dementia in the next ten years. The NHS needs to start taking dementia seriously.
'At least ??80 million a year and probably hundreds of millions could be saved if people with dementia are enabled to leave hospital one week earlier. Hospitals must commit to reducing the length of stay if we are to stop people with dementia deteriorating in hospital and lessen the chance of people being discharged to a care home.'
Broadcaster, journalist and Alzheimer's Society Ambassador, Angela Rippon, who's supporting the campaign, says,
'I know only too well how scary it can be for a person with dementia to go into hospital. It was awful watching my mother so vulnerable and frightened in this strange, noisy environment full of people she did not know. Some people with dementia are not able to eat or drink due to a lack of appropriate dementia care and many are not being treated with dignity and respect. But good hospitals show us that with the right investment and training, quality dementia care is possible.'
Ann Reid, 63, from Eastbourne, whose mother has dementia, says,
'My mum quickly became confused and frightened in hospital. One day the staff left a sign next to her bed telling her: "you are not well, you need to stay in hospital. Just sit there, rest, relax and don't bang the table". My mum did not understand: she did not have her reading glasses with her and could not remember anything for more than two seconds.
'This was very upsetting for me - I nursed my husband through severe dementia until his death six months earlier. He too received poor care in hospital. He went in walking, and within ten days he was unable to walk and barely able to talk. I knew my mum deserved better.'
Counting the Cost: caring for people with dementia on hospital wards, based on a survey of 2,427 people with dementia, carers, nursing staff and nurse managers, found:
- 47% of carers said being in hospital had a significant negative effect on the person with dementia's health.
- 54% of carers said being in hospital had a significant negative effect on the person's dementia.
- 77% of carers dissatisfied with the quality of dementia care.
- 35% of carers complained and 38% would have liked to but didn't.
- 36% of people with dementia who go into hospital from living in their own homes are discharged to a care home.
- 34% of nurses don't receive enough dementia training.
- 54% nurses don't receive any dementia training.
- 89% nurses said people with dementia are treated with dignity and respect but 36% of carers said they were not.
(Breakdown of respondents: Carers - 1,291, Nursing Staff - 657, Nurse/Ward Managers - 479)
Notes
- Case studies, good practice examples and spokespeople available for interviews on request.
- Find out more about Alzheimer's Society's campaign to improve hospital care by visiting alzheimers.uk/countingthecost.
- People with dementia occupy one quarter of hospital beds at any one time.
- The report provides evidence on the quality of dementia care provided on general wards in hospitals across England, Wales and Northern Ireland.
- One in three people over 65 will die with dementia.
- Alzheimer's Society research shows that 700,000 people in the UK have a form of dementia, more than half have Alzheimer's disease. In less than 20 years nearly a million people will be living with dementia. This will soar to 1.7 million people by 2051.
- Alzheimer's Society champions the rights of people living with dementia and the millions of people who care for them.
Source
Alzheimer's Society
вторник, 11 октября 2011 г.
Clues To The Role Of Brain Plaques Typical In Alzheimer's Patients
A study from EPFL's (Ecole Polytechnique Federale de Lausanne) Laboratory of Neuroenergetics and Cellular Dynamics in Lausanne Switzerland, published today in the Journal of Neuroscience, may lead to new forms of treatment following a better understanding of how Amyloid-Beta found in cerebral plaques, typically present in the brain of Alzheimer's patients, may lead to neurodegeneration. Researchers in Lausanne have studied how the functions of certain cells called astrocytes - which normally protect, repair, and transfer energy to neurons - are impaired when "possessed" by aggregated Amyloid-Beta.
Alzheimer's disease currently affects more than 26 million people worldwide and estimates of up to four times as many sufferers by 2050 has made studying its causes a top priority for neuroscientists.
While the exact mechanisms by which the formation of plaques occurs and how they cause neurodegeneration and dementia is still a matter of debate in the scientific world, this study sheds a new light on how astrocytes may participate in the development of Alzheimer's disease. This new understanding of the interaction between Amyloid-Beta and astrocytes could lead to more effective therapies for Alzheimer's disease by trying to rescue astrocytic functions by deactivating the scavenger receptors.
The current study explores the causal relationship between the build-up of the Amyloid-Beta protein, associated with the formation of plaques, and the impairment of astrocyte's functions. Pierre Magistretti, director of the Brain Mind Institute and the Center for Psychiatric Neurosciences at CHUV/UNIL, and Igor Allaman, post doctoral fellow in Magistretti's lab, have succeeded in determining how built-up Amyloid-Beta infiltrates the astrocyte cells and alters their proper functioning, thus leading to the death of surrounding neurons. "To penetrate the astrocyte, the pathological protein goes through a 'scavenger' receptor." explains Igor Allaman. "Our study has shown that if we impair Amyloid-Beta build-up, or activation of this receptor, astrocytes continue to fulfill their normal neuroprotective functions even in the presence of the Amyloid-Beta."
The authors include Igor Allaman, from the Laboratory of Neuroenergetics and Cellular Dynamics in the Brain Mind Institute (EPFL), Mathilde Gavillet from the Laboratory of Neuroenergetics and Cellular Dynamics in the Brain Mind Institute (EPFL), Mireille B?©langer from the Laboratory of Neuroenergetics and Cellular Dynamics in the Brain Mind Institute (EPFL), Thierry Laroche from the Cellular Imaging Facility in the Brain Mind Institute (EPFL), David Viertl from the Laboratory of Molecular Neurobiology and Functionnal Neuroproteomics in the Brain Mind Institute (EPFL), Hilal A. Lashuel from the Laboratory of Molecular Neurobiology and Functionnal Neuroproteomics in the Brain Mind Institute (EPFL), and Pierre J. Magistretti from the Laboratory of Neuroenergetics and Cellular Dynamics in the Brain Mind Institute (EPFL) and the Centre de Neurosciences Psychiatriques, Centre Hospitalier Universitaire Vaudois, De??partement de Psychiatrie, Site de Cery, CH-1008 Prilly/Lausanne, Switzerland.
Amyloid-Beta Aggregates Cause Alterations of Astrocytic Metabolic Phenotype: Impact on Neuronal Viability, Journal of Neuroscience, March 3, 2010, issue 9
Source:
Michael Mitchell
Ecole Polytechnique F?©d?©rale de Lausanne
Alzheimer's disease currently affects more than 26 million people worldwide and estimates of up to four times as many sufferers by 2050 has made studying its causes a top priority for neuroscientists.
While the exact mechanisms by which the formation of plaques occurs and how they cause neurodegeneration and dementia is still a matter of debate in the scientific world, this study sheds a new light on how astrocytes may participate in the development of Alzheimer's disease. This new understanding of the interaction between Amyloid-Beta and astrocytes could lead to more effective therapies for Alzheimer's disease by trying to rescue astrocytic functions by deactivating the scavenger receptors.
The current study explores the causal relationship between the build-up of the Amyloid-Beta protein, associated with the formation of plaques, and the impairment of astrocyte's functions. Pierre Magistretti, director of the Brain Mind Institute and the Center for Psychiatric Neurosciences at CHUV/UNIL, and Igor Allaman, post doctoral fellow in Magistretti's lab, have succeeded in determining how built-up Amyloid-Beta infiltrates the astrocyte cells and alters their proper functioning, thus leading to the death of surrounding neurons. "To penetrate the astrocyte, the pathological protein goes through a 'scavenger' receptor." explains Igor Allaman. "Our study has shown that if we impair Amyloid-Beta build-up, or activation of this receptor, astrocytes continue to fulfill their normal neuroprotective functions even in the presence of the Amyloid-Beta."
The authors include Igor Allaman, from the Laboratory of Neuroenergetics and Cellular Dynamics in the Brain Mind Institute (EPFL), Mathilde Gavillet from the Laboratory of Neuroenergetics and Cellular Dynamics in the Brain Mind Institute (EPFL), Mireille B?©langer from the Laboratory of Neuroenergetics and Cellular Dynamics in the Brain Mind Institute (EPFL), Thierry Laroche from the Cellular Imaging Facility in the Brain Mind Institute (EPFL), David Viertl from the Laboratory of Molecular Neurobiology and Functionnal Neuroproteomics in the Brain Mind Institute (EPFL), Hilal A. Lashuel from the Laboratory of Molecular Neurobiology and Functionnal Neuroproteomics in the Brain Mind Institute (EPFL), and Pierre J. Magistretti from the Laboratory of Neuroenergetics and Cellular Dynamics in the Brain Mind Institute (EPFL) and the Centre de Neurosciences Psychiatriques, Centre Hospitalier Universitaire Vaudois, De??partement de Psychiatrie, Site de Cery, CH-1008 Prilly/Lausanne, Switzerland.
Amyloid-Beta Aggregates Cause Alterations of Astrocytic Metabolic Phenotype: Impact on Neuronal Viability, Journal of Neuroscience, March 3, 2010, issue 9
Source:
Michael Mitchell
Ecole Polytechnique F?©d?©rale de Lausanne
суббота, 8 октября 2011 г.
Education Protects Against Pre Alzheimer's Memory Loss
People with more education and more mentally demanding occupations may have protection against the memory loss that precedes Alzheimer's disease, according to a study published in the October 21, 2008, issue of Neurology®, the medical journal of the American Academy of Neurology.
The study involved 242 people with Alzheimer's disease, 72 people with mild cognitive impairment, and 144 people with no memory problems. Mild cognitive impairment is a transition stage when some memory problems are occurring beyond what is normal for a person's age but not the serious problems of Alzheimer's disease.
Researchers tested the participants' memory and cognitive skills and used brain scans to measure the amount of brain glucose metabolism, which shows how much the brain has been affected by the plaques and tangles of Alzheimer's disease. The participants were followed for an average of 14 months. During that time, 21 of the people with mild cognitive impairment developed Alzheimer's disease.
The study found that in people with the same level of memory impairment, people with more education and more mentally demanding jobs had significantly more changes and damage in their brains from Alzheimer's disease than people with less education and less mentally demanding jobs.
"The theory is that education and demanding jobs create a buffer against the effects of dementia on the brain, or a cognitive reserve," said study author Valentina Garibotto, MD, of the San Raffaele University and Scientific Institute and the National Institute of Neuroscience in Milan, Italy. "Their brains are able to compensate for the damage and allow them to maintain functioning in spite of damage. There are two possible explanations. The brain could be made stronger through education and occupational challenges. Or, genetic factors that enabled people to achieve higher education and occupational achievement might determine the amount of brain reserve. It isn't possible to determine which accounts for our findings."
The results were found in both people with Alzheimer's and people with mild cognitive impairment who developed Alzheimer's during the study, suggesting that the cognitive reserve is already in effect during the mild cognitive impairment phase before Alzheimer's begins, Garibotto said.
People with Alzheimer's disease and people with mild cognitive impairment who developed Alzheimer's during the study had metabolic dysfunction in the areas of the brain consistent with Alzheimer's disease, whereas the healthy people and those with mild cognitive impairment who did not develop Alzheimer's disease had no brain metabolism problems.
The study was supported by NEST-DD (Network for Efficiency and Standardization of Dementia Diagnosis), 5th European Research Program and DIMI (Diagnostic Molecular Imaging) Network of Excellence, 6th European Research Program.
The American Academy of Neurology, an association of more than 21,000 neurologists and neuroscience professionals, is dedicated to improving patient care through education and research. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as epilepsy, dystonia, migraine, Huntington's disease, and dementia. For more information about the American Academy of Neurology, visit aan.
American Academy of Neurology (AAN)
1080 Montreal Ave.
St. Paul, MN 55116
United States
neurology
The study involved 242 people with Alzheimer's disease, 72 people with mild cognitive impairment, and 144 people with no memory problems. Mild cognitive impairment is a transition stage when some memory problems are occurring beyond what is normal for a person's age but not the serious problems of Alzheimer's disease.
Researchers tested the participants' memory and cognitive skills and used brain scans to measure the amount of brain glucose metabolism, which shows how much the brain has been affected by the plaques and tangles of Alzheimer's disease. The participants were followed for an average of 14 months. During that time, 21 of the people with mild cognitive impairment developed Alzheimer's disease.
The study found that in people with the same level of memory impairment, people with more education and more mentally demanding jobs had significantly more changes and damage in their brains from Alzheimer's disease than people with less education and less mentally demanding jobs.
"The theory is that education and demanding jobs create a buffer against the effects of dementia on the brain, or a cognitive reserve," said study author Valentina Garibotto, MD, of the San Raffaele University and Scientific Institute and the National Institute of Neuroscience in Milan, Italy. "Their brains are able to compensate for the damage and allow them to maintain functioning in spite of damage. There are two possible explanations. The brain could be made stronger through education and occupational challenges. Or, genetic factors that enabled people to achieve higher education and occupational achievement might determine the amount of brain reserve. It isn't possible to determine which accounts for our findings."
The results were found in both people with Alzheimer's and people with mild cognitive impairment who developed Alzheimer's during the study, suggesting that the cognitive reserve is already in effect during the mild cognitive impairment phase before Alzheimer's begins, Garibotto said.
People with Alzheimer's disease and people with mild cognitive impairment who developed Alzheimer's during the study had metabolic dysfunction in the areas of the brain consistent with Alzheimer's disease, whereas the healthy people and those with mild cognitive impairment who did not develop Alzheimer's disease had no brain metabolism problems.
The study was supported by NEST-DD (Network for Efficiency and Standardization of Dementia Diagnosis), 5th European Research Program and DIMI (Diagnostic Molecular Imaging) Network of Excellence, 6th European Research Program.
The American Academy of Neurology, an association of more than 21,000 neurologists and neuroscience professionals, is dedicated to improving patient care through education and research. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as epilepsy, dystonia, migraine, Huntington's disease, and dementia. For more information about the American Academy of Neurology, visit aan.
American Academy of Neurology (AAN)
1080 Montreal Ave.
St. Paul, MN 55116
United States
neurology
среда, 5 октября 2011 г.
Promising Alzheimer's Disease Treatment Revealed By Early Study
A drug once approved as an antihistamine in Russia improved thinking processes and ability to function in patients with Alzheimer's disease in a study conducted there, said an expert at Baylor College of Medicine in Houston. The findings are published in the current issue of the journal The Lancet.
"More research is needed, but we are encouraged by the effect the drug Dimebon had on Alzheimer's patients" said Dr. Rachelle Doody, professor of neurology at BCM and lead author of the study.
In the study, the authors noted that Dimebon is the first drug for Alzheimer's disease that demonstrated continued improvement in patients over a 12 month period. Other approved drugs do not have this effect.
Half of the 183 patients in the Russian study received Dimebon; the other half were given a placebo or an inactive pill. Clinicians at the study sites then monitored the patients' progress over the next year on five different outcomes. All of those in the study had mild to moderate Alzheimer's disease.
"What we saw in the clinical trial is that people on the medication continued to improve over time," Doody said. "Those on placebo continued to decline."
Researchers believe the medication works by stabilizing mitochondria, the cellular components that produce energy, and possibly by inhibiting brain cell death. Researchers evaluated patients' thinking and memory ability, overall function, psychiatric and behavioral symptoms, and ability to perform daily activities.
"Usually at this point in a drug's development, we are happy to see improvement in one of the outcome measures," Doody said. "We saw improvement in all five."
Some participants complained of occasional dry mouth, but no one opted out of the study because of the side effects.
"As we continue research, we hope to replicate these results," Doody said. "My belief is that this drug will turn out to be useful for Alzheimer's disease, regardless of the stage of the disease."
Doody said this is only the first study looking into the effects of Dimebon on Alzheimer's disease. She also noted that it involved only a relatively small population from one specific region of the world. The ongoing Phase 3 study will include several international locations including the United States.
Other researchers who contributed to this study include: Dr. Svetlana I. Gavrilova, Russian Academy of Medical Sciences, Moscow, Russia; Dr. Mary Sano, Mount Sinai School of Medicine, New York City, NY; Dr. Ronald G. Thomas, University of California, San Diego, La Jolla, CA; Dr. Paul S. Aisen, formerly with Georgetown University School of Medicine, Washington, DC and now at the University of California, San Diego; ; Dr. Sergey O. Bachurin, Russian Academy of Sciences, Institute of Physiologically Active Compounds, Chernogolovka, Russia; Drs. Lynn Seely and David Hung, Medivation, Inc., San Francisco, CA.
Funding for this study came from Medivation, Inc., the company developing the drug worldwide. Doody is also a member of the Scientific and Clinical Advisory board for Medivation, Inc.
The full report can be found at thelancet/
More information on science research at Baylor College of Medicine can be found at bcm/fromthelab or bcm/findings.
Source: Graciela Gutierrez
Baylor College of Medicine
"More research is needed, but we are encouraged by the effect the drug Dimebon had on Alzheimer's patients" said Dr. Rachelle Doody, professor of neurology at BCM and lead author of the study.
In the study, the authors noted that Dimebon is the first drug for Alzheimer's disease that demonstrated continued improvement in patients over a 12 month period. Other approved drugs do not have this effect.
Half of the 183 patients in the Russian study received Dimebon; the other half were given a placebo or an inactive pill. Clinicians at the study sites then monitored the patients' progress over the next year on five different outcomes. All of those in the study had mild to moderate Alzheimer's disease.
"What we saw in the clinical trial is that people on the medication continued to improve over time," Doody said. "Those on placebo continued to decline."
Researchers believe the medication works by stabilizing mitochondria, the cellular components that produce energy, and possibly by inhibiting brain cell death. Researchers evaluated patients' thinking and memory ability, overall function, psychiatric and behavioral symptoms, and ability to perform daily activities.
"Usually at this point in a drug's development, we are happy to see improvement in one of the outcome measures," Doody said. "We saw improvement in all five."
Some participants complained of occasional dry mouth, but no one opted out of the study because of the side effects.
"As we continue research, we hope to replicate these results," Doody said. "My belief is that this drug will turn out to be useful for Alzheimer's disease, regardless of the stage of the disease."
Doody said this is only the first study looking into the effects of Dimebon on Alzheimer's disease. She also noted that it involved only a relatively small population from one specific region of the world. The ongoing Phase 3 study will include several international locations including the United States.
Other researchers who contributed to this study include: Dr. Svetlana I. Gavrilova, Russian Academy of Medical Sciences, Moscow, Russia; Dr. Mary Sano, Mount Sinai School of Medicine, New York City, NY; Dr. Ronald G. Thomas, University of California, San Diego, La Jolla, CA; Dr. Paul S. Aisen, formerly with Georgetown University School of Medicine, Washington, DC and now at the University of California, San Diego; ; Dr. Sergey O. Bachurin, Russian Academy of Sciences, Institute of Physiologically Active Compounds, Chernogolovka, Russia; Drs. Lynn Seely and David Hung, Medivation, Inc., San Francisco, CA.
Funding for this study came from Medivation, Inc., the company developing the drug worldwide. Doody is also a member of the Scientific and Clinical Advisory board for Medivation, Inc.
The full report can be found at thelancet/
More information on science research at Baylor College of Medicine can be found at bcm/fromthelab or bcm/findings.
Source: Graciela Gutierrez
Baylor College of Medicine
воскресенье, 2 октября 2011 г.
Soybean Product Fights Abnormal Protein Involved In Alzheimer's Disease
A vegan food renowned in Asia for its ability to protect against heart attacks also shows a powerful ability in lab experiments to prevent formation of the clumps of tangled protein involved in Alzheimer's disease, scientists in Taiwan are reporting. Their study is in the Feb. 11 issue of ACS' Journal of Agricultural and Food Chemistry, a bi-weekly publication.
Rita P. Y. Chen and colleagues point out that people in Asia have been eating natto - a fermented food made from boiled soybeans -for more than 1,000 years. Natto contains an enzyme, nattokinase, that has effects similar to clot-busting drugs used in heart disease. Nattokinase is sold a dietary supplement to improve the body's circulatory system. The scientists term this the first study on whether nattokinase also can dissolve amyloids. Those tangled proteins are involved in Alzheimer's disease and several other health problems.
In the study, the nattokinase degraded several kinds of amyloid fibrils, suggesting its possible use in the treatment of amyloid-related diseases. "Moreover, since natto has been ingested by humans for a long time, it would be worthwhile to carry out an epidemiological study on the rate of occurrence of various amyloid-related diseases in a population regularly consuming natto," the scientists say.
"Amyloid-Degrading Ability of Nattokinase from Bacillus subtilis Natto"
DOWNLOAD FULL TEXT ARTICLE
American Chemical Society
The world's largest scientific society.
acs
Rita P. Y. Chen and colleagues point out that people in Asia have been eating natto - a fermented food made from boiled soybeans -for more than 1,000 years. Natto contains an enzyme, nattokinase, that has effects similar to clot-busting drugs used in heart disease. Nattokinase is sold a dietary supplement to improve the body's circulatory system. The scientists term this the first study on whether nattokinase also can dissolve amyloids. Those tangled proteins are involved in Alzheimer's disease and several other health problems.
In the study, the nattokinase degraded several kinds of amyloid fibrils, suggesting its possible use in the treatment of amyloid-related diseases. "Moreover, since natto has been ingested by humans for a long time, it would be worthwhile to carry out an epidemiological study on the rate of occurrence of various amyloid-related diseases in a population regularly consuming natto," the scientists say.
"Amyloid-Degrading Ability of Nattokinase from Bacillus subtilis Natto"
DOWNLOAD FULL TEXT ARTICLE
American Chemical Society
The world's largest scientific society.
acs
четверг, 29 сентября 2011 г.
Research Suggests Alcohol Consumption Helps Stave Off Dementia
Experts agree that long-term alcohol abuse is detrimental to memory function and can cause neuro-degenerative disease. However, according to a study published in Age and Ageing by Oxford University Press today, there is evidence that light-to-moderate alcohol consumption may decrease the risk of cognitive decline or dementia.
Estimates from various studies have suggested the prevalence of alcohol-related dementia to be about 10% of all cases of dementia. Now researchers have found after analyzing 23 longitudinal studies of subjects aged 65 years and older that the impact of small amounts of alcohol was associated with lower incidence rates of overall dementia and Alzheimer dementia, but not of vascular dementia and cognitive decline. It is still an open question whether different alcoholic beverages, such as beer, wine, and spirits, all have a similar effect. Some studies have shown a positive effect of wine only, which may be due either to the level of ethanol, the complex mixture that comprises wine, or to the healthier life-style ascribed to wine drinkers.
A total of 3,327 patients were interviewed in their homes by trained investigators (physicians, psychologists, gerontologists) and reassessed one and a half years and three years later. Information on the cognitive status of those who had died in the interim was collected from family members, caregivers or primary care physicians.
Among the 3,327 patients interviewed at baseline, 84.8% (n=2,820) could be personally interviewed one and a half years later and 73.9% (n=2,460) three years later. For the vast majority of subjects who could not be personally interviewed, systematic assessments (follow-up 1: 482; follow-up 2: 336) focusing particularly on dementia could be obtained from GPs, relatives or caregivers. Within three years, follow-up assessments were unavailable for only 49 subjects (1.5%). Proxy information could be obtained for 98.0% (n=295) of the 301 patients who had died in the interim. Since dementia is associated with a higher mortality rate, proxy information is particularly important in order to avoid underestimation of incident dementia cases.
At baseline there were 3,202 persons without dementia. Alcohol consumption information was available for 3,180 subjects:
50.0% were abstinent
24.8% consumed less than one drink (10 grams of alcohol) per day
12.8% consumed 10-19 grams of alcohol per day
12.4% consumed 20 or more grams per day
A small subgroup of 25 participants fulfilled the criteria of harmful drinking (>60 grams of alcohol per day for men, respectively >40 grams for women)
One man (>120 grams of alcohol per day) and one woman (>80 grams of alcohol per day) reported an extremely high consumption of alcohol
Among the consumers of alcohol almost half (48.6%) drank wine only
29.0% drank beer only
22.4% drank mixed alcohol beverages (wine, beer, or spirits)
Alcohol consumption was significantly associated with male gender, younger age, higher level of education, not living alone, and not being depressed.
The calculation of incident cases of dementia is based on 3,202 subjects who had no dementia at baseline. Within the follow-up period of three years:
217 cases of dementia (6.8%) were diagnosed, whereby 111 subjects (3.5%) suffered from Alzheimer dementia. Due to the relatively small numbers, other subgroups of dementia (vascular dementia: n=42; other specific dementia, e.g. dementia in Parkinson's disease, Lewy body dementia, alcohol dementia: n=14; dementia with unknown aetiology: n=50) were not considered in the following analyses.
Univariate and multivariate analyses revealed that alcohol consumption was significantly associated with a lower incidence of overall dementia and Alzheimer dementia. In line with a large-scale study also based on GP attenders aged 75 years and older, the study found that light-to-moderate alcohol consumption was associated with relatively good physical and mental health. This three-year follow-up study included, at baseline, only those subjects 75 years of age and older, the mean age was 80.2 years, much higher than that in most other studies.
Acknowledgements
This study is part of the German Research Network on Dementia (KND) and the German Research Network on Degenerative Dementia (KNDD) and was funded by the German Federal Ministry of Education and Research (grants KND: 01GI0102, 01GI0420, 01GI0422, 01GI0423, 01GI0429, 01GI0431, 01GI0433, 01GI0434; grants KNDD: O1GI0710, 01GI0711, 01GI0712, 01GI0713, 01GI0714, 01GI0715, 01GI0716). The funding bodies have had no influence on the paper or the decision to publish.
Citation
"Current alcohol consumption and its relationship to incident dementia: results from a 3-year follow-up study among primary
care attenders aged 75 years and older"
Siegfriedweyerer1, Martina Sch?¤ufele1, Birgittwiese 2, Wolfgangmaier3, Franziskatebarth3,
Hendrik Van Den Bussche4, Michael Pentzek5, Horst Bickel6, Melanie Luppa7,
Steffi G. Riedel-Heller7 for the German AGECODE study group (German Study On Ageing,
Cognition and Dementia in Primary Care Patients)
1 Central Institute of Mental Health, Mannheim, Germany
2 Institute for Biometrics, Hannover Medical School, Hannover, Germany
3 Department of Psychiatry, University of Bonn, Bonn, Germany
4 Institute of Primary Medical Care, University Medical Center Hamburg-Eppendorf, Hamburg, Germany
5 Department of General Practice, University Medical Center D??sseldorf, Dusseldorf, Germany
6 Department of Psychiatry, Technical University of Munich, Munich, Germany
7 Department of Psychiatry, University of Leipzig, Leipzig, Germany
Age and Ageing 2011; 0: 1-7, doi: 10.1093/ageing/afr007
Estimates from various studies have suggested the prevalence of alcohol-related dementia to be about 10% of all cases of dementia. Now researchers have found after analyzing 23 longitudinal studies of subjects aged 65 years and older that the impact of small amounts of alcohol was associated with lower incidence rates of overall dementia and Alzheimer dementia, but not of vascular dementia and cognitive decline. It is still an open question whether different alcoholic beverages, such as beer, wine, and spirits, all have a similar effect. Some studies have shown a positive effect of wine only, which may be due either to the level of ethanol, the complex mixture that comprises wine, or to the healthier life-style ascribed to wine drinkers.
A total of 3,327 patients were interviewed in their homes by trained investigators (physicians, psychologists, gerontologists) and reassessed one and a half years and three years later. Information on the cognitive status of those who had died in the interim was collected from family members, caregivers or primary care physicians.
Among the 3,327 patients interviewed at baseline, 84.8% (n=2,820) could be personally interviewed one and a half years later and 73.9% (n=2,460) three years later. For the vast majority of subjects who could not be personally interviewed, systematic assessments (follow-up 1: 482; follow-up 2: 336) focusing particularly on dementia could be obtained from GPs, relatives or caregivers. Within three years, follow-up assessments were unavailable for only 49 subjects (1.5%). Proxy information could be obtained for 98.0% (n=295) of the 301 patients who had died in the interim. Since dementia is associated with a higher mortality rate, proxy information is particularly important in order to avoid underestimation of incident dementia cases.
At baseline there were 3,202 persons without dementia. Alcohol consumption information was available for 3,180 subjects:
50.0% were abstinent
24.8% consumed less than one drink (10 grams of alcohol) per day
12.8% consumed 10-19 grams of alcohol per day
12.4% consumed 20 or more grams per day
A small subgroup of 25 participants fulfilled the criteria of harmful drinking (>60 grams of alcohol per day for men, respectively >40 grams for women)
One man (>120 grams of alcohol per day) and one woman (>80 grams of alcohol per day) reported an extremely high consumption of alcohol
Among the consumers of alcohol almost half (48.6%) drank wine only
29.0% drank beer only
22.4% drank mixed alcohol beverages (wine, beer, or spirits)
Alcohol consumption was significantly associated with male gender, younger age, higher level of education, not living alone, and not being depressed.
The calculation of incident cases of dementia is based on 3,202 subjects who had no dementia at baseline. Within the follow-up period of three years:
217 cases of dementia (6.8%) were diagnosed, whereby 111 subjects (3.5%) suffered from Alzheimer dementia. Due to the relatively small numbers, other subgroups of dementia (vascular dementia: n=42; other specific dementia, e.g. dementia in Parkinson's disease, Lewy body dementia, alcohol dementia: n=14; dementia with unknown aetiology: n=50) were not considered in the following analyses.
Univariate and multivariate analyses revealed that alcohol consumption was significantly associated with a lower incidence of overall dementia and Alzheimer dementia. In line with a large-scale study also based on GP attenders aged 75 years and older, the study found that light-to-moderate alcohol consumption was associated with relatively good physical and mental health. This three-year follow-up study included, at baseline, only those subjects 75 years of age and older, the mean age was 80.2 years, much higher than that in most other studies.
Acknowledgements
This study is part of the German Research Network on Dementia (KND) and the German Research Network on Degenerative Dementia (KNDD) and was funded by the German Federal Ministry of Education and Research (grants KND: 01GI0102, 01GI0420, 01GI0422, 01GI0423, 01GI0429, 01GI0431, 01GI0433, 01GI0434; grants KNDD: O1GI0710, 01GI0711, 01GI0712, 01GI0713, 01GI0714, 01GI0715, 01GI0716). The funding bodies have had no influence on the paper or the decision to publish.
Citation
"Current alcohol consumption and its relationship to incident dementia: results from a 3-year follow-up study among primary
care attenders aged 75 years and older"
Siegfriedweyerer1, Martina Sch?¤ufele1, Birgittwiese 2, Wolfgangmaier3, Franziskatebarth3,
Hendrik Van Den Bussche4, Michael Pentzek5, Horst Bickel6, Melanie Luppa7,
Steffi G. Riedel-Heller7 for the German AGECODE study group (German Study On Ageing,
Cognition and Dementia in Primary Care Patients)
1 Central Institute of Mental Health, Mannheim, Germany
2 Institute for Biometrics, Hannover Medical School, Hannover, Germany
3 Department of Psychiatry, University of Bonn, Bonn, Germany
4 Institute of Primary Medical Care, University Medical Center Hamburg-Eppendorf, Hamburg, Germany
5 Department of General Practice, University Medical Center D??sseldorf, Dusseldorf, Germany
6 Department of Psychiatry, Technical University of Munich, Munich, Germany
7 Department of Psychiatry, University of Leipzig, Leipzig, Germany
Age and Ageing 2011; 0: 1-7, doi: 10.1093/ageing/afr007
понедельник, 26 сентября 2011 г.
Decreased TGF-beta Signaling Might Make You Demented
The physical changes that occur in the brain of patients with Alzheimer's disease (AD), the most common cause of dementia in the elderly, have been well characterized, but the cause(s) of this disease and the development of therapies has remained elusive. Now, in a study appearing in the November issue of the Journal of Clinical Investigation, researchers from Stanford University have shown that decreased signaling through a receptor known as T-beta-RII -- expression of which is decreased in the neurons of patients with AD -- increases neurodegeneration in mice.
Tony Wyss-Coray and colleagues found that neuron expression of T-beta-RII is decreased at an early stage of disease in the brains of individuals with AD. So they generated mice in which signaling by the molecule that triggers T-beta-RII, TGF-beta, is decreased. Analysis of these mice showed age-dependent neurodegeneration and beta-amyloid peptide accumulation in the brain, as is seen in the brain of patients with AD. The authors therefore suggest that increasing TGF-beta signaling in the brain might reduce neurodegeneration and be of benefit to individuals with AD.
In an accompanying commentary, Pritam Das and Todd Golde from the Mayo Clinic in Jacksonville outline how a decrease in TGF-beta signaling in the brain might promote neurodegeneration and beta-amyloid peptide accumulation, but warn that further studies to determine what causes the decreased expression of T-beta-RII are required.
TITLE: Deficiency in neuronal TGF-beta signaling promotes neurodegeneration and Alzheimer's pathology
AUTHOR CONTACT:
Tony Wyss-Coray
Stanford University, Stanford, California, USA.
ACCOMPANYING COMMENTARY
TITLE: Dysfunction of TGF-beta in Alzheimer's disease
AUTHOR CONTACT:
Todd Golde
Mayo Clinic Jacksonville, Jacksonville, Florida, USA. P
Pritam Das
Mayo Clinic Jacksonville, Jacksonville, Florida, USA.
Contact: Karen Honey
Journal of Clinical Investigation
Tony Wyss-Coray and colleagues found that neuron expression of T-beta-RII is decreased at an early stage of disease in the brains of individuals with AD. So they generated mice in which signaling by the molecule that triggers T-beta-RII, TGF-beta, is decreased. Analysis of these mice showed age-dependent neurodegeneration and beta-amyloid peptide accumulation in the brain, as is seen in the brain of patients with AD. The authors therefore suggest that increasing TGF-beta signaling in the brain might reduce neurodegeneration and be of benefit to individuals with AD.
In an accompanying commentary, Pritam Das and Todd Golde from the Mayo Clinic in Jacksonville outline how a decrease in TGF-beta signaling in the brain might promote neurodegeneration and beta-amyloid peptide accumulation, but warn that further studies to determine what causes the decreased expression of T-beta-RII are required.
TITLE: Deficiency in neuronal TGF-beta signaling promotes neurodegeneration and Alzheimer's pathology
AUTHOR CONTACT:
Tony Wyss-Coray
Stanford University, Stanford, California, USA.
ACCOMPANYING COMMENTARY
TITLE: Dysfunction of TGF-beta in Alzheimer's disease
AUTHOR CONTACT:
Todd Golde
Mayo Clinic Jacksonville, Jacksonville, Florida, USA. P
Pritam Das
Mayo Clinic Jacksonville, Jacksonville, Florida, USA.
Contact: Karen Honey
Journal of Clinical Investigation
пятница, 23 сентября 2011 г.
Government's Carer Support Strategy Is "Pathetic" Says Southport Dementia Pioneer, UK
A dementia care and support pioneer says that the government has missed the boat spectacularly in its "dabbling and pathetic" response to the needs of family and home carers in the UK.
Dan Lingard, Chief Executive of Melton Heath Care Limited, which owns the innovative Birch Abbey care centre in Southport, says that the government's reaction to the Commons Work and Pensions Committee report into the plight of the country's six million unpaid carers who don't want to use professional care services such as home carers and care homes is another illustration of how out-of-touch ministers are.
The committee says that state help for carers is now of critical importance.
"It is not just critical, it is massively urgent. On the one hand the government is telling us that we are in some quarters enjoying better health and longevity than ever before, but they are simply not grasping the nettle and moving fast enough to address the issues that come with living longer,"
said Dan Lingard.
"The longer we live, the more likely we are to fall into ill-health and to start to be affected by conditions such as dementia.
"Somebody has to help the growing population of people with dementia, and while some families' circumstances allow them to bring in professional support offered by organisations such as ours, there are many families whose circumstances do not permit such input and support, or, in fact, have decided they don't want to use 'professional' carers at home or from a care home.
"The committee said that it was disappointed that the government had not addressed the issue of financial help for carers in its Carers Strategy, which was launched earlier this year, and it has hit the nail on the head with regard to the key issue.
"As somebody who is frontline in supporting people with dementia - and their families - I can only say that the government is doing what it has typically done for this much misunderstood and undervalued group of
people: it has nibbled round the edges, dabbled, put off a decision and provided a pathetic response.
"My team are professional carers and supporters of people with dementia and their families; at a professional level it is challenging - and in witnessing the challenges facing families on a daily basis I can provide cast-iron assurances that the efforts and commitment of family carers is absolutely immense.
"In effect many give up a great deal of their lives to care for loved ones with dementia. Financial support for carers should be an immediate priority, not something that has been put on the backburner in the Carers Strategy until 2011."
Dan Lingard, Chief Executive of Altrincham-based Melton Health Care Limited, which owns Birch Abbey care home in Southport, is a former software developer working with IBM and the BBC. He says much-misunderstood dementia needs to be fought, and people with the condition, and their family and friends, supported and inspired rather than simply have their basic needs attended to.
Dan and his team at Birch Abbey invented and pioneered a specialist monitoring system to support people with dementia, MyAmego (myamego), an award-winning world first, which is now being installed in care homes and day centres, "extra care" flats and for use at home.
MyAmego
Dan Lingard, Chief Executive of Melton Heath Care Limited, which owns the innovative Birch Abbey care centre in Southport, says that the government's reaction to the Commons Work and Pensions Committee report into the plight of the country's six million unpaid carers who don't want to use professional care services such as home carers and care homes is another illustration of how out-of-touch ministers are.
The committee says that state help for carers is now of critical importance.
"It is not just critical, it is massively urgent. On the one hand the government is telling us that we are in some quarters enjoying better health and longevity than ever before, but they are simply not grasping the nettle and moving fast enough to address the issues that come with living longer,"
said Dan Lingard.
"The longer we live, the more likely we are to fall into ill-health and to start to be affected by conditions such as dementia.
"Somebody has to help the growing population of people with dementia, and while some families' circumstances allow them to bring in professional support offered by organisations such as ours, there are many families whose circumstances do not permit such input and support, or, in fact, have decided they don't want to use 'professional' carers at home or from a care home.
"The committee said that it was disappointed that the government had not addressed the issue of financial help for carers in its Carers Strategy, which was launched earlier this year, and it has hit the nail on the head with regard to the key issue.
"As somebody who is frontline in supporting people with dementia - and their families - I can only say that the government is doing what it has typically done for this much misunderstood and undervalued group of
people: it has nibbled round the edges, dabbled, put off a decision and provided a pathetic response.
"My team are professional carers and supporters of people with dementia and their families; at a professional level it is challenging - and in witnessing the challenges facing families on a daily basis I can provide cast-iron assurances that the efforts and commitment of family carers is absolutely immense.
"In effect many give up a great deal of their lives to care for loved ones with dementia. Financial support for carers should be an immediate priority, not something that has been put on the backburner in the Carers Strategy until 2011."
Dan Lingard, Chief Executive of Altrincham-based Melton Health Care Limited, which owns Birch Abbey care home in Southport, is a former software developer working with IBM and the BBC. He says much-misunderstood dementia needs to be fought, and people with the condition, and their family and friends, supported and inspired rather than simply have their basic needs attended to.
Dan and his team at Birch Abbey invented and pioneered a specialist monitoring system to support people with dementia, MyAmego (myamego), an award-winning world first, which is now being installed in care homes and day centres, "extra care" flats and for use at home.
MyAmego
вторник, 20 сентября 2011 г.
Scientists Use Shared Genome Data To Confirm SORL1 Gene Linked To Alzheimer's
Until recently, only one of the approximately 30,000 genes in the human genome has been linked to risk of late-onset Alzheimer's disease (AD). Now, a new NIH-supported study in the Nov. 19, 2007, issue of NeuroReport (now online) used a publicly shared genome dataset to strongly support findings that variation in the sequence of the SORL1 gene may be a second risk factor gene for late-onset disease. Identifying the genes involved in AD ultimately may help determine who may be at greater risk and enable researchers to zero in on pathways to develop new treatments.
The National Institute on Aging (NIA), part of the National Institutes of Health (NIH), funded the study, along with the Canadian Institutes of Health Research and a number of private foundations in the U.S., Canada and Japan.
Three mutated genes - amyloid precursor protein (APP) and the presenilins (PS1 and PS2) - have been shown to cause rare, early-onset, familial forms of the disease which mostly occur in middle age. A gene variant - apolipoprotein ?µ4 (APO-?µ4) - was the first confirmed risk factor for the common form of late-onset AD, which typically occurs after age 65.
Earlier this year, researchers first linked variations in the gene SORL1 to late-onset AD. The analysis involved 14 collaborating institutions in North America, Europe and Asia, and 6,600 people who donated blood and tissue for genetic typing. To learn more, go to here.
This new study confirms those findings and in a novel way. Lindsay A. Farrer, Ph.D., of the Boston University School of Medicine and colleagues accessed data from a genome-wide association study (GWAS) recently made publicly available online by the Translational Genomics Research Institute (TGen), a nonprofit research institute promoting genomics research. GWAS involves rapidly scanning for markers across the complete set of DNA of many people to find genetic variations related to a particular disease. By analyzing TGen's data on the DNA of 1,408 cases and controls, Dr. Farrer's study replicated the findings of the earlier studies that linked SORL1 data to late-onset AD.
"These results are especially remarkable since this gene was not a focus of the original TGen study which generated the data used to test our hypothesis," Farrer said.
"This is the first example of publicly available data from a genome-wide association study to confirm the identification of a risk factor gene," said Marcelle Morrison-Bogorad, Ph.D., director of the Neuroscience and Neuropsychology Program at NIA. "This shows the tremendous benefit of highly collaborative interaction and rapid data sharing. Sample sharing greatly increases the likelihood of finding new risk factor genes relatively quickly and inexpensively."
Collaboration was a hallmark of the study, with TGen conducting the GWAS using brain tissues and blood samples made available by NIA Alzheimer Center brain banks, NIA-funded investigators, and other collaborating institutes. The Boston University Linux Cluster for Genetic Analysis, funded by the National Center for Research Resources (NCRR) at the NIH, provided Dr. Farrer's group high-speed computer analysis.
NIA leads the federal effort on understanding the biomedical, social and behavioral aspects of aging and the problems of older people by conducting and supporting research into these areas. For more information on aging-related research and the NIA, please visit nia.nih. The NIA provides information on age-related cognitive change and neurodegenerative disease specifically at its Alzheimer's Disease Education and Referral (ADEAR) Center site at nia.nih/alzheimers.
The National Institutes of Health (NIH) - The Nation's Medical Research Agency - includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit nih.
The National Institute on Aging (NIA), part of the National Institutes of Health (NIH), funded the study, along with the Canadian Institutes of Health Research and a number of private foundations in the U.S., Canada and Japan.
Three mutated genes - amyloid precursor protein (APP) and the presenilins (PS1 and PS2) - have been shown to cause rare, early-onset, familial forms of the disease which mostly occur in middle age. A gene variant - apolipoprotein ?µ4 (APO-?µ4) - was the first confirmed risk factor for the common form of late-onset AD, which typically occurs after age 65.
Earlier this year, researchers first linked variations in the gene SORL1 to late-onset AD. The analysis involved 14 collaborating institutions in North America, Europe and Asia, and 6,600 people who donated blood and tissue for genetic typing. To learn more, go to here.
This new study confirms those findings and in a novel way. Lindsay A. Farrer, Ph.D., of the Boston University School of Medicine and colleagues accessed data from a genome-wide association study (GWAS) recently made publicly available online by the Translational Genomics Research Institute (TGen), a nonprofit research institute promoting genomics research. GWAS involves rapidly scanning for markers across the complete set of DNA of many people to find genetic variations related to a particular disease. By analyzing TGen's data on the DNA of 1,408 cases and controls, Dr. Farrer's study replicated the findings of the earlier studies that linked SORL1 data to late-onset AD.
"These results are especially remarkable since this gene was not a focus of the original TGen study which generated the data used to test our hypothesis," Farrer said.
"This is the first example of publicly available data from a genome-wide association study to confirm the identification of a risk factor gene," said Marcelle Morrison-Bogorad, Ph.D., director of the Neuroscience and Neuropsychology Program at NIA. "This shows the tremendous benefit of highly collaborative interaction and rapid data sharing. Sample sharing greatly increases the likelihood of finding new risk factor genes relatively quickly and inexpensively."
Collaboration was a hallmark of the study, with TGen conducting the GWAS using brain tissues and blood samples made available by NIA Alzheimer Center brain banks, NIA-funded investigators, and other collaborating institutes. The Boston University Linux Cluster for Genetic Analysis, funded by the National Center for Research Resources (NCRR) at the NIH, provided Dr. Farrer's group high-speed computer analysis.
NIA leads the federal effort on understanding the biomedical, social and behavioral aspects of aging and the problems of older people by conducting and supporting research into these areas. For more information on aging-related research and the NIA, please visit nia.nih. The NIA provides information on age-related cognitive change and neurodegenerative disease specifically at its Alzheimer's Disease Education and Referral (ADEAR) Center site at nia.nih/alzheimers.
The National Institutes of Health (NIH) - The Nation's Medical Research Agency - includes 27 Institutes and Centers and is a component of the U.S. Department of Health and Human Services. It is the primary federal agency for conducting and supporting basic, clinical and translational medical research, and it investigates the causes, treatments, and cures for both common and rare diseases. For more information about NIH and its programs, visit nih.
суббота, 17 сентября 2011 г.
Eisai Submits Application to FDA for ARICEPT(R) for Treatment of Severe Alzheimer's Disease
Eisai Co, Ltd and Eisai Inc announced that on their behalf, Eisai Medical Research Inc. (Headquarters: Ridgefield Park, President Mindell Seidlin, MD) has submitted a supplemental New Drug Application (sNDA) to the U.S. Food and Drug Administration for ARICEPT(R) (donepezil HCl tablets) for treatment of severe Alzheimer's disease (AD). ARICEPT, which is co-promoted in the United States by Eisai Inc. and Pfizer Inc, is currently approved for treatment of mild to moderate AD.
"Our goal to provide ARICEPT to people with severe Alzheimer's disease is consistent with Eisai's human health care mission to improve the lives of patients and their families," said Lonnel Coats, president and COO, Eisai Inc.
The August 31 submission is based on data from a six-month, multi-center, randomized, double-blind, placebo-controlled clinical trial conducted in approximately 250 nursing home patients with severe AD. In the pivotal study, patients with severe AD (Mini Mental State Examination scores 1-10) treated with ARICEPT had a statistically significant improvement compared to those taking placebo on both primary measures of efficacy: the Severe Impairment Battery (SIB scale) and the Modified Alzheimer's Disease Cooperative Study Activities of Daily Living Inventory for Severe Alzheimer's Disease (ADCS ADL severe scale). The SIB measures cognition in a more severe population. The ADCS ADL measures patient function and ability to conduct activities of daily living.
Treatment with ARICEPT(R) (donepezil HCl tablets) was generally well tolerated. The most common adverse events in ARICEPT-treated patients reported at more than twice the rate of placebo-treated patients were diarrhea and hallucinations. The rate of discontinuation for adverse events was greater in the ARICEPT-treated patients than in the placebo-treated patients (15.6 % vs 6.7%).
AD is a progressive brain disease that gradually destroys a person's memory and ability to learn, reason, make judgments, communicate and carry out daily activities. AD affects 4.5 million Americans. One in 10 persons over age 65 has AD, and nearly half of those over 85 have it. The levels of acetylcholine (ACh), a brain chemical involved in memory and thinking, decrease in people with AD. ARICEPT is believed to work by inhibiting the breakdown of ACh, thereby increasing available levels of this chemical in the brain.
Information About ARICEPT Treatment in Alzheimer's disease
While there is no cure for Alzheimer's disease, medical treatments are available to help manage symptoms of the disease. Once-a-day prescription ARICEPT is indicated for mild to moderate Alzheimer's disease.
In a progressively degenerative disease such as Alzheimer's, improvement, stabilization or a less-than-expected decline over time is considered a positive response to treatment. These types of responses have been observed in patients treated with ARICEPT in clinical trials for Alzheimer's disease. Individual responses to treatment vary, and some patients may not respond.
ARICEPT is well tolerated but may not be for everyone. Some people may have nausea, diarrhea, not sleep well or vomit. Some people may have muscle cramps, feel very tired or may not want to eat. In studies, these side effects were usually mild and went away over time. People at risk for stomach ulcers or who take certain other medicines should tell their doctors, because serious stomach problems, such as bleeding, may get worse. Some people who take ARICEPT may experience fainting.
ARICEPT is the number one prescribed Alzheimer's disease therapy worldwide, with more than 1 billion patient days of ARICEPT therapy. More than 1.7 million people in the United States alone have begun ARICEPT therapy.
ARICEPT(R) (donepezil HCl tablets) was discovered and developed and is manufactured and distributed by Eisai.
For more information about managing Alzheimer's disease and about ARICEPT, see accompanying full prescribing information or call (888) 999-9616 or visit aricept.
About Eisai Co., Ltd.
Eisai Co., Ltd. is a research-based human health care company that discovers, develops and markets products in more than 30 countries. 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 7,700 people worldwide.
About Eisai Medical Research Inc.
Eisai Medical Research Inc. is a U.S. pharmaceutical subsidiary of Eisai Co., Ltd. Eisai Medical Research Inc. was established to focus solely on clinical research and to expedite clinical drug development of new chemical entities and of new indications for marketed products.
About Eisai Inc.
Eisai Inc. is a U.S. pharmaceutical subsidiary of Eisai Co., Ltd. Established in 1995, Eisai Inc. began marketing its first product in the United States in 1997 and has rapidly grown to become an integrated pharmaceutical business with sales of approximately $2 billion in fiscal year 2004 (year ended March 31, 2005).
About Pfizer Inc
Pfizer Inc discovers, develops, manufactures and markets leading prescription medicines for humans and animals and many of the world's best-known consumer brands.
eisai
View drug information on ARICEPT.
"Our goal to provide ARICEPT to people with severe Alzheimer's disease is consistent with Eisai's human health care mission to improve the lives of patients and their families," said Lonnel Coats, president and COO, Eisai Inc.
The August 31 submission is based on data from a six-month, multi-center, randomized, double-blind, placebo-controlled clinical trial conducted in approximately 250 nursing home patients with severe AD. In the pivotal study, patients with severe AD (Mini Mental State Examination scores 1-10) treated with ARICEPT had a statistically significant improvement compared to those taking placebo on both primary measures of efficacy: the Severe Impairment Battery (SIB scale) and the Modified Alzheimer's Disease Cooperative Study Activities of Daily Living Inventory for Severe Alzheimer's Disease (ADCS ADL severe scale). The SIB measures cognition in a more severe population. The ADCS ADL measures patient function and ability to conduct activities of daily living.
Treatment with ARICEPT(R) (donepezil HCl tablets) was generally well tolerated. The most common adverse events in ARICEPT-treated patients reported at more than twice the rate of placebo-treated patients were diarrhea and hallucinations. The rate of discontinuation for adverse events was greater in the ARICEPT-treated patients than in the placebo-treated patients (15.6 % vs 6.7%).
AD is a progressive brain disease that gradually destroys a person's memory and ability to learn, reason, make judgments, communicate and carry out daily activities. AD affects 4.5 million Americans. One in 10 persons over age 65 has AD, and nearly half of those over 85 have it. The levels of acetylcholine (ACh), a brain chemical involved in memory and thinking, decrease in people with AD. ARICEPT is believed to work by inhibiting the breakdown of ACh, thereby increasing available levels of this chemical in the brain.
Information About ARICEPT Treatment in Alzheimer's disease
While there is no cure for Alzheimer's disease, medical treatments are available to help manage symptoms of the disease. Once-a-day prescription ARICEPT is indicated for mild to moderate Alzheimer's disease.
In a progressively degenerative disease such as Alzheimer's, improvement, stabilization or a less-than-expected decline over time is considered a positive response to treatment. These types of responses have been observed in patients treated with ARICEPT in clinical trials for Alzheimer's disease. Individual responses to treatment vary, and some patients may not respond.
ARICEPT is well tolerated but may not be for everyone. Some people may have nausea, diarrhea, not sleep well or vomit. Some people may have muscle cramps, feel very tired or may not want to eat. In studies, these side effects were usually mild and went away over time. People at risk for stomach ulcers or who take certain other medicines should tell their doctors, because serious stomach problems, such as bleeding, may get worse. Some people who take ARICEPT may experience fainting.
ARICEPT is the number one prescribed Alzheimer's disease therapy worldwide, with more than 1 billion patient days of ARICEPT therapy. More than 1.7 million people in the United States alone have begun ARICEPT therapy.
ARICEPT(R) (donepezil HCl tablets) was discovered and developed and is manufactured and distributed by Eisai.
For more information about managing Alzheimer's disease and about ARICEPT, see accompanying full prescribing information or call (888) 999-9616 or visit aricept.
About Eisai Co., Ltd.
Eisai Co., Ltd. is a research-based human health care company that discovers, develops and markets products in more than 30 countries. 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 7,700 people worldwide.
About Eisai Medical Research Inc.
Eisai Medical Research Inc. is a U.S. pharmaceutical subsidiary of Eisai Co., Ltd. Eisai Medical Research Inc. was established to focus solely on clinical research and to expedite clinical drug development of new chemical entities and of new indications for marketed products.
About Eisai Inc.
Eisai Inc. is a U.S. pharmaceutical subsidiary of Eisai Co., Ltd. Established in 1995, Eisai Inc. began marketing its first product in the United States in 1997 and has rapidly grown to become an integrated pharmaceutical business with sales of approximately $2 billion in fiscal year 2004 (year ended March 31, 2005).
About Pfizer Inc
Pfizer Inc discovers, develops, manufactures and markets leading prescription medicines for humans and animals and many of the world's best-known consumer brands.
eisai
View drug information on ARICEPT.
среда, 14 сентября 2011 г.
Delirium Presentation Predicts Mortality
The way certain patients present in the post-acute hospital setting with delirium, a common, preventable but life-threatening acute confusional state, predicts mortality, according to a study conducted by the Institute for Aging Research of Hebrew SeniorLife.
Patients with severe, hypoactive delirium, characterized by slowing or lack of movement and unresponsiveness, have the worst six-month survival rate of any class of the disease. Those with mild, hypoactive delirium have a significantly higher likelihood of dying than patients with other, milder symptoms.
"The association of the delirium classes on mortality depends on the presence or absence of dementia," says lead author Frances Yang, Ph.D., an assistant scientist at the Institute for Aging Research and an instructor in psychiatry at Brigham and Women's Hospital and Harvard Medical School. "Among patients who did not have dementia, it was delirium severity rather than motoric subtype that was associated with higher risk of mortality at six months."
The study, published in the May/June issue of the journal Psychosomatics, is the first to link characteristics of delirium, called subtypes, with disease severity. The four subtypes of delirium are normal, hypoactive, hyperactive (symptoms range from mild restlessness to constant movement and agitation) and mixed, which combines both hypo- and hyperactive elements.
Using two standard assessment tools, researchers at the Institute's Aging Brain Center examined whether the classic psychomotor subtypes of delirium are reflected by delirium severity. In addition, they sought to determine if the subtypes were able to predict mortality.
Dr. Yang's co-author, Edward Marcantonio, M.D., an associate professor of medicine at Beth Israel Deaconess Medical Center and Harvard Medical School, and colleagues screened more than 4,000 patients at eight Boston-area skilled nursing facilities using the Confusion Assessment Method and the Memorial Delirium Assessment Scale, two standard tools to detect delirium. More than 400 of these patients were found to have delirium and were followed over six months.
Delirium is an acute and relatively sudden - over hours or days - decline in attention, perception and cognition. It is generally caused by severe physical illness, often in the elderly, or any process that interferes with the normal metabolism and function of the brain. An estimated 14 percent to 24 percent of patients admitted to the hospital suffer from episodes of delirium. A recent study by Aging Brain Center investigators found that delirium rapidly accelerates memory decline in Alzheimer's disease patients.
"Our data reinforce the need to systematically assess patients for delirium at post-acute care admission, while considering dementia status," says Dr. Yang. "The findings demonstrate the importance of examining psychomotor subtype and the severity of delirium in predicting mortality."
Source:
Scott Edwards
Hebrew SeniorLife Institute for Aging Research
Patients with severe, hypoactive delirium, characterized by slowing or lack of movement and unresponsiveness, have the worst six-month survival rate of any class of the disease. Those with mild, hypoactive delirium have a significantly higher likelihood of dying than patients with other, milder symptoms.
"The association of the delirium classes on mortality depends on the presence or absence of dementia," says lead author Frances Yang, Ph.D., an assistant scientist at the Institute for Aging Research and an instructor in psychiatry at Brigham and Women's Hospital and Harvard Medical School. "Among patients who did not have dementia, it was delirium severity rather than motoric subtype that was associated with higher risk of mortality at six months."
The study, published in the May/June issue of the journal Psychosomatics, is the first to link characteristics of delirium, called subtypes, with disease severity. The four subtypes of delirium are normal, hypoactive, hyperactive (symptoms range from mild restlessness to constant movement and agitation) and mixed, which combines both hypo- and hyperactive elements.
Using two standard assessment tools, researchers at the Institute's Aging Brain Center examined whether the classic psychomotor subtypes of delirium are reflected by delirium severity. In addition, they sought to determine if the subtypes were able to predict mortality.
Dr. Yang's co-author, Edward Marcantonio, M.D., an associate professor of medicine at Beth Israel Deaconess Medical Center and Harvard Medical School, and colleagues screened more than 4,000 patients at eight Boston-area skilled nursing facilities using the Confusion Assessment Method and the Memorial Delirium Assessment Scale, two standard tools to detect delirium. More than 400 of these patients were found to have delirium and were followed over six months.
Delirium is an acute and relatively sudden - over hours or days - decline in attention, perception and cognition. It is generally caused by severe physical illness, often in the elderly, or any process that interferes with the normal metabolism and function of the brain. An estimated 14 percent to 24 percent of patients admitted to the hospital suffer from episodes of delirium. A recent study by Aging Brain Center investigators found that delirium rapidly accelerates memory decline in Alzheimer's disease patients.
"Our data reinforce the need to systematically assess patients for delirium at post-acute care admission, while considering dementia status," says Dr. Yang. "The findings demonstrate the importance of examining psychomotor subtype and the severity of delirium in predicting mortality."
Source:
Scott Edwards
Hebrew SeniorLife Institute for Aging Research
воскресенье, 11 сентября 2011 г.
Conscientious People Less Likely To Develop Alzheimer's Disease
If you are a conscientious person; you have a tendency to be thorough, determined and self-disciplined, you may have a lower chance of developing Alzheimer's disease, compared to a person who has a low level of conscientiousness, according to an article in Archives of General Psychiatry (JAMA/Archives).
Conscientiousness is also known as will, work and dependability - it refers to an individual's tendency to control impulses and be goal directed, explain the authors. It may be important for maintaining general good health.
Robert S. Wilson, Ph.D., Rush University Medical Center, Chicago, and team, in 1994, started examining 997 Catholic nuns, priests and monks who did not have dementia - they were all elderly. They were all checked for their medical history, had neurologic examinations and underwent cognitive testing. A 12-item inventory was used to measure conscientiousness - the participants had to rate agreement with each item, such as "I am a productive person who always gets the job done," on a scale of 1 to 5. Annual follow-up examinations were carried out until the end of 2006 - 7.9 evaluations were carried out per person on average.
The average conscientiousness score of the 997 participants was 34 out of a maximum of 48. Through a maximum period of 12 years of follow-up, 176 people developed Alzheimer's disease. Those who had scored at least 40 points in conscientiousness had an 89% lower chance of developing Alzheimer's disease, compared to those who scored 28 points or less. Even after controlling for known Alzheimer's disease factors the figures did not change significantly.
The researchers also found that conscientiousness was also linked to a slower rate of cognitive decline and a reduced risk of mild cognitive impairment (which may precede Alzheimer's disease).
Brain autopsies of 324 individuals who had died during the studies were analyzed by the researchers. In these patients, conscientiousness was not associated to any of the hallmark signs of Alzheimer's disease, such as brain plaques or tangles. Nevertheless, conscientiousness did seem to modify the association of these brain changes with a person's cognitive abilities before death.
The authors suggest that there may be many ways by which conscientiousness may guard against Alzheimer's disease. Conscientious people have a greater chance of succeeding educationally and occupationally; both factors which reduce the risk of Alzheimer's disease. Additionally, conscientiousness has been associated with resilience and to coping actively with difficulties. The authors noted "These factors might lessen the adverse consequences of negative life events and chronic psychological distress, which have been associated with risk of dementia in old age."
The writers continued "In conclusion, level of conscientiousness is associated with incidence of mild cognitive impairment and Alzheimer's disease but not with the pathologic hallmarks of these conditions. Understanding the mechanisms linking conscientiousness to maintenance of cognition in old age may suggest novel strategies for delaying the symptoms of Alzheimer's disease."
Arch Gen Psychiatry. 2007;64(10):1204-1212
archpsyc.ama-assn
Written by:
Conscientiousness is also known as will, work and dependability - it refers to an individual's tendency to control impulses and be goal directed, explain the authors. It may be important for maintaining general good health.
Robert S. Wilson, Ph.D., Rush University Medical Center, Chicago, and team, in 1994, started examining 997 Catholic nuns, priests and monks who did not have dementia - they were all elderly. They were all checked for their medical history, had neurologic examinations and underwent cognitive testing. A 12-item inventory was used to measure conscientiousness - the participants had to rate agreement with each item, such as "I am a productive person who always gets the job done," on a scale of 1 to 5. Annual follow-up examinations were carried out until the end of 2006 - 7.9 evaluations were carried out per person on average.
The average conscientiousness score of the 997 participants was 34 out of a maximum of 48. Through a maximum period of 12 years of follow-up, 176 people developed Alzheimer's disease. Those who had scored at least 40 points in conscientiousness had an 89% lower chance of developing Alzheimer's disease, compared to those who scored 28 points or less. Even after controlling for known Alzheimer's disease factors the figures did not change significantly.
The researchers also found that conscientiousness was also linked to a slower rate of cognitive decline and a reduced risk of mild cognitive impairment (which may precede Alzheimer's disease).
Brain autopsies of 324 individuals who had died during the studies were analyzed by the researchers. In these patients, conscientiousness was not associated to any of the hallmark signs of Alzheimer's disease, such as brain plaques or tangles. Nevertheless, conscientiousness did seem to modify the association of these brain changes with a person's cognitive abilities before death.
The authors suggest that there may be many ways by which conscientiousness may guard against Alzheimer's disease. Conscientious people have a greater chance of succeeding educationally and occupationally; both factors which reduce the risk of Alzheimer's disease. Additionally, conscientiousness has been associated with resilience and to coping actively with difficulties. The authors noted "These factors might lessen the adverse consequences of negative life events and chronic psychological distress, which have been associated with risk of dementia in old age."
The writers continued "In conclusion, level of conscientiousness is associated with incidence of mild cognitive impairment and Alzheimer's disease but not with the pathologic hallmarks of these conditions. Understanding the mechanisms linking conscientiousness to maintenance of cognition in old age may suggest novel strategies for delaying the symptoms of Alzheimer's disease."
Arch Gen Psychiatry. 2007;64(10):1204-1212
archpsyc.ama-assn
Written by:
четверг, 8 сентября 2011 г.
Accera, Inc. Announces Results Of Phase II Study In Alzheimer's Disease At American Academy Of Neurology Meeting
Accera Inc. is presenting
topline data today from its Phase IIb study of its lead compound AC-1202 in
Alzheimer's disease (AD) at the American Academy of Neurology (AAN) 59th
Annual Meeting in Boston. Judged by the AAN to be in the top five percent
of the program, the data will also be featured in the Scientific Highlights
Plenary Session.
The randomized, double-blinded, placebo-controlled Phase IIb trial
evaluated 152 subjects that had previously been diagnosed with mild to
moderate AD. Consistent with the findings of Accera's Phase IIa study,
subjects who did not have the ApoE4 genotype-a known genetic risk factor
that occurs in half of all AD patients-responded particularly well to
treatment, as reflected in statistically significant improvement in AD
Assessment Scale- Cognitive (ADAS-Cog) scores.
Subjects underwent pharmacogenomic analysis for a variety of genetic
markers and were evaluated through a battery of neuropsychometric tests at
Day 0, 45, and 90. Compared to the placebo group, the ADAS-Cog scores of
the AC- 1202-treated ApoE4(-) population improved 3.5 points in twelve
weeks (p=0.01), and statistically significant improvement was seen in just
45 days.
Interestingly, ApoE4(-) subjects who also exhibited a genetic variation
that affects glucose regulation showed a 5 point improvement in ADAS-Cog
scores compared to placebo, providing further insight into the disease.
"The profound effect we see in the population without the ApoE4 risk factor
supports the findings of an earlier study linking efficacy to a certain
pharmacogenomic profile," said Dr. Lauren Costantini, Accera's vice
president of clinical development. "It also provides further evidence of
the link between Alzheimer's disease and glucose metabolism."
Regardless of genotype, subjects treated with AC-1202 showed a trend
toward improvement (p=.072), suggesting the compound's disease modifying
potential. Taken in addition to an existing AD treatment, AC-1202 was well
tolerated, making it a promising co-therapeutic candidate for the chronic
treatment of the disease.
Dr. Lauren Costantini is presenting the abstract, "Clinical Efficacy of
AC-1202 in Mild to Moderate Alzheimer's Disease" at the Late Breaking
Science session today at 3:45 p.m. EDT. The plenary session will be held at
5:15 p.m. EDT on Friday, May 4.
The trial was conducted at 25 centers across the United States, and all
subjects were given the opportunity to participate in a six-month
open-label extension upon completion of the three-month blinded study. The
results of the open-label extension will be presented at the Alzheimer's
Association's International Prevention Conference in early June.
About AC-1202
Brain imaging techniques performed on AD patients reveal a dramatically
decreased uptake of glucose, the brain's preferred source of energy.
AC-1202 is an orally available, liquid compound that is efficiently
converted by the liver into ketone bodies, an alternative energy source
that the brain can metabolize even when it cannot process glucose. Thus
preserving the glucose- deprived brain cells, AC-1202 has disease modifying
potential in AD and a number other neurodegenerative diseases characterized
by neuronal metabolism. The potentially neuroprotective mechanism of this
first-in-class compound is also being evaluated in age-associated memory
impairment, Parkinson's disease, and canine cognitive dysfunction.
About Accera, Inc.
Based in Broomfield, CO, Accera, Inc. is a privately held
biopharmaceutical company focused on developing novel drugs for
neurodegenerative diseases. The company's lead candidate, AC-1202, is a
first- in-class molecule currently in Phase II clinical trials for
Alzheimer's disease and age-associated memory impairment. A key element of
Accera's strategy is to develop AC-1202 and other small molecule compounds
in its pipeline with corporate partners for a range of memory and cognition
disorders associated with neurological conditions and aging.
accerapharma
Accera Inc.
accerapharma
topline data today from its Phase IIb study of its lead compound AC-1202 in
Alzheimer's disease (AD) at the American Academy of Neurology (AAN) 59th
Annual Meeting in Boston. Judged by the AAN to be in the top five percent
of the program, the data will also be featured in the Scientific Highlights
Plenary Session.
The randomized, double-blinded, placebo-controlled Phase IIb trial
evaluated 152 subjects that had previously been diagnosed with mild to
moderate AD. Consistent with the findings of Accera's Phase IIa study,
subjects who did not have the ApoE4 genotype-a known genetic risk factor
that occurs in half of all AD patients-responded particularly well to
treatment, as reflected in statistically significant improvement in AD
Assessment Scale- Cognitive (ADAS-Cog) scores.
Subjects underwent pharmacogenomic analysis for a variety of genetic
markers and were evaluated through a battery of neuropsychometric tests at
Day 0, 45, and 90. Compared to the placebo group, the ADAS-Cog scores of
the AC- 1202-treated ApoE4(-) population improved 3.5 points in twelve
weeks (p=0.01), and statistically significant improvement was seen in just
45 days.
Interestingly, ApoE4(-) subjects who also exhibited a genetic variation
that affects glucose regulation showed a 5 point improvement in ADAS-Cog
scores compared to placebo, providing further insight into the disease.
"The profound effect we see in the population without the ApoE4 risk factor
supports the findings of an earlier study linking efficacy to a certain
pharmacogenomic profile," said Dr. Lauren Costantini, Accera's vice
president of clinical development. "It also provides further evidence of
the link between Alzheimer's disease and glucose metabolism."
Regardless of genotype, subjects treated with AC-1202 showed a trend
toward improvement (p=.072), suggesting the compound's disease modifying
potential. Taken in addition to an existing AD treatment, AC-1202 was well
tolerated, making it a promising co-therapeutic candidate for the chronic
treatment of the disease.
Dr. Lauren Costantini is presenting the abstract, "Clinical Efficacy of
AC-1202 in Mild to Moderate Alzheimer's Disease" at the Late Breaking
Science session today at 3:45 p.m. EDT. The plenary session will be held at
5:15 p.m. EDT on Friday, May 4.
The trial was conducted at 25 centers across the United States, and all
subjects were given the opportunity to participate in a six-month
open-label extension upon completion of the three-month blinded study. The
results of the open-label extension will be presented at the Alzheimer's
Association's International Prevention Conference in early June.
About AC-1202
Brain imaging techniques performed on AD patients reveal a dramatically
decreased uptake of glucose, the brain's preferred source of energy.
AC-1202 is an orally available, liquid compound that is efficiently
converted by the liver into ketone bodies, an alternative energy source
that the brain can metabolize even when it cannot process glucose. Thus
preserving the glucose- deprived brain cells, AC-1202 has disease modifying
potential in AD and a number other neurodegenerative diseases characterized
by neuronal metabolism. The potentially neuroprotective mechanism of this
first-in-class compound is also being evaluated in age-associated memory
impairment, Parkinson's disease, and canine cognitive dysfunction.
About Accera, Inc.
Based in Broomfield, CO, Accera, Inc. is a privately held
biopharmaceutical company focused on developing novel drugs for
neurodegenerative diseases. The company's lead candidate, AC-1202, is a
first- in-class molecule currently in Phase II clinical trials for
Alzheimer's disease and age-associated memory impairment. A key element of
Accera's strategy is to develop AC-1202 and other small molecule compounds
in its pipeline with corporate partners for a range of memory and cognition
disorders associated with neurological conditions and aging.
accerapharma
Accera Inc.
accerapharma
понедельник, 5 сентября 2011 г.
New Technique Paves Way For Medical Discoveries
Researchers have previously been able to analyse which sugar structures are to be found on certain proteins, but not exactly where on the protein they are positioned. This is now possible thanks to a new technique developed at the Sahlgrenska Academy at the University of Gothenburg, Sweden.
The technique entails preparing samples in a new way and is a development of applied mass spectrometry. Presented in the latest issue of renowned journal Nature Methods, the technique will enable medical researchers to study the mechanisms behind diseases in more detail and, with luck, find new ways of treating them.
"When we developed the method, we were analysing cerebrospinal fluid from healthy subjects and could see that many proteins had sugar structures previously unknown to us," says Jonas Nilsson, a researcher at the Department of Clinical Chemistry and Transfusion Medicine at the Sahlgrenska Academy. "We know that some of these proteins play a role in diseases such as Alzheimer's disease, and now it's possible to study whether faults in these sugar structures are responsible for the development of the disease."
There are more than 20,000 proteins in the human body. These proteins ensure that the instructions from the genes are carried out. Around half of them have sugar structures on their surface consisting of chains of sugar molecules. These sugar structures mean that the protein can be recognised by other proteins. Some of these structures can act as a locking mechanism when proteins bind to cells and other proteins. Sugar structures are also found on the surface of cells, where they determine, among other things, which blood group we belong to.
"Sugar structures often play an important role in how a cell or protein functions and how it affects different systems in the body," says Nilsson. "Being able to study them in more detail is a major step forward for biomedical research."
The chains of sugars in these structures are attached to the proteins at only one end. The new technique entails attaching a plastic bead to the loose end of these chains and separating the sugared proteins from those that do not have sugar structures. The proteins are then chopped into pieces and the sugar chain is released from the plastic bead, leaving the sugar chain attached to a chunk of protein known as a peptide. The researchers can then study the sugar structure on the peptide and see which protein the peptide belonged to and where on the protein it sat.
Journal: Nature Methods
Title of article: Enrichment of Glycopeptides for Glycan Structure and Attachment Site Identification
Authors: Jonas Nilsson, Ulla R??etschi, Adnan Halim, Camilla Hesse, Elisabet Carlsohn, Gunnar Brinkmalm and G?¶ran Larson
Source:
Jonas Nilsson
University of Gothenburg
The technique entails preparing samples in a new way and is a development of applied mass spectrometry. Presented in the latest issue of renowned journal Nature Methods, the technique will enable medical researchers to study the mechanisms behind diseases in more detail and, with luck, find new ways of treating them.
"When we developed the method, we were analysing cerebrospinal fluid from healthy subjects and could see that many proteins had sugar structures previously unknown to us," says Jonas Nilsson, a researcher at the Department of Clinical Chemistry and Transfusion Medicine at the Sahlgrenska Academy. "We know that some of these proteins play a role in diseases such as Alzheimer's disease, and now it's possible to study whether faults in these sugar structures are responsible for the development of the disease."
There are more than 20,000 proteins in the human body. These proteins ensure that the instructions from the genes are carried out. Around half of them have sugar structures on their surface consisting of chains of sugar molecules. These sugar structures mean that the protein can be recognised by other proteins. Some of these structures can act as a locking mechanism when proteins bind to cells and other proteins. Sugar structures are also found on the surface of cells, where they determine, among other things, which blood group we belong to.
"Sugar structures often play an important role in how a cell or protein functions and how it affects different systems in the body," says Nilsson. "Being able to study them in more detail is a major step forward for biomedical research."
The chains of sugars in these structures are attached to the proteins at only one end. The new technique entails attaching a plastic bead to the loose end of these chains and separating the sugared proteins from those that do not have sugar structures. The proteins are then chopped into pieces and the sugar chain is released from the plastic bead, leaving the sugar chain attached to a chunk of protein known as a peptide. The researchers can then study the sugar structure on the peptide and see which protein the peptide belonged to and where on the protein it sat.
Journal: Nature Methods
Title of article: Enrichment of Glycopeptides for Glycan Structure and Attachment Site Identification
Authors: Jonas Nilsson, Ulla R??etschi, Adnan Halim, Camilla Hesse, Elisabet Carlsohn, Gunnar Brinkmalm and G?¶ran Larson
Source:
Jonas Nilsson
University of Gothenburg
пятница, 2 сентября 2011 г.
Breakthrough In Caregiver Support For Rare Dementia FTD
The FTD Support Forum (ftdsupportforum) has just registered it's 1000th new member world-wide since being established 9 months ago.
This on line support group's mission is to provide a place for safe and secure communications for people who have been diagnosed with FTD and those who care for loved ones with FTD.
Members are dedicated to supporting one another in a sensitive, respectful and sincere manner.
This forum also encourages increased awareness of FTD within the medical community and the general public, with the belief that knowledge will bring improved access to support networks that are emerging on the internet and elsewhere.
As many as seven million Americans may be afflicted with a form of dementia. Frontotemporal Dementia may account for 2-5 percent or 140,000 - 350,000 cases of dementia and for as many as 25 percent of early age on-set (pre-senile) dementias.1 Unless scientists discover a way to delay or halt these brain attacks, some 8 million people are expected to have some form of dementia by 2030, and by 2050 that toll could reach 17 million.2 That may mean almost 400,000 FTD sufferers by 2030 and 850,000 by 2050.
Worldwide the statistics are alarming: 62 million people between the ages of 30 and 69 are suffering some form of dementia.3 & 4 By 2050, with global population of 9.191 billion there may be 85 million people suffering from FTD" 4 & 3
The term Pick's Complex, identified in 1903 as different than Alzheimer's disease is now transitioning and becoming known as one category within the Frontotemporal Lobar Degeneration diseases. Due to tauopathies (protein brain deposits ) research and ever improving brain imaging technologies ".... it is only perhaps in the last decade that we (scientists, academians and doctors) have become more comfortable calling a dementia condition, a possible or probable frontotemporal lobar degeneration (FTLD) and then trying to identify which one of the FTLDs might be the best fit" says Dr. Leilani Doty, PhD, Director, University of Florida Cognitive and Memory Disorder Clinics, McKnight Brain Institute.
For more information on FTD please visit ftd-picks, ftdSupport, and pdsg.uk
References
1. caregiver/caregiver/j...jsp?nodeid=573
2. msnbc.msn/id/17694931/ based on this statement: Unless scientists discover a way to delay Alzheimer's brain attack, some 7.7 million people are expected to have the disease by 2030, the report says. By 2050, that toll could reach 16 million. (if FTD='s 5% of total cases, and Alz is 7.7, then total would be over 8 mil and 5% is 385,000{"almost 400,000"}. By 2050, 16mil Alz's patients would be part of a total of 17 mil total dementias and 5% is 850,000 FTD's
3. alzheimer-europe/?lm2...h=6FB10D101364
The purpose of this forum is to provide a place for safe and secure communications for people who have been diagnosed with FTD and those who care for loved ones with FTD.
FTD Support Forum
This on line support group's mission is to provide a place for safe and secure communications for people who have been diagnosed with FTD and those who care for loved ones with FTD.
Members are dedicated to supporting one another in a sensitive, respectful and sincere manner.
This forum also encourages increased awareness of FTD within the medical community and the general public, with the belief that knowledge will bring improved access to support networks that are emerging on the internet and elsewhere.
As many as seven million Americans may be afflicted with a form of dementia. Frontotemporal Dementia may account for 2-5 percent or 140,000 - 350,000 cases of dementia and for as many as 25 percent of early age on-set (pre-senile) dementias.1 Unless scientists discover a way to delay or halt these brain attacks, some 8 million people are expected to have some form of dementia by 2030, and by 2050 that toll could reach 17 million.2 That may mean almost 400,000 FTD sufferers by 2030 and 850,000 by 2050.
Worldwide the statistics are alarming: 62 million people between the ages of 30 and 69 are suffering some form of dementia.3 & 4 By 2050, with global population of 9.191 billion there may be 85 million people suffering from FTD" 4 & 3
The term Pick's Complex, identified in 1903 as different than Alzheimer's disease is now transitioning and becoming known as one category within the Frontotemporal Lobar Degeneration diseases. Due to tauopathies (protein brain deposits ) research and ever improving brain imaging technologies ".... it is only perhaps in the last decade that we (scientists, academians and doctors) have become more comfortable calling a dementia condition, a possible or probable frontotemporal lobar degeneration (FTLD) and then trying to identify which one of the FTLDs might be the best fit" says Dr. Leilani Doty, PhD, Director, University of Florida Cognitive and Memory Disorder Clinics, McKnight Brain Institute.
For more information on FTD please visit ftd-picks, ftdSupport, and pdsg.uk
References
1. caregiver/caregiver/j...jsp?nodeid=573
2. msnbc.msn/id/17694931/ based on this statement: Unless scientists discover a way to delay Alzheimer's brain attack, some 7.7 million people are expected to have the disease by 2030, the report says. By 2050, that toll could reach 16 million. (if FTD='s 5% of total cases, and Alz is 7.7, then total would be over 8 mil and 5% is 385,000{"almost 400,000"}. By 2050, 16mil Alz's patients would be part of a total of 17 mil total dementias and 5% is 850,000 FTD's
3. alzheimer-europe/?lm2...h=6FB10D101364
The purpose of this forum is to provide a place for safe and secure communications for people who have been diagnosed with FTD and those who care for loved ones with FTD.
FTD Support Forum
вторник, 30 августа 2011 г.
Mechanism Explains Link Between Apolipoprotein E And Alzheimer's Disease
Scientists have discovered a previously unknown mechanism by which apolipoprotein E, a molecule whose mutation is linked to Alzheimer's disease (AD), stimulates degradation of sticky amyloid beta (A) protein within the brain. The research, published by Cell Press in the June 12 issue of the journal Neuron, may lead to a powerful new therapy for this devastating disease.
One of the primary characteristics of AD is the accumulation and deposition of neuron-damaging clumps of A protein. Apolipoprotein E (ApoE), a cholesterol transport protein, is known to be a key regulator of brain A levels, and it is likely that processes that regulate ApoE activity will influence A deposition and clearance. "An isoform of ApoE, ApoE4, has been shown to confer dramatically increased risk for late-onset AD; however, the basis for this remains one of the major unanswered questions of disease pathogenesis," writes study author Dr. Gary E. Landreth from the Alzheimer Research Laboratory at Case Western Reserve University School of Medicine in Cleveland, Ohio.
Dr. Landreth and colleagues sought to unravel the link between ApoE, A clearance in the brain, and an enhanced risk for AD. The researchers found that ApoE profoundly enhanced the intracellular and extracellular degradation of A?. This enhancement varied for different isoforms of ApoE with the ApoE4 isoform exhibiting an impaired ability to promote A degradation when compared to other ApoE isoforms. The number of lipid molecules associated with ApoE was also critical to its ability to stimulate A degradation. Activation of liver X receptors (LXRs) to enhance expression of lipidated ApoE significantly facilitated A degradation. Importantly, use of an LXR agonist to increase lipidated forms of ApoE in a mouse model of AD resulted in reduced A? plaque levels and an improvement in contextual memory.
The results of this study document a major role for ApoE in the stimulation of A degradation within the brain and highlight the importance of lipidation to the function of ApoE. This work also explains the previous observation that inactivation of a gene which helps the brain to process lipids (called Abca1) resulted in decreased levels of ApoE along with a seemingly paradoxical elevation of A levels and plaque formation in mice. "Our data suggest that therapeutic agents that increase the levels of lipidated forms of ApoE, including LXR agonists, represent a potentially efficacious therapy for AD," concludes Dr. Landreth.
The researchers include Qingguang Jiang, Case Western Reserve University School of Medicine, Cleveland, OH; C.Y. Daniel Lee, Case Western Reserve University School of Medicine, Cleveland, OH; Shweta Mandrekar, Case Western Reserve University School of Medicine, Cleveland, OH; Brandy Wilkinson, Case Western Reserve University School of Medicine, Cleveland, OH; Paige Cramer, Case Western Reserve University School of Medicine, Cleveland, OH; Noam Zelcer, Howard Hughes Medical Institute, University of California, Los Angeles, Los Angeles, CA; Karen Mann, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH; Bruce Lamb, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH; Timothy M. Willson, GlaxoSmithKline, Discovery Research, Research Triangle Park, NC; Jon L. Collins, GlaxoSmithKline, Discovery Research, Research Triangle Park, NC; Jill C. Richardson, GlaxoSmithKline, New Frontiers Science Park, Harlow, UK; Jonathan D. Smith, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH; Thomas A. Comery, Wyeth Research, Princeton, NJ; David Riddell, Wyeth Research, Princeton, NJ ; David M. Holtzman, Washington University School of Medicine, St. Louis, MO; Peter Tontonoz, Howard Hughes Medical Institute, University of California, Los Angeles, Los Angeles, CA; and Gary E. Landreth, Case Western Reserve University School of Medicine, Cleveland, OH.
Source: Cathleen Genova
Cell Press
One of the primary characteristics of AD is the accumulation and deposition of neuron-damaging clumps of A protein. Apolipoprotein E (ApoE), a cholesterol transport protein, is known to be a key regulator of brain A levels, and it is likely that processes that regulate ApoE activity will influence A deposition and clearance. "An isoform of ApoE, ApoE4, has been shown to confer dramatically increased risk for late-onset AD; however, the basis for this remains one of the major unanswered questions of disease pathogenesis," writes study author Dr. Gary E. Landreth from the Alzheimer Research Laboratory at Case Western Reserve University School of Medicine in Cleveland, Ohio.
Dr. Landreth and colleagues sought to unravel the link between ApoE, A clearance in the brain, and an enhanced risk for AD. The researchers found that ApoE profoundly enhanced the intracellular and extracellular degradation of A?. This enhancement varied for different isoforms of ApoE with the ApoE4 isoform exhibiting an impaired ability to promote A degradation when compared to other ApoE isoforms. The number of lipid molecules associated with ApoE was also critical to its ability to stimulate A degradation. Activation of liver X receptors (LXRs) to enhance expression of lipidated ApoE significantly facilitated A degradation. Importantly, use of an LXR agonist to increase lipidated forms of ApoE in a mouse model of AD resulted in reduced A? plaque levels and an improvement in contextual memory.
The results of this study document a major role for ApoE in the stimulation of A degradation within the brain and highlight the importance of lipidation to the function of ApoE. This work also explains the previous observation that inactivation of a gene which helps the brain to process lipids (called Abca1) resulted in decreased levels of ApoE along with a seemingly paradoxical elevation of A levels and plaque formation in mice. "Our data suggest that therapeutic agents that increase the levels of lipidated forms of ApoE, including LXR agonists, represent a potentially efficacious therapy for AD," concludes Dr. Landreth.
The researchers include Qingguang Jiang, Case Western Reserve University School of Medicine, Cleveland, OH; C.Y. Daniel Lee, Case Western Reserve University School of Medicine, Cleveland, OH; Shweta Mandrekar, Case Western Reserve University School of Medicine, Cleveland, OH; Brandy Wilkinson, Case Western Reserve University School of Medicine, Cleveland, OH; Paige Cramer, Case Western Reserve University School of Medicine, Cleveland, OH; Noam Zelcer, Howard Hughes Medical Institute, University of California, Los Angeles, Los Angeles, CA; Karen Mann, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH; Bruce Lamb, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH; Timothy M. Willson, GlaxoSmithKline, Discovery Research, Research Triangle Park, NC; Jon L. Collins, GlaxoSmithKline, Discovery Research, Research Triangle Park, NC; Jill C. Richardson, GlaxoSmithKline, New Frontiers Science Park, Harlow, UK; Jonathan D. Smith, Lerner Research Institute, Cleveland Clinic Foundation, Cleveland, OH; Thomas A. Comery, Wyeth Research, Princeton, NJ; David Riddell, Wyeth Research, Princeton, NJ ; David M. Holtzman, Washington University School of Medicine, St. Louis, MO; Peter Tontonoz, Howard Hughes Medical Institute, University of California, Los Angeles, Los Angeles, CA; and Gary E. Landreth, Case Western Reserve University School of Medicine, Cleveland, OH.
Source: Cathleen Genova
Cell Press
суббота, 27 августа 2011 г.
Why Alzheimer's Disease Kills Some Neuron Types First
Bioengineers from the University of California, San Diego developed an explanation for why some types of neurons die sooner than others in the brains of people with Alzheimer's disease. These insights, published in the journal Nature Biotechnology, come from detailed models of brain energy metabolism developed in the Department of Bioengineering at the UC San Diego Jacobs School of Engineering.
The Alzheimer's insights demonstrate how fundamental insights on human metabolism can be gleaned from computer models that incorporate large genomic and proteomic data sets with information from biochemical studies. UC San Diego bioengineering professor Bernhard Palsson and his students and collaborators first developed this "in silico" modeling approach for E. coli and other prokaryotes, and later extended it to human tissues.
The Nature Biotechnology paper describes the first time this modeling approach has been used to capture how the metabolism of specific human cell types affect the metabolism of other cell types.
"In human tissues, different cells have different roles. We're trying to predict how the behavior of one cell type will affect the behavior of other cell types," said Nathan Lewis, a Ph.D. candidate in the Department of Bioengineering at the UC San Diego Jacobs School of Engineering and the first author on the Nature Biotechnology paper, which also includes authors from the University of Heidelberg, Massachusetts Institute of Technology, and the German Cancer Research Center (DKFZ).
Similar approaches can be used to identify potential off-target effects of drugs, provide insights on disease progression, and offer new tools for uncovering the underlying biological mechanisms in a wide range of human tissues and cell types.
Why Some Neurons Die First in the Alzheimer's Brain
In the brains of people with Alzheimer's disease, certain cells, such as glutamatergic and cholinergic neurons, tend to die in much larger numbers in moderate stages of Alzheimer's disease, while GABAergic neurons are relatively unaffected until later stages of the disease.
"There is a big question as to what is causing this cell-type specificity," said Lewis.
The researchers built Palsson Lab: Systems Biology Research Group computational models that captured the metabolic interactions between each of the three neuron types and their associated astrocyte cells. Next, the bioengineersknocked down ?±-ketoglutarate, a gene known to be damaged in patients with Alzheimer's disease, and let their models of brain metabolism run to see what happens.
The results from the models agreed with clinical data. When the bioengineers disrupted the ?±-ketoglutarate enzyme in the models for cholinergic and glutamatergic neurons, the metabolic rate of these neurons dropped, leading to cell death. "But then you have the GABAergic neurons that show no effect. So the cell types that are known to be lost early on in Alzheimer's show slowed metabolic rates," explained Lewis.
Analysis of their models then led the bioengineers to the biochemical pathways that allowed the GABAergic neurons to be relatively unaffected despite the disrupted gene.
"We looked at what upstream is allowing this and found a GABA-specific enzyme called glutamate decarboxylase," said Lewis.
When the researchers added this enzyme to the models of the other neuron types, the metabolic rates of these neurons improved as well. Thus the model allowed the researchers to identify a gene and how it contributes to the whole cell to potentially prolong the life of certain cells in Alzheimer's disease.
Large Scale Modeling of Metabolic Interactions
The new Nature Biotechnology paper uses the Alzheimer's brain study as an example of how to build models of metabolism that go one level deeper than previous work by taking into account the tissue microenvironment and metabolic interactions between specific cell types.
The models for each cell can be represented like a circuit, with certain inputs and outputs. For example, sugars, like glucose, are inputs, and the models detail how these inputs are used to build cell parts and secrete byproducts as outputs. The metabolic models the bioengineers built provide a means to study these networks.
For example, each cell type has different biochemical pathways that can take the sugars from point A to B. If you knock out a gene in between, the network might find a different route, produce different products, or predict cell death. When models for multiple cells are combined, additional insight can be gained since the inputs and outputs of each model begin to affect the other cells.
"There are many potential applications for these models. For example, this modeling approach could be useful for predicting off target side effects of drugs. You could theoretically take a cell line, throw a drug at it and see which metabolic pathways are significantly affected. Thus, you could decrease the amount of resources spent on drug development if the model suggests negative side effects that may cause it to fail," said Lewis.
Notes:
"Large-scale in silico modeling of metabolic interactions between cell types in the human brain," by Nathan E Lewis (1), Gunnar Schramm (2,5), Aarash Bordbar (1), Jan Schellenberger (3), Michael P Andersen (1), Jeffrey K Cheng (1), Nilam Patel (1), Alex Yee (1), Randall A Lewis (4), Roland Eils (2,5), Rainer K?¶nig (2,5) & Bernhard ?? Palsson (1); published online on November 21, 2010 in Nature Biotechnology.
(1) Department of Bioengineering, University of California, San Diego, La Jolla, California, USA.
(2) Department of Bioinformatics and Functional Genomics, Institute of Pharmacy and Molecular Biotechnology and Bioquant, University of Heidelberg, Heidelberg, Germany.
(3) Bioinformatics Program, University of California, San Diego, La Jolla, California, USA.
(4) Department of Economics, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA.
(5) Department of Theoretical Bioinformatics, German Cancer Research Center (DKFZ), Heidelberg, Germany.
This work was funded in part by a Fulbright fellowship, a National Science Foundation IGERT Plant Systems Biology training grant (no. DGE-0504645), a US National Institutes of Health grant 2R01GM068837_05A1 and the Helmholtz Alliance on Systems Biology and the BMBF by the NGFN+ neuroblastoma project ENGINE.
Source:
Daniel Kane
University of California - San Diego
The Alzheimer's insights demonstrate how fundamental insights on human metabolism can be gleaned from computer models that incorporate large genomic and proteomic data sets with information from biochemical studies. UC San Diego bioengineering professor Bernhard Palsson and his students and collaborators first developed this "in silico" modeling approach for E. coli and other prokaryotes, and later extended it to human tissues.
The Nature Biotechnology paper describes the first time this modeling approach has been used to capture how the metabolism of specific human cell types affect the metabolism of other cell types.
"In human tissues, different cells have different roles. We're trying to predict how the behavior of one cell type will affect the behavior of other cell types," said Nathan Lewis, a Ph.D. candidate in the Department of Bioengineering at the UC San Diego Jacobs School of Engineering and the first author on the Nature Biotechnology paper, which also includes authors from the University of Heidelberg, Massachusetts Institute of Technology, and the German Cancer Research Center (DKFZ).
Similar approaches can be used to identify potential off-target effects of drugs, provide insights on disease progression, and offer new tools for uncovering the underlying biological mechanisms in a wide range of human tissues and cell types.
Why Some Neurons Die First in the Alzheimer's Brain
In the brains of people with Alzheimer's disease, certain cells, such as glutamatergic and cholinergic neurons, tend to die in much larger numbers in moderate stages of Alzheimer's disease, while GABAergic neurons are relatively unaffected until later stages of the disease.
"There is a big question as to what is causing this cell-type specificity," said Lewis.
The researchers built Palsson Lab: Systems Biology Research Group computational models that captured the metabolic interactions between each of the three neuron types and their associated astrocyte cells. Next, the bioengineersknocked down ?±-ketoglutarate, a gene known to be damaged in patients with Alzheimer's disease, and let their models of brain metabolism run to see what happens.
The results from the models agreed with clinical data. When the bioengineers disrupted the ?±-ketoglutarate enzyme in the models for cholinergic and glutamatergic neurons, the metabolic rate of these neurons dropped, leading to cell death. "But then you have the GABAergic neurons that show no effect. So the cell types that are known to be lost early on in Alzheimer's show slowed metabolic rates," explained Lewis.
Analysis of their models then led the bioengineers to the biochemical pathways that allowed the GABAergic neurons to be relatively unaffected despite the disrupted gene.
"We looked at what upstream is allowing this and found a GABA-specific enzyme called glutamate decarboxylase," said Lewis.
When the researchers added this enzyme to the models of the other neuron types, the metabolic rates of these neurons improved as well. Thus the model allowed the researchers to identify a gene and how it contributes to the whole cell to potentially prolong the life of certain cells in Alzheimer's disease.
Large Scale Modeling of Metabolic Interactions
The new Nature Biotechnology paper uses the Alzheimer's brain study as an example of how to build models of metabolism that go one level deeper than previous work by taking into account the tissue microenvironment and metabolic interactions between specific cell types.
The models for each cell can be represented like a circuit, with certain inputs and outputs. For example, sugars, like glucose, are inputs, and the models detail how these inputs are used to build cell parts and secrete byproducts as outputs. The metabolic models the bioengineers built provide a means to study these networks.
For example, each cell type has different biochemical pathways that can take the sugars from point A to B. If you knock out a gene in between, the network might find a different route, produce different products, or predict cell death. When models for multiple cells are combined, additional insight can be gained since the inputs and outputs of each model begin to affect the other cells.
"There are many potential applications for these models. For example, this modeling approach could be useful for predicting off target side effects of drugs. You could theoretically take a cell line, throw a drug at it and see which metabolic pathways are significantly affected. Thus, you could decrease the amount of resources spent on drug development if the model suggests negative side effects that may cause it to fail," said Lewis.
Notes:
"Large-scale in silico modeling of metabolic interactions between cell types in the human brain," by Nathan E Lewis (1), Gunnar Schramm (2,5), Aarash Bordbar (1), Jan Schellenberger (3), Michael P Andersen (1), Jeffrey K Cheng (1), Nilam Patel (1), Alex Yee (1), Randall A Lewis (4), Roland Eils (2,5), Rainer K?¶nig (2,5) & Bernhard ?? Palsson (1); published online on November 21, 2010 in Nature Biotechnology.
(1) Department of Bioengineering, University of California, San Diego, La Jolla, California, USA.
(2) Department of Bioinformatics and Functional Genomics, Institute of Pharmacy and Molecular Biotechnology and Bioquant, University of Heidelberg, Heidelberg, Germany.
(3) Bioinformatics Program, University of California, San Diego, La Jolla, California, USA.
(4) Department of Economics, Massachusetts Institute of Technology, Cambridge, Massachusetts, USA.
(5) Department of Theoretical Bioinformatics, German Cancer Research Center (DKFZ), Heidelberg, Germany.
This work was funded in part by a Fulbright fellowship, a National Science Foundation IGERT Plant Systems Biology training grant (no. DGE-0504645), a US National Institutes of Health grant 2R01GM068837_05A1 and the Helmholtz Alliance on Systems Biology and the BMBF by the NGFN+ neuroblastoma project ENGINE.
Source:
Daniel Kane
University of California - San Diego
среда, 24 августа 2011 г.
Combining Vitamins E and C May Reduce Risk of Alzheimer's
Contact: Kenna Brigham
410-955-6878
JAMA and Archives Journals Website
(JAMA = Journal of the American Medical Association)
CHICAGO (USA) - Elderly persons who take individual vitamin E and C supplements together may reduce their risk of Alzheimer disease (AD), according to an article in the January issue of The Archives of Neurology, one of the JAMA/Archives journals.
According to the article, the public health threat of AD will continue to grow as people live longer. Previous studies have shown that antioxidant vitamins may protect the brain against damage caused by free radicals and other reactive oxygen species - molecular byproducts of basic cellular metabolism.
Neurons are especially sensitive to damage caused by free radicals, which is believed to be partially responsible for the development of AD. Incorporating antioxidants (which help to neutralize these free radicals) into the diet through food or supplementation may help protect neurons.
Peter P. Zandi, Ph.D., of The Johns Hopkins University Bloomberg School of Public Health, Baltimore, and colleagues examined the relationship between antioxidant supplement use and risk of AD.
The researchers assessed the prevalence of dementia and AD in 4,740 elderly (65 years or older) residents of Cache County, Utah in 1995 to 1997 and collected information about supplement use.
These residents were followed-up in 1998 to 2000 for new cases of dementia or AD. The researchers identified 200 cases of AD (prevalent cases) between 1995 and 1997, and 104 new cases (incident cases) of AD during follow-up.
The researchers categorized participants as vitamin E users if they reported taking an individual supplement of vitamin E or a multivitamin containing more than 400 IU (international units) of vitamin E.
Vitamin C users reported taking vitamin C supplements or multivitamins containing at least 500 micrograms of ascorbic acid.
Individuals were classified as multivitamin users if they reported taking multivitamins containing lower doses of vitamin E or C.
The researchers found the greatest reduction in both prevalence and incidence of AD in participants who used individual vitamin E and C supplements in combination, with or without an additional multivitamin.
'Use of vitamin E and C (ascorbic acid) supplements in combination reduced AD prevalence [by about 78 percent] and incidence [by about 64 percent],' the authors write.
The researchers also found 'no appreciable association with the use of vitamin C alone, vitamin E alone, or vitamin C and multivitamins in combination,' and prevalence of AD.
'The current??? recommended daily allowance for vitamin E is 22 IU (15 micrograms), and for vitamin C (ascorbic acid), 75 to 90 micrograms,' the researchers write.
'Multivitamin preparations typically contain these approximate quantities of both vitamins E and C (more vitamin C in some instances), while individual supplements typically contain doses up to 1,000 IU of vitamin E and 500 to 1,000 micrograms or more of vitamin C (ascorbic acid). Our findings suggest that vitamins E and C may offer protection against AD when taken together in the higher doses available from individual supplements.'
To contact Peter P. Zandi, Ph.D., call Kenna Brigham at 410-955-6878.
(Arch Neurol. 2004;61:82-88. Available post-embargo at
archneurol)
Editor's Note: This study was supported by grants from the National Institutes of Health, Bethesda, Md., and a grant from the National Institute of Mental Health, Bethesda, Md.
For more information, contact JAMA/Archives Media Relations at 312-464-JAMA (5262) or e-mail mediarelationsjama-archives
410-955-6878
JAMA and Archives Journals Website
(JAMA = Journal of the American Medical Association)
CHICAGO (USA) - Elderly persons who take individual vitamin E and C supplements together may reduce their risk of Alzheimer disease (AD), according to an article in the January issue of The Archives of Neurology, one of the JAMA/Archives journals.
According to the article, the public health threat of AD will continue to grow as people live longer. Previous studies have shown that antioxidant vitamins may protect the brain against damage caused by free radicals and other reactive oxygen species - molecular byproducts of basic cellular metabolism.
Neurons are especially sensitive to damage caused by free radicals, which is believed to be partially responsible for the development of AD. Incorporating antioxidants (which help to neutralize these free radicals) into the diet through food or supplementation may help protect neurons.
Peter P. Zandi, Ph.D., of The Johns Hopkins University Bloomberg School of Public Health, Baltimore, and colleagues examined the relationship between antioxidant supplement use and risk of AD.
The researchers assessed the prevalence of dementia and AD in 4,740 elderly (65 years or older) residents of Cache County, Utah in 1995 to 1997 and collected information about supplement use.
These residents were followed-up in 1998 to 2000 for new cases of dementia or AD. The researchers identified 200 cases of AD (prevalent cases) between 1995 and 1997, and 104 new cases (incident cases) of AD during follow-up.
The researchers categorized participants as vitamin E users if they reported taking an individual supplement of vitamin E or a multivitamin containing more than 400 IU (international units) of vitamin E.
Vitamin C users reported taking vitamin C supplements or multivitamins containing at least 500 micrograms of ascorbic acid.
Individuals were classified as multivitamin users if they reported taking multivitamins containing lower doses of vitamin E or C.
The researchers found the greatest reduction in both prevalence and incidence of AD in participants who used individual vitamin E and C supplements in combination, with or without an additional multivitamin.
'Use of vitamin E and C (ascorbic acid) supplements in combination reduced AD prevalence [by about 78 percent] and incidence [by about 64 percent],' the authors write.
The researchers also found 'no appreciable association with the use of vitamin C alone, vitamin E alone, or vitamin C and multivitamins in combination,' and prevalence of AD.
'The current??? recommended daily allowance for vitamin E is 22 IU (15 micrograms), and for vitamin C (ascorbic acid), 75 to 90 micrograms,' the researchers write.
'Multivitamin preparations typically contain these approximate quantities of both vitamins E and C (more vitamin C in some instances), while individual supplements typically contain doses up to 1,000 IU of vitamin E and 500 to 1,000 micrograms or more of vitamin C (ascorbic acid). Our findings suggest that vitamins E and C may offer protection against AD when taken together in the higher doses available from individual supplements.'
To contact Peter P. Zandi, Ph.D., call Kenna Brigham at 410-955-6878.
(Arch Neurol. 2004;61:82-88. Available post-embargo at
archneurol)
Editor's Note: This study was supported by grants from the National Institutes of Health, Bethesda, Md., and a grant from the National Institute of Mental Health, Bethesda, Md.
For more information, contact JAMA/Archives Media Relations at 312-464-JAMA (5262) or e-mail mediarelationsjama-archives
воскресенье, 21 августа 2011 г.
Antipsychotic Drugs Have Too Many Side Effects For Alzheimer's Patients
Antipsychotic drugs, such as Zyprexa, Seroquel and Risperdal, have side effects which are greater than their benefits for Alzheimer's patients, say researchers from the USA. These drugs are regularly prescribed to treat psychosis and aggression in patients with Alzheimer's disease.
You can read about this new study in the New England Journal of Medicine (NEJM).
Study leader, Dr. Lon Schneider, Unviersity of Southern California, USA, said the drugs do have some effects in treating symptoms, when compared to a placebo. However, the intolerable side-effects they bring with them offset the benefits for this vulnerable population.
Antipsychotic drugs are commonly used for Alzheimer's patients, despite there being no compelling evidence that their benefits are greater than their shortcomings. This new study provides the evidence - showing the drawbacks tend to outweigh the benefits.
In this 42-site, double-blind, placebo-controlled trial, the team examined 421 Alzheimer's patients - they all also suffered from aggression, delusions, hallucinations and/or agitation. They were given either a placebo or one of the three antipsychotic drugs - olanzapine (mean dose, 5.5 mg per day), quetiapine (mean dose, 56.5 mg per day), risperidone (mean dose, 1.0 mg per day). All the patients were followed up during 36 weeks. Doses were adjusted as needed.
Eventually, 85% of patients stopped taking the prescription drugs - either because of the magnitude of the side-effects, or because they did not work. Between 26% - 32% of those on the prescription drugs improved, compared to 21% of those on the placebo.
The antipsychotic drugs made the patients gain weight, as well as making them confused and sleepy.
The team concluded that the prescription medications were no better than the placebo.
"Effectiveness of Atypical Antipsychotic Drugs in Patients with Alzheimer's Disease"
Lon S. Schneider, M.D., Pierre N. Tariot, M.D., Karen S. Dagerman, M.S., Sonia M. Davis, Dr.P.H., John K. Hsiao, M.D., M. Saleem Ismail, M.D., Barry D. Lebowitz, Ph.D., Constantine G. Lyketsos, M.D., M.H.S., J. Michael Ryan, M.D., T. Scott Stroup, M.D., David L. Sultzer, M.D., Daniel Weintraub, M.D., Jeffrey A. Lieberman, M.D., for the CATIE-AD Study Group
NEJM Volume 355:1525-1538 October 12, 2006 Number 15
Click here to see abstract online
Written by:
View drug information on Risperdal Oral Formulation; Seroquel; Zyprexa.
You can read about this new study in the New England Journal of Medicine (NEJM).
Study leader, Dr. Lon Schneider, Unviersity of Southern California, USA, said the drugs do have some effects in treating symptoms, when compared to a placebo. However, the intolerable side-effects they bring with them offset the benefits for this vulnerable population.
Antipsychotic drugs are commonly used for Alzheimer's patients, despite there being no compelling evidence that their benefits are greater than their shortcomings. This new study provides the evidence - showing the drawbacks tend to outweigh the benefits.
In this 42-site, double-blind, placebo-controlled trial, the team examined 421 Alzheimer's patients - they all also suffered from aggression, delusions, hallucinations and/or agitation. They were given either a placebo or one of the three antipsychotic drugs - olanzapine (mean dose, 5.5 mg per day), quetiapine (mean dose, 56.5 mg per day), risperidone (mean dose, 1.0 mg per day). All the patients were followed up during 36 weeks. Doses were adjusted as needed.
Eventually, 85% of patients stopped taking the prescription drugs - either because of the magnitude of the side-effects, or because they did not work. Between 26% - 32% of those on the prescription drugs improved, compared to 21% of those on the placebo.
The antipsychotic drugs made the patients gain weight, as well as making them confused and sleepy.
The team concluded that the prescription medications were no better than the placebo.
"Effectiveness of Atypical Antipsychotic Drugs in Patients with Alzheimer's Disease"
Lon S. Schneider, M.D., Pierre N. Tariot, M.D., Karen S. Dagerman, M.S., Sonia M. Davis, Dr.P.H., John K. Hsiao, M.D., M. Saleem Ismail, M.D., Barry D. Lebowitz, Ph.D., Constantine G. Lyketsos, M.D., M.H.S., J. Michael Ryan, M.D., T. Scott Stroup, M.D., David L. Sultzer, M.D., Daniel Weintraub, M.D., Jeffrey A. Lieberman, M.D., for the CATIE-AD Study Group
NEJM Volume 355:1525-1538 October 12, 2006 Number 15
Click here to see abstract online
Written by:
View drug information on Risperdal Oral Formulation; Seroquel; Zyprexa.
четверг, 18 августа 2011 г.
Quality-of-life for those with dementia in long-term residential care, USA
Recent estimates reveal that approximately 50 percent or one million residents in long-term care assisted living and nursing homes have dementia. This figure is expected to increase substantially as the population ages, making the need for dementia care staff training critical.
In a special issue of The Gerontologist released this month, 16 articles explored quality of life and specific care needs for people with dementia in assisted living and nursing homes. The volume, titled "Dementia Care and Quality of Life in Assisted Living and Nursing Homes," was made possible through a grant from the Alzheimer's Association and was guest edited by Richard Schulz, Ph.D, of the University Center for Social and Urban Research at The University of Pittsburgh.
"This research forms part of the foundation of the Alzheimer's Association Campaign for Quality Residential Care initiated to enhance care for individuals with dementia in long-term care residential settings," said Harry Johns, president and CEO of the Alzheimer's Association. "The findings of this research reinforce our Campaign and the Association's mission to support and improve the quality of lives of those with Alzheimer's, their families and caregivers."
By 2050, the number of people with Alzheimer's disease could reach 16 million and for many families, long-term residential care will be the care option of choice.
The Gerontologist is a refereed publication of The Gerontological Society of America, the oldest and largest national multidisciplinary scientific organization devoted to the advancement of gerontological research. Founded in 1945, its membership includes some 5,000+ researchers, educators, practitioners, and other professionals in the field of aging. The Society's principal missions are to promote research and education in aging and to encourage the dissemination of research results to other scientists, decision makers, and practitioners.
The Alzheimer's Association, the world leader in Alzheimer research and support, is the first and largest voluntary health organization dedicated to finding prevention methods, treatments and an eventual cure for Alzheimer's. For nearly 25 years, the donor-supported, not-for-profit Alzheimer's Association has provided reliable information and care consultation; created supportive services for families; increased funding for dementia research; and influenced public policy changes.
Todd Kluss
tklussgeron
The Gerontological Society of America
geron
In a special issue of The Gerontologist released this month, 16 articles explored quality of life and specific care needs for people with dementia in assisted living and nursing homes. The volume, titled "Dementia Care and Quality of Life in Assisted Living and Nursing Homes," was made possible through a grant from the Alzheimer's Association and was guest edited by Richard Schulz, Ph.D, of the University Center for Social and Urban Research at The University of Pittsburgh.
"This research forms part of the foundation of the Alzheimer's Association Campaign for Quality Residential Care initiated to enhance care for individuals with dementia in long-term care residential settings," said Harry Johns, president and CEO of the Alzheimer's Association. "The findings of this research reinforce our Campaign and the Association's mission to support and improve the quality of lives of those with Alzheimer's, their families and caregivers."
By 2050, the number of people with Alzheimer's disease could reach 16 million and for many families, long-term residential care will be the care option of choice.
The Gerontologist is a refereed publication of The Gerontological Society of America, the oldest and largest national multidisciplinary scientific organization devoted to the advancement of gerontological research. Founded in 1945, its membership includes some 5,000+ researchers, educators, practitioners, and other professionals in the field of aging. The Society's principal missions are to promote research and education in aging and to encourage the dissemination of research results to other scientists, decision makers, and practitioners.
The Alzheimer's Association, the world leader in Alzheimer research and support, is the first and largest voluntary health organization dedicated to finding prevention methods, treatments and an eventual cure for Alzheimer's. For nearly 25 years, the donor-supported, not-for-profit Alzheimer's Association has provided reliable information and care consultation; created supportive services for families; increased funding for dementia research; and influenced public policy changes.
Todd Kluss
tklussgeron
The Gerontological Society of America
geron
понедельник, 15 августа 2011 г.
Revealing A Surprising Link Between Diabetes And Alzheimer's Disease
Blindness, heart disease, nerve damage, and kidney failure are not the only complications facing the nation's estimated 24 million people with diabetes. Although not widely known, those with the disease face up to double the risk of developing Alzheimer's disease (AD) than non-diabetics, according to an article scheduled for the May 18 issue of Chemical & Engineering News, ACS' weekly newsmagazine.
C&EN senior editor Sophie Rovner explains in the article that people with diabetes tend to have a higher risk of getting AD, and possibly get it at an earlier age, than the general population. Five million people in the United States have Alzheimer's, a brain disorder that causes severe memory loss. Diabetes results from the body's inability to produce or use insulin. Newer research now suggests that insulin is critical for healthy nerve cells in the brain. As the hormone declines in the brains of people with Alzheimer's, so does their memory.
Some research even suggests that diabetes and Alzheimer's are part of the same disease process that affects different parts of the body and that Alzheimer's may be considered "Type 3" diabetes. If so, then doctors might treat Alzheimer's in the same way as diabetes, which includes giving patients insulin or other medications - including so-called "insulin sensitizing" drugs - the article states.
Source
American Chemical Society
C&EN senior editor Sophie Rovner explains in the article that people with diabetes tend to have a higher risk of getting AD, and possibly get it at an earlier age, than the general population. Five million people in the United States have Alzheimer's, a brain disorder that causes severe memory loss. Diabetes results from the body's inability to produce or use insulin. Newer research now suggests that insulin is critical for healthy nerve cells in the brain. As the hormone declines in the brains of people with Alzheimer's, so does their memory.
Some research even suggests that diabetes and Alzheimer's are part of the same disease process that affects different parts of the body and that Alzheimer's may be considered "Type 3" diabetes. If so, then doctors might treat Alzheimer's in the same way as diabetes, which includes giving patients insulin or other medications - including so-called "insulin sensitizing" drugs - the article states.
Source
American Chemical Society
пятница, 12 августа 2011 г.
Alzheimer's Foundation Of America Sets Standard Of Excellence For Dementia Settings
As part of its ongoing efforts to
raise the bar on dementia care, the Alzheimer's Foundation of America (AFA)
has developed a nationwide standard of excellence for settings that provide
care to individuals with Alzheimer's disease or related dementias.
The new initiative, called Excellence in Care, involves on-site
evaluations of dementia care settings and assistance in meeting the
comprehensive set of standards. The standards reflect what AFA believes to
be essential components of any quality dementia care program.
Facilities that comply with the standards will earn the status of AFA
Excellence in Care Dementia Program of Distinction.
This is believed to be the first national program involving standards
and on-site evaluation for dementia care settings, such as assisted living
and skilled nursing facilities, continuum of care residential communities,
adult day and adult day healthcare care programs.
"As the incidence of Alzheimer's disease continues to rise, this
population deserves to be cared for in settings that meet a gold standard.
Quality of life and safety are paramount," said Eric J. Hall, AFA's chief
executive officer.
"Through Excellence in Care, we hope to promote continual improvement
of care and best practices throughout the country. This program gives care
settings the opportunity to ensure that optimal care is given to their
clients, and it will assist families as they select programs for their
loved ones," he said.
AFA designed the program with input from the Avila Institute of
Gerontology, an AFA member organization based in Germantown, NY that
provides high-quality education programs, as well as other AFA member
organizations, national organizations and industry experts.
Areas of evaluation include the physical environment, safety
procedures, program activities, staff-client interaction, and training of
staff and families.
AFA's trained Excellence in Care specialists will conduct the on-site
evaluations, and they will collaborate with settings found to have
shortcomings to upgrade their programs to meet the requirements.
AFA's first class of Excellence in Care specialists was trained this
past month and will begin evaluating facilities that sign up for the
Excellence in Care program.
The Alzheimer's Foundation of America is a national nonprofit
organization headquartered in New York and is made up of hundreds of member
organizations that provide hands-on programs to meet the educational,
emotional, practical and social needs of families. AFA's services include a
toll-free hot line, counseling, educational materials, a free caregiver
magazine, and professional training. For information, call (toll-free)
866-AFA-8484 or visit alzfdn.
Alzheimer's Foundation of America
alzfdn
raise the bar on dementia care, the Alzheimer's Foundation of America (AFA)
has developed a nationwide standard of excellence for settings that provide
care to individuals with Alzheimer's disease or related dementias.
The new initiative, called Excellence in Care, involves on-site
evaluations of dementia care settings and assistance in meeting the
comprehensive set of standards. The standards reflect what AFA believes to
be essential components of any quality dementia care program.
Facilities that comply with the standards will earn the status of AFA
Excellence in Care Dementia Program of Distinction.
This is believed to be the first national program involving standards
and on-site evaluation for dementia care settings, such as assisted living
and skilled nursing facilities, continuum of care residential communities,
adult day and adult day healthcare care programs.
"As the incidence of Alzheimer's disease continues to rise, this
population deserves to be cared for in settings that meet a gold standard.
Quality of life and safety are paramount," said Eric J. Hall, AFA's chief
executive officer.
"Through Excellence in Care, we hope to promote continual improvement
of care and best practices throughout the country. This program gives care
settings the opportunity to ensure that optimal care is given to their
clients, and it will assist families as they select programs for their
loved ones," he said.
AFA designed the program with input from the Avila Institute of
Gerontology, an AFA member organization based in Germantown, NY that
provides high-quality education programs, as well as other AFA member
organizations, national organizations and industry experts.
Areas of evaluation include the physical environment, safety
procedures, program activities, staff-client interaction, and training of
staff and families.
AFA's trained Excellence in Care specialists will conduct the on-site
evaluations, and they will collaborate with settings found to have
shortcomings to upgrade their programs to meet the requirements.
AFA's first class of Excellence in Care specialists was trained this
past month and will begin evaluating facilities that sign up for the
Excellence in Care program.
The Alzheimer's Foundation of America is a national nonprofit
organization headquartered in New York and is made up of hundreds of member
organizations that provide hands-on programs to meet the educational,
emotional, practical and social needs of families. AFA's services include a
toll-free hot line, counseling, educational materials, a free caregiver
magazine, and professional training. For information, call (toll-free)
866-AFA-8484 or visit alzfdn.
Alzheimer's Foundation of America
alzfdn
вторник, 9 августа 2011 г.
Perceptive Informatics Introduces Medical Imaging Methodology To Accelerate Development Decisions About Alzheimer's Treatments
Perceptive Informatics, the industry's leading eClinical solutions provider and a subsidiary of PAREXEL International Corporation (Nasdaq: PRXL), announced that it has developed a robust medical imaging methodology for Central Nervous System (CNS) clinical trials involving Alzheimer's disease. The method, based on measuring ventricular size, provides a new approach to monitor brain atrophy in Alzheimer's disease and potential treatment effects. The technique was presented on April 26, 2009 in Seattle, Washington during an invitation-only meeting of the Alzheimer's Disease Neuroimaging Initiative (ADNI).
The advantages of this method include providing higher quality, reproducible, and regulatory compliant assessments with the potential to help clinical trial sponsors make better and faster development decisions about Alzheimer's treatments in development. To develop this method, the Perceptive Informatics team collected Magnetic Resonance Imaging (MRI) scans from the ADNI database using Perceptive's medical imaging system and regulatory compliant processes.
"It is more critical than ever that biopharmaceutical companies have the ability to make accurate go/no go decisions as early as possible for new compounds. Medical imaging is increasingly being used as a surrogate endpoint or biomarker of drug efficacy in all phases of CNS trials. With this new methodology, we believe that Perceptive's therapeutic area experts are able to help sponsors advance neuroimaging and bring important CNS treatments to patients sooner," said Kenneth G. Faulkner, Ph.D., Vice President of Medical Imaging, Perceptive Informatics.
"Based on ADNI data, measuring ventricular change may be one of the most robust outcomes for imaging progression of Alzheimer's disease. Perceptive has developed a novel method of ventricular measurement that accurately reflects brain atrophy," said James Paskavitz, M.D., Medical Director, Perceptive Informatics. "We believe that this method can support sponsors in reducing the time, cost, and risk associated with clinical development of Alzheimer's treatments by providing medical image data that informs early phase decisions and is reproducible for later phase, multi-center trials."
The Perceptive Informatics Medical Imaging Group has helped to develop and validate novel surrogate endpoints for a variety of CNS disorders. Perceptive offers a range of capabilities in the application of imaging techniques from early clinical development through late phase studies. The medical imaging team operates globally and services a wide range of therapeutic areas, including oncology, central nervous system, musculoskeletal, cardiovascular, and metabolism/endocrinology imaging.
ADNI is focused on defining the rate of progress of mild cognitive impairment and Alzheimer's disease, developing improved methods for clinical trials in this area, and providing a large database to improve design of treatment trials. A goal of ADNI is to provide information and methods to help lead to effective treatments for Alzheimer's disease, leading to effective prevention.
About Perceptive Informatics
Perceptive Informatics, a subsidiary of PAREXEL, is the industry's leading eClinical solutions provider. Perceptive Informatics offers unprecedented access to innovative eClinical technologies and resources, providing clinical trial sponsors, CROs, and other service providers with the benefits of an extensive line of products and services throughout the entire clinical development lifecycle. In August, 2008 Perceptive was joined with ClinPhone plc, and the newly combined organization offers eClinical software and services that increase the efficiency and productivity of clinical research. Perceptive's expansive product portfolio includes Interactive Voice and Web Response Systems (IVRS/IWRS), Medical Imaging, Electronic Data Capture (EDC) systems, Clinical Trial Management Systems (CTMS) and Electronic Patient Reported Outcomes (ePRO) solutions, as well as eClinical systems integration and implementation services.
About PAREXEL International
PAREXEL International Corporation is a leading global biopharmaceutical services organization, providing a broad range of knowledge-based contract research, medical communications and consulting services to the worldwide pharmaceutical, biotechnology and medical device industries. Committed to providing solutions that expedite time-to-market and peak-market penetration, PAREXEL has developed significant expertise across the development and commercialization continuum, from drug development and regulatory consulting to clinical pharmacology, clinical trials management, medical education and reimbursement. Perceptive Informatics, Inc., a subsidiary of PAREXEL, provides advanced technology solutions, including medical imaging, to facilitate the clinical development process. Headquartered near Boston, Massachusetts, PAREXEL operates in 69 locations throughout 52 countries around the world, and has over 9,400 employees.
This release contains "forward-looking" statements regarding future results and events. For this purpose, any statements contained herein that are not statements of historical fact may be deemed forward-looking statements. Without limiting the foregoing, the words "believes," "anticipates," "plans," "expects," "intends," "appears," "estimates," "projects," "targets," and similar expressions are also intended to identify forward-looking statements. The forward-looking statements in this release involve a number of risks and uncertainties. The Company's actual future results may differ significantly from the results discussed in the forward-looking statements contained in this release. Important factors that might cause such a difference include, but are not limited to, risks associated with: actual operating performance; actual expense savings and other operating improvements resulting from recent restructurings; the loss, modification, or delay of contracts which would, among other things, adversely impact the Company's recognition of revenue included in backlog; the Company's dependence on certain industries and clients; the Company's ability to win new business, manage growth and costs, and attract and retain employees; the Company's ability to complete additional acquisitions and to integrate newly acquired businesses or enter into new lines of business, including, but not limited to, the successful business integration and anticipated synergy achievements in connection with the ClinPhone acquisition; the impact on the Company's business of government regulation of the drug, medical device and biotechnology industry; consolidation within the pharmaceutical industry and competition within the biopharmaceutical services industry; the potential for significant liability to clients and third parties; the potential adverse impact of health care reform; and the effects of exchange rate fluctuations and other international economic, political, and other risks. Such factors and others are discussed more fully in the section entitled "Risk Factors" of the Company's Quarterly Report on Form 10-Q for the quarter ended December 31, 2008 as filed with the SEC on February 9, 2009, which "Risk Factors" discussion is incorporated by reference in this press release. The forward-looking statements included in this press release represent the Company's estimates as of the date of this release. The Company specifically disclaims any obligation to update these forward-looking statements in the future. These forward-looking statements should not be relied upon as representing the Company's estimates or views as of any date subsequent to the date of this press release.
PAREXEL is a registered trademark of PAREXEL International Corporation, and Perceptive Informatics is a trademark of Perceptive Informatics, Inc. All other names or marks may be registered trademarks or trademarks of PAREXEL International Corporation, Perceptive Informatics, Inc. or their respective owners and are hereby acknowledged.
Source: PAREXEL International Corporation
The advantages of this method include providing higher quality, reproducible, and regulatory compliant assessments with the potential to help clinical trial sponsors make better and faster development decisions about Alzheimer's treatments in development. To develop this method, the Perceptive Informatics team collected Magnetic Resonance Imaging (MRI) scans from the ADNI database using Perceptive's medical imaging system and regulatory compliant processes.
"It is more critical than ever that biopharmaceutical companies have the ability to make accurate go/no go decisions as early as possible for new compounds. Medical imaging is increasingly being used as a surrogate endpoint or biomarker of drug efficacy in all phases of CNS trials. With this new methodology, we believe that Perceptive's therapeutic area experts are able to help sponsors advance neuroimaging and bring important CNS treatments to patients sooner," said Kenneth G. Faulkner, Ph.D., Vice President of Medical Imaging, Perceptive Informatics.
"Based on ADNI data, measuring ventricular change may be one of the most robust outcomes for imaging progression of Alzheimer's disease. Perceptive has developed a novel method of ventricular measurement that accurately reflects brain atrophy," said James Paskavitz, M.D., Medical Director, Perceptive Informatics. "We believe that this method can support sponsors in reducing the time, cost, and risk associated with clinical development of Alzheimer's treatments by providing medical image data that informs early phase decisions and is reproducible for later phase, multi-center trials."
The Perceptive Informatics Medical Imaging Group has helped to develop and validate novel surrogate endpoints for a variety of CNS disorders. Perceptive offers a range of capabilities in the application of imaging techniques from early clinical development through late phase studies. The medical imaging team operates globally and services a wide range of therapeutic areas, including oncology, central nervous system, musculoskeletal, cardiovascular, and metabolism/endocrinology imaging.
ADNI is focused on defining the rate of progress of mild cognitive impairment and Alzheimer's disease, developing improved methods for clinical trials in this area, and providing a large database to improve design of treatment trials. A goal of ADNI is to provide information and methods to help lead to effective treatments for Alzheimer's disease, leading to effective prevention.
About Perceptive Informatics
Perceptive Informatics, a subsidiary of PAREXEL, is the industry's leading eClinical solutions provider. Perceptive Informatics offers unprecedented access to innovative eClinical technologies and resources, providing clinical trial sponsors, CROs, and other service providers with the benefits of an extensive line of products and services throughout the entire clinical development lifecycle. In August, 2008 Perceptive was joined with ClinPhone plc, and the newly combined organization offers eClinical software and services that increase the efficiency and productivity of clinical research. Perceptive's expansive product portfolio includes Interactive Voice and Web Response Systems (IVRS/IWRS), Medical Imaging, Electronic Data Capture (EDC) systems, Clinical Trial Management Systems (CTMS) and Electronic Patient Reported Outcomes (ePRO) solutions, as well as eClinical systems integration and implementation services.
About PAREXEL International
PAREXEL International Corporation is a leading global biopharmaceutical services organization, providing a broad range of knowledge-based contract research, medical communications and consulting services to the worldwide pharmaceutical, biotechnology and medical device industries. Committed to providing solutions that expedite time-to-market and peak-market penetration, PAREXEL has developed significant expertise across the development and commercialization continuum, from drug development and regulatory consulting to clinical pharmacology, clinical trials management, medical education and reimbursement. Perceptive Informatics, Inc., a subsidiary of PAREXEL, provides advanced technology solutions, including medical imaging, to facilitate the clinical development process. Headquartered near Boston, Massachusetts, PAREXEL operates in 69 locations throughout 52 countries around the world, and has over 9,400 employees.
This release contains "forward-looking" statements regarding future results and events. For this purpose, any statements contained herein that are not statements of historical fact may be deemed forward-looking statements. Without limiting the foregoing, the words "believes," "anticipates," "plans," "expects," "intends," "appears," "estimates," "projects," "targets," and similar expressions are also intended to identify forward-looking statements. The forward-looking statements in this release involve a number of risks and uncertainties. The Company's actual future results may differ significantly from the results discussed in the forward-looking statements contained in this release. Important factors that might cause such a difference include, but are not limited to, risks associated with: actual operating performance; actual expense savings and other operating improvements resulting from recent restructurings; the loss, modification, or delay of contracts which would, among other things, adversely impact the Company's recognition of revenue included in backlog; the Company's dependence on certain industries and clients; the Company's ability to win new business, manage growth and costs, and attract and retain employees; the Company's ability to complete additional acquisitions and to integrate newly acquired businesses or enter into new lines of business, including, but not limited to, the successful business integration and anticipated synergy achievements in connection with the ClinPhone acquisition; the impact on the Company's business of government regulation of the drug, medical device and biotechnology industry; consolidation within the pharmaceutical industry and competition within the biopharmaceutical services industry; the potential for significant liability to clients and third parties; the potential adverse impact of health care reform; and the effects of exchange rate fluctuations and other international economic, political, and other risks. Such factors and others are discussed more fully in the section entitled "Risk Factors" of the Company's Quarterly Report on Form 10-Q for the quarter ended December 31, 2008 as filed with the SEC on February 9, 2009, which "Risk Factors" discussion is incorporated by reference in this press release. The forward-looking statements included in this press release represent the Company's estimates as of the date of this release. The Company specifically disclaims any obligation to update these forward-looking statements in the future. These forward-looking statements should not be relied upon as representing the Company's estimates or views as of any date subsequent to the date of this press release.
PAREXEL is a registered trademark of PAREXEL International Corporation, and Perceptive Informatics is a trademark of Perceptive Informatics, Inc. All other names or marks may be registered trademarks or trademarks of PAREXEL International Corporation, Perceptive Informatics, Inc. or their respective owners and are hereby acknowledged.
Source: PAREXEL International Corporation
суббота, 6 августа 2011 г.
FDA Seeks To Include Those Most Affected By Alzheimer's Disease In The Drug Review Process
The U.S. Food and Drug Administration (FDA) has expanded its Patient Consultant and Patient Representative programs to include individuals in the early stages of Alzheimer's disease and their caregivers. The FDA made the change in response to a request by the Alzheimer's Association encouraging the agency to give people directly affected by Alzheimer's a more active role in the review and approval of new Alzheimer drugs.
"People who are living with this terrible disease have much to offer to the pharmaceutical industry, researchers and government regulators, and their voices must be heard," said Harry Johns, president and CEO of the Alzheimer's Association. "We are pleased that the FDA understands the value of involving Alzheimer families in regulatory decisions that affect them and appreciate that the agency was so responsive in expanding their patient consultant program."
Similar to the programs that already exist for those with cancer and Parkinson's disease, the Alzheimer patient consultants and representatives will participate in FDA advisory committee meetings and advise on topics such as clinical trial design and the development of guidelines for clinical research. Involving those with the disease and their primary caregivers will increase the FDA's capacity to make informed regulatory decisions that are sensitive to the needs and preferences of this population. Following rigorous training by FDA staff, all involved will have access to materials for review and the opportunity to offer input on a variety of issues.
The Alzheimer's Association's request to the FDA grew out of extensive conversations with families across the nation struggling with the disease, many of whom felt that the drug development process was not always responsive to their needs. The Association held a Research Roundtable meeting in Washington at which persons with Alzheimer's, family caregivers, researchers, FDA regulators and Alzheimer's Association leaders discussed the risk and benefit trade-offs involved in drug development.
Following the meeting, the Association published articles on the issue in its scientific journal and subsequently forwarded the recommendation on the patient consultancy program to the FDA. This was followed by meetings with FDA leadership to move the issue forward.
"The FDA has been quite open to working with the Alzheimer's Association on ways to increase the attention and priority of Alzheimer issues within the agency," said Stephen McConnell, vice president of Advocacy and Public Policy for the Alzheimer's Association. "The Alzheimer's Association's goal is to ensure treatments that are safe and effective can get through the regulatory review process as quickly and efficiently as possible, while also being responsive to the special perspective of those who will benefit from them. The FDA has been a willing partner with the Association in this effort."
About the Alzheimer's Association
The Alzheimer's Association is the leading voluntary health organization in Alzheimer care, support and research. Our mission is to eliminate Alzheimer's disease through the advancement of research; to provide and enhance care and support for all affected; and to reduce the risk of dementia through the promotion of brain health. Our vision is a world without Alzheimer's.
Alzheimer's Association
"People who are living with this terrible disease have much to offer to the pharmaceutical industry, researchers and government regulators, and their voices must be heard," said Harry Johns, president and CEO of the Alzheimer's Association. "We are pleased that the FDA understands the value of involving Alzheimer families in regulatory decisions that affect them and appreciate that the agency was so responsive in expanding their patient consultant program."
Similar to the programs that already exist for those with cancer and Parkinson's disease, the Alzheimer patient consultants and representatives will participate in FDA advisory committee meetings and advise on topics such as clinical trial design and the development of guidelines for clinical research. Involving those with the disease and their primary caregivers will increase the FDA's capacity to make informed regulatory decisions that are sensitive to the needs and preferences of this population. Following rigorous training by FDA staff, all involved will have access to materials for review and the opportunity to offer input on a variety of issues.
The Alzheimer's Association's request to the FDA grew out of extensive conversations with families across the nation struggling with the disease, many of whom felt that the drug development process was not always responsive to their needs. The Association held a Research Roundtable meeting in Washington at which persons with Alzheimer's, family caregivers, researchers, FDA regulators and Alzheimer's Association leaders discussed the risk and benefit trade-offs involved in drug development.
Following the meeting, the Association published articles on the issue in its scientific journal and subsequently forwarded the recommendation on the patient consultancy program to the FDA. This was followed by meetings with FDA leadership to move the issue forward.
"The FDA has been quite open to working with the Alzheimer's Association on ways to increase the attention and priority of Alzheimer issues within the agency," said Stephen McConnell, vice president of Advocacy and Public Policy for the Alzheimer's Association. "The Alzheimer's Association's goal is to ensure treatments that are safe and effective can get through the regulatory review process as quickly and efficiently as possible, while also being responsive to the special perspective of those who will benefit from them. The FDA has been a willing partner with the Association in this effort."
About the Alzheimer's Association
The Alzheimer's Association is the leading voluntary health organization in Alzheimer care, support and research. Our mission is to eliminate Alzheimer's disease through the advancement of research; to provide and enhance care and support for all affected; and to reduce the risk of dementia through the promotion of brain health. Our vision is a world without Alzheimer's.
Alzheimer's Association
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