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
четверг, 29 сентября 2011 г.
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
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