People at all stages of Alzheimer's will now be able to access drugs on the NHS that can slow the progression of the disease.
The development comes following final guidance published by The National Institute for Health and Clinical Excellence (NICE). Alzheimer's Society services are holding celebrations around the country all week to mark the occasion.
The decision is a reversal of NICE's previous position - in place since 2007 - limiting access to only those in the moderate stages of the disease.
Andrew Chidgey, Head of Policy and Public Affairs at Alzheimer's Society, says,
'This is a victory for people with Alzheimer's and their carers, many of whom have been campaigning for this day for years. These drugs don't work for everyone, but for some people they can radically improve their quality of life. We now need more people to be diagnosed early and for them to receive the treatment, support and advice that they desperately need.'
There are currently 465,000 people living with Alzheimer's in the UK and a further 62,000 people are developing Alzheimer's each year. The drugs - Aricept, Exelon and Reminyl - will now be available on prescription for people in the early and moderate stages of Alzheimer's disease. These treatments have up to now been restricted to people in the moderate stages. A fourth drug, called Ebixa, will also be made available to people in the moderate to late stages.
Heather Roberts, 56, from Derby has Alzheimer's disease and has been heavily involved in the campaign since 2007. She says,
'It's absolutely fantastic that NICE has changed its guidelines on Alzheimer's drugs, but it's not before time. NICE should be ashamed of itself for restricting access to these essential drugs in the first place. Within six months of taking Aricept my memory had improved to how it had been two years previously. That is a measure of the difference it has made to me. I am still very independent - I've got my driving licence, regularly play tennis and enjoy going on holiday. Thank heavens NICE has finally seen sense.'
Notes
- The final decision by NICE comes following the publication in October 2010 of draft guidance and is part of a review cycle of Alzheimer's drug treatments.
- For more information on the background of Alzheimer's Society's campaigning work around NICE guidance on Alzheimer's drugs, visit here.
- If people are worried about their memory they should visit their GP. For information on drug treatments, an Alzheimer's Society factsheet is available.
Source:
Alzheimer's Society
View drug information on ARICEPT; Exelon; Reminyl.
воскресенье, 8 мая 2011 г.
суббота, 7 мая 2011 г.
Hispanics Have More Risk Factors For Developing Alzheimer's Disease Than Other Groups, Research Suggests
The New York Times on Tuesday examined research that found "many Hispanics may have more risk factors for developing dementia than other groups" and that a "significant number appear to be getting Alzheimer's earlier" than most U.S. residents, who commonly develop the disease in their 70s or 80s. According to the Alzheimer's Association, about 200,000 Hispanics in the U.S. have the condition but the number could increase to 1.3 million by 2050. "This is the tip of the iceberg of a huge public health challenge," Yanira Cruz, president of the National Hispanic Council on Aging, said, adding, "We really need to do more research in this population to really understand why it is that we're developing these conditions much earlier."
Overall, the number of U.S. residents with Alzheimer's is expected to increase from five million in 2008 to 16 million in 2050. According to experts, Hispanics are not more genetically predisposed to Alzheimer's but factors related to low income or cultural dislocation -- such as higher rates of diabetes, obesity, cardiovascular disease, stroke and high blood pressure -- may put them at a higher risk for dementia. Cruz said the immigration experience, along with the changes in diet and social network that it entails, could play a role in increased the risk of Alzheimer's. She said, "As you acculturate, you lose those protective factors linked to nutrition, physical activity [and a] social support system that come with you when you first arrive here."
According to the Times, less education also could make this group more vulnerable to risk factors and to dementia because, scientists say, education may increase the plasticity of the brain and its ability to compensate for symptoms. Some research also cites stress related to financial troubles or cultural adjustment as risk factors for dementia. In addition, Hispanics, who are less likely to see doctors because of financial and language barriers, often mistake the symptoms of dementia as a result of aging, according to the Times. "There's some taboos," Liany Arroyo, director of the Institute for Hispanic Health at the National Council of La Raza, said, adding that surveys his group completed indicated that some Hispanics "do not necessarily understand" what Alzheimer's is.
Alzheimer's and Hispanic groups have responded to such findings by setting up health fairs and support groups, the Times reports. Some Alzheimer's centers have opened offices in Hispanic neighborhoods, according to the Times (Belluck, New York Times, 10/21).
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.
Overall, the number of U.S. residents with Alzheimer's is expected to increase from five million in 2008 to 16 million in 2050. According to experts, Hispanics are not more genetically predisposed to Alzheimer's but factors related to low income or cultural dislocation -- such as higher rates of diabetes, obesity, cardiovascular disease, stroke and high blood pressure -- may put them at a higher risk for dementia. Cruz said the immigration experience, along with the changes in diet and social network that it entails, could play a role in increased the risk of Alzheimer's. She said, "As you acculturate, you lose those protective factors linked to nutrition, physical activity [and a] social support system that come with you when you first arrive here."
According to the Times, less education also could make this group more vulnerable to risk factors and to dementia because, scientists say, education may increase the plasticity of the brain and its ability to compensate for symptoms. Some research also cites stress related to financial troubles or cultural adjustment as risk factors for dementia. In addition, Hispanics, who are less likely to see doctors because of financial and language barriers, often mistake the symptoms of dementia as a result of aging, according to the Times. "There's some taboos," Liany Arroyo, director of the Institute for Hispanic Health at the National Council of La Raza, said, adding that surveys his group completed indicated that some Hispanics "do not necessarily understand" what Alzheimer's is.
Alzheimer's and Hispanic groups have responded to such findings by setting up health fairs and support groups, the Times reports. Some Alzheimer's centers have opened offices in Hispanic neighborhoods, according to the Times (Belluck, New York Times, 10/21).
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.
пятница, 6 мая 2011 г.
Recovery Funds Advance Alzheimer's Disease Research
American Recovery and Reinvestment Funds are being used to promote the national research efforts to better understand, diagnose and treat Alzheimer's disease. The National Institute on Aging (NIA), part of the National Institutes of Health, has targeted promising areas of research in granting the awards, such as new and ongoing studies to identify additional risk factor genes associated with Alzheimer's, improve diagnostic tools, find biomarkers, develop therapies, conduct clinical trials and explore preventive measures.
"We are delighted to announce the award of Recovery Act funds to many dedicated, hardworking scientists committed to advancing scientific discovery into Alzheimer's disease and cognitive impairment," said NIA Director Richard J. Hodes, M.D. "Over the next two years, the recipients will use this unprecedented boost in research funds to help reach our ultimate goal of understanding age-related cognitive decline and reducing the individual and societal burden of this devastating disease."
More than 100 Alzheimer's or Alzheimer's-related research grants were awarded under the Recovery Act. The full list of NIH grants can be found at grants.nih/recovery/. The grants featured here highlight how these funds will expand research. Some of the funding will advance the work of existing NIA initiatives that benefit from large-scale collaborative, interdisciplinary research:
The Neuroimaging Initiative - Identifying brain changes before symptoms appear
The Alzheimer's Disease Neuroimaging Initiative (ADNI) will receive $24 million in stimulus funds - half from the NIA and half contributed by the NIH Office of the Director - to further groundbreaking research to establish neuroimaging and biomarker measures. These funds will enable researchers - and ultimately practicing physicians - to track changes in the living brain as older people transition from normal cognitive aging to amnestic mild cognitive impairment (MCI), in which individuals have a memory deficit but generally retain other cognitive abilities, and from MCI to Alzheimer's disease. ADNI, a research partnership supported primarily by the NIA with private sector support through the Foundation for NIH, seeks to find neuroimaging and other biological markers that can be used to detect Alzheimer's disease progression and measure the effectiveness of potential therapies.
The original ADNI involved the study of 800 people who ranged from normal to those with late-stage MCI or overt Alzheimer's disease. This new grant expands the scope of ongoing research under ADNI by allowing for the enrollment of participants at an earlier stage of MCI, when symptoms are milder. Furthermore, the funding for this new grant will allow ADNI investigators to extend the length of the original study to better assess changes in individuals over time. All of the participants will have neuroimaging scans and blood and cerebrospinal fluid analyses to look for changes in the brain.
The overall impact of the added funding will be increased knowledge of the sequence and timing of events leading to MCI and Alzheimer's disease and development of better clinical and imaging/fluid biomarker methods for early detection and for monitoring the progression of these conditions. This will facilitate clinical trials of treatments to slow disease progression and will ultimately contribute to the prevention of Alzheimer's disease. Just this year, ADNI made a significant step forward in developing a test to help diagnose the beginning stages of Alzheimer's disease sooner and more accurately by measuring levels of two biomarkers - tau and beta-amyloid proteins - in cerebrospinal fluid.
"Researchers and clinicians need imaging and biomarker tools to detect and understand the very earliest signs of pathology that cause changes in the brain some 10 to 20 years before any clinical symptoms of cognitive impairment or Alzheimer's may appear,"said ADNI Principal Investigator Michael Weiner, M.D., of the San Francisco Department of Veterans Affairs Medical Center and the University of California, San Francisco. "This grant will help us in our goal of establishing a panel of biomarkers that predict those at risk of developing the disease and also reveal which therapies may be effective in treating the disease or preventing its progression."
The grant was awarded to the Northern California Institute for Research and Education, a nonprofit research foundation affiliated with the San Francisco VA Medical Center. ADNI is the largest public-private partnership on brain research under way at the NIH. In addition to the NIA, the federal ADNI partners are the National Institute of Biomedical Imaging and Bioengineering, also part of NIH, and the U.S. Food and Drug Administration, another agency of the U.S. Department of Health and Human Services.
The AD Genetics Consortium and more " Identifying genes affecting risk for late-onset Alzheimer's
A grant of more than $5.4 million will add 3,800 Alzheimer's patients and an equal number of people free of the disease to a previously funded study by the Alzheimer' Disease Genetics Consortium (ADGC). Gerard Schellenberg, Ph.D., University of Pennsylvania School of Medicine, Philadelphia, leads the consortium, which aims to identify the additional risk factor genes for late-onset Alzheimer's disease. All of these study participants are currently enrolled in the NIA-funded national network of 29 Alzheimer's Disease Centers. When added to the samples from other sources, this will make available one of the largest collections of samples to perform genome-wide association studies (GWAS) in an effort to identify the susceptibility and protective genes influencing the onset and progression of late-onset disease. The large number of DNA samples brought together in this study may enable the researchers to detect genes whose individual effects in the disorder may be small but may still play a role.
The ADGC will use research infrastructures previously established by NIA to store and make available to qualified researchers DNA samples, datasets containing a wealth of information about participants, and genetic analysis data. The combined resources will allow scientists also to search for genes associated with a number of traits associated with Alzheimer's, as well as for genes related to cognitive decline.
"This funding will bring us closer to identifying the elusive genetic variations that contribute to overall risk and development of late-onset Alzheimer's disease," said Marcelle Morrison-Bogorad, Ph.D., director of the NIA Division of Neuroscience. "With this large sample size and the rapid DNA sample and data sharing, there are tremendous opportunities for defining new disease pathways that could lead to the development of new therapies."
Additionally, $4.7 million in Recovery Act funds will be used for another important study - a GWAS project examining cognitive decline in older African-Americans. Denis Evans, M.D., of Rush University Medical Center in Chicago, will collect and analyze the DNA of 4,140 elderly African-Americans enrolled in NIA-funded aging studies already taking place in Chicago and Indianapolis. Data from this analysis will also be shared with the ADGC to help identify risk factor genes for cognitive decline and late-onset Alzheimer's. The study will assess the associations of over 900,000 genetic markers with other co-morbidities, including stroke and high blood pressure.
Another $820,000 in Recovery Act funds will advance Alzheimer's genetics research by developing methods for identifying combinations of genes that might influence age-related risk of AD. The role of different forms of translocase of outer mitochondrial membrane (TOMM40), a gene that makes a protein thought to play a role in disease onset, will be studied by Allen Roses, M.D., of the Duke University School of Medicine in Durham, N.C.; Roses discovered the link between the apolipoprotein E (APOE)-epsilon 4 gene and increased risk for late-onset Alzheimer's disease. This new study will investigate whether particular variants of TOMM40 that tend to co-occur with the APOE3 gene also interact with that gene, and if this interaction plays a role in the age of disease onset.
Additional Recovery Act research opportunities
Other studies made possible by the Recovery Act range from clinical trials to epigenomic studies to translational research:
Drug, exercise clinical trials - A clinical trial exploring whether low doses of an anti-epileptic seizure drug, levetiracetam, can improve memory and affect brain function in people with MCI will be conducted with $1.2 million in support. Michela Gallagher, Ph.D., of Johns Hopkins University, Baltimore, will use functional MRI to visualize activity in the hippocampus - a brain area that becomes overactive in MCI patients - while the clinical trial participants receiving either the drug or a placebo engage in memory tasks. In another trial, researchers will examine how exercise training, cognitive training, or a combination of both, might impact immune and inflammatory biomarkers and cognitive health in older adults with MCI. The randomized trial, under a $1 million grant to David Lowenstein, Ph.D., of the University of Miami, will examine a broad array of outcomes and will include Hispanic and non-Hispanic volunteers.
Epigenetics/translational research - A $1 million grant will support a study exploring whether changes in histone acetylation (an epigenetic, or non-genetic factor that causes genes to behave differently) are one way in which a variety of life experiences may influence the risk of developing age-related cognitive decline and dementia. David Bennett, M.D., of Rush University Medical Center, Chicago, will use brain tissues from the NIA-funded Memory and Aging Project and the Religious Orders Study to examine this question. Another epigenomics grant of $819,000 will be used in translational research to test whether overexpressing histone deacetylase (HDAC1) with small molecule probes in the brain may demonstrate therapeutic potential for Alzheimer's and stroke patients. Li-Huei Tsai, Ph.D., of Massachusetts Institute of Technology, Boston, will lead the study, which seeks to find out whether abnormal regulation of the protein may play a role in neurological disorders.
The NIA leads the federal effort supporting and conducting research on aging and the medical, social and behavioral issues of older people. For more information on research and aging, go to 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. To sign up for e-mail alerts about new findings or publications, please visit either website.
Source
National Institutes of Health (NIH)
"We are delighted to announce the award of Recovery Act funds to many dedicated, hardworking scientists committed to advancing scientific discovery into Alzheimer's disease and cognitive impairment," said NIA Director Richard J. Hodes, M.D. "Over the next two years, the recipients will use this unprecedented boost in research funds to help reach our ultimate goal of understanding age-related cognitive decline and reducing the individual and societal burden of this devastating disease."
More than 100 Alzheimer's or Alzheimer's-related research grants were awarded under the Recovery Act. The full list of NIH grants can be found at grants.nih/recovery/. The grants featured here highlight how these funds will expand research. Some of the funding will advance the work of existing NIA initiatives that benefit from large-scale collaborative, interdisciplinary research:
The Neuroimaging Initiative - Identifying brain changes before symptoms appear
The Alzheimer's Disease Neuroimaging Initiative (ADNI) will receive $24 million in stimulus funds - half from the NIA and half contributed by the NIH Office of the Director - to further groundbreaking research to establish neuroimaging and biomarker measures. These funds will enable researchers - and ultimately practicing physicians - to track changes in the living brain as older people transition from normal cognitive aging to amnestic mild cognitive impairment (MCI), in which individuals have a memory deficit but generally retain other cognitive abilities, and from MCI to Alzheimer's disease. ADNI, a research partnership supported primarily by the NIA with private sector support through the Foundation for NIH, seeks to find neuroimaging and other biological markers that can be used to detect Alzheimer's disease progression and measure the effectiveness of potential therapies.
The original ADNI involved the study of 800 people who ranged from normal to those with late-stage MCI or overt Alzheimer's disease. This new grant expands the scope of ongoing research under ADNI by allowing for the enrollment of participants at an earlier stage of MCI, when symptoms are milder. Furthermore, the funding for this new grant will allow ADNI investigators to extend the length of the original study to better assess changes in individuals over time. All of the participants will have neuroimaging scans and blood and cerebrospinal fluid analyses to look for changes in the brain.
The overall impact of the added funding will be increased knowledge of the sequence and timing of events leading to MCI and Alzheimer's disease and development of better clinical and imaging/fluid biomarker methods for early detection and for monitoring the progression of these conditions. This will facilitate clinical trials of treatments to slow disease progression and will ultimately contribute to the prevention of Alzheimer's disease. Just this year, ADNI made a significant step forward in developing a test to help diagnose the beginning stages of Alzheimer's disease sooner and more accurately by measuring levels of two biomarkers - tau and beta-amyloid proteins - in cerebrospinal fluid.
"Researchers and clinicians need imaging and biomarker tools to detect and understand the very earliest signs of pathology that cause changes in the brain some 10 to 20 years before any clinical symptoms of cognitive impairment or Alzheimer's may appear,"said ADNI Principal Investigator Michael Weiner, M.D., of the San Francisco Department of Veterans Affairs Medical Center and the University of California, San Francisco. "This grant will help us in our goal of establishing a panel of biomarkers that predict those at risk of developing the disease and also reveal which therapies may be effective in treating the disease or preventing its progression."
The grant was awarded to the Northern California Institute for Research and Education, a nonprofit research foundation affiliated with the San Francisco VA Medical Center. ADNI is the largest public-private partnership on brain research under way at the NIH. In addition to the NIA, the federal ADNI partners are the National Institute of Biomedical Imaging and Bioengineering, also part of NIH, and the U.S. Food and Drug Administration, another agency of the U.S. Department of Health and Human Services.
The AD Genetics Consortium and more " Identifying genes affecting risk for late-onset Alzheimer's
A grant of more than $5.4 million will add 3,800 Alzheimer's patients and an equal number of people free of the disease to a previously funded study by the Alzheimer' Disease Genetics Consortium (ADGC). Gerard Schellenberg, Ph.D., University of Pennsylvania School of Medicine, Philadelphia, leads the consortium, which aims to identify the additional risk factor genes for late-onset Alzheimer's disease. All of these study participants are currently enrolled in the NIA-funded national network of 29 Alzheimer's Disease Centers. When added to the samples from other sources, this will make available one of the largest collections of samples to perform genome-wide association studies (GWAS) in an effort to identify the susceptibility and protective genes influencing the onset and progression of late-onset disease. The large number of DNA samples brought together in this study may enable the researchers to detect genes whose individual effects in the disorder may be small but may still play a role.
The ADGC will use research infrastructures previously established by NIA to store and make available to qualified researchers DNA samples, datasets containing a wealth of information about participants, and genetic analysis data. The combined resources will allow scientists also to search for genes associated with a number of traits associated with Alzheimer's, as well as for genes related to cognitive decline.
"This funding will bring us closer to identifying the elusive genetic variations that contribute to overall risk and development of late-onset Alzheimer's disease," said Marcelle Morrison-Bogorad, Ph.D., director of the NIA Division of Neuroscience. "With this large sample size and the rapid DNA sample and data sharing, there are tremendous opportunities for defining new disease pathways that could lead to the development of new therapies."
Additionally, $4.7 million in Recovery Act funds will be used for another important study - a GWAS project examining cognitive decline in older African-Americans. Denis Evans, M.D., of Rush University Medical Center in Chicago, will collect and analyze the DNA of 4,140 elderly African-Americans enrolled in NIA-funded aging studies already taking place in Chicago and Indianapolis. Data from this analysis will also be shared with the ADGC to help identify risk factor genes for cognitive decline and late-onset Alzheimer's. The study will assess the associations of over 900,000 genetic markers with other co-morbidities, including stroke and high blood pressure.
Another $820,000 in Recovery Act funds will advance Alzheimer's genetics research by developing methods for identifying combinations of genes that might influence age-related risk of AD. The role of different forms of translocase of outer mitochondrial membrane (TOMM40), a gene that makes a protein thought to play a role in disease onset, will be studied by Allen Roses, M.D., of the Duke University School of Medicine in Durham, N.C.; Roses discovered the link between the apolipoprotein E (APOE)-epsilon 4 gene and increased risk for late-onset Alzheimer's disease. This new study will investigate whether particular variants of TOMM40 that tend to co-occur with the APOE3 gene also interact with that gene, and if this interaction plays a role in the age of disease onset.
Additional Recovery Act research opportunities
Other studies made possible by the Recovery Act range from clinical trials to epigenomic studies to translational research:
Drug, exercise clinical trials - A clinical trial exploring whether low doses of an anti-epileptic seizure drug, levetiracetam, can improve memory and affect brain function in people with MCI will be conducted with $1.2 million in support. Michela Gallagher, Ph.D., of Johns Hopkins University, Baltimore, will use functional MRI to visualize activity in the hippocampus - a brain area that becomes overactive in MCI patients - while the clinical trial participants receiving either the drug or a placebo engage in memory tasks. In another trial, researchers will examine how exercise training, cognitive training, or a combination of both, might impact immune and inflammatory biomarkers and cognitive health in older adults with MCI. The randomized trial, under a $1 million grant to David Lowenstein, Ph.D., of the University of Miami, will examine a broad array of outcomes and will include Hispanic and non-Hispanic volunteers.
Epigenetics/translational research - A $1 million grant will support a study exploring whether changes in histone acetylation (an epigenetic, or non-genetic factor that causes genes to behave differently) are one way in which a variety of life experiences may influence the risk of developing age-related cognitive decline and dementia. David Bennett, M.D., of Rush University Medical Center, Chicago, will use brain tissues from the NIA-funded Memory and Aging Project and the Religious Orders Study to examine this question. Another epigenomics grant of $819,000 will be used in translational research to test whether overexpressing histone deacetylase (HDAC1) with small molecule probes in the brain may demonstrate therapeutic potential for Alzheimer's and stroke patients. Li-Huei Tsai, Ph.D., of Massachusetts Institute of Technology, Boston, will lead the study, which seeks to find out whether abnormal regulation of the protein may play a role in neurological disorders.
The NIA leads the federal effort supporting and conducting research on aging and the medical, social and behavioral issues of older people. For more information on research and aging, go to 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. To sign up for e-mail alerts about new findings or publications, please visit either website.
Source
National Institutes of Health (NIH)
четверг, 5 мая 2011 г.
Mayo Clinic Women's HealthSource Special Report On Deciphering Dementia: Many Disorders Can Cause Loss Of Brain Function
Occasional misplaced keys or forgotten names don't mark the beginning of dementia. All dementia isn't Alzheimer's disease. Some dementia symptoms can be reversed. Those facts and many more are covered in Deciphering Dementia, a supplemental Special Report to the July issue of Mayo Clinic Women's HealthSource.
The report provides in-depth coverage of the causes, risk factors, diagnoses and treatment options for dementia. Some highlights from the report include:
Types and causes of dementia: While Alzheimer's is the most common cause of dementia in people 65 and older, there are many other causes. For example, vascular dementia results from stroke. Lewy body dementia occurs when abnormal round structures called Lewy bodies develop in regions of the brain involved with thinking, movement and sleep. Visual hallucinations can be the first sign of this type of dementia.
Infections such as meningitis and encephalitis can cause dementia symptoms, and so can leukemia and multiple sclerosis. Depression can cause people to appear slow, confused or forgetful. In these situations, symptoms of dementia may improve with treatment for the underlying disease.
Ways to protect the brain: Lowering cholesterol or blood pressure levels can help thwart the buildup of plaques in arteries and can help prevent stroke, one of the major causes of vascular dementia. Some research has indicated that statin drugs, which help lower cholesterol, may help lower dementia risk.
Other protective strategies include keeping the mind active, being physically and socially active and eating a diet rich in fruits, vegetables and omega-3 fatty acids found in certain fish and nuts.
What's normal memory loss and what isn't: Occasional lapses in memory are different from the type of memory loss associated with dementia. Needing directions when driving to a place visited only occasionally is normal. Losing one's way driving home from a familiar location, such as the grocery store, is not.
When dementia-like symptoms start to become a concern, it's time to see a physician. Memory loss and other dementia symptoms have many causes, so diagnosis can be a challenge. Nevertheless, early and accurate diagnosis allows for treatment that might help reverse, lessen or delay the progression of symptoms.
Source:
Mayo Clinic
The report provides in-depth coverage of the causes, risk factors, diagnoses and treatment options for dementia. Some highlights from the report include:
Types and causes of dementia: While Alzheimer's is the most common cause of dementia in people 65 and older, there are many other causes. For example, vascular dementia results from stroke. Lewy body dementia occurs when abnormal round structures called Lewy bodies develop in regions of the brain involved with thinking, movement and sleep. Visual hallucinations can be the first sign of this type of dementia.
Infections such as meningitis and encephalitis can cause dementia symptoms, and so can leukemia and multiple sclerosis. Depression can cause people to appear slow, confused or forgetful. In these situations, symptoms of dementia may improve with treatment for the underlying disease.
Ways to protect the brain: Lowering cholesterol or blood pressure levels can help thwart the buildup of plaques in arteries and can help prevent stroke, one of the major causes of vascular dementia. Some research has indicated that statin drugs, which help lower cholesterol, may help lower dementia risk.
Other protective strategies include keeping the mind active, being physically and socially active and eating a diet rich in fruits, vegetables and omega-3 fatty acids found in certain fish and nuts.
What's normal memory loss and what isn't: Occasional lapses in memory are different from the type of memory loss associated with dementia. Needing directions when driving to a place visited only occasionally is normal. Losing one's way driving home from a familiar location, such as the grocery store, is not.
When dementia-like symptoms start to become a concern, it's time to see a physician. Memory loss and other dementia symptoms have many causes, so diagnosis can be a challenge. Nevertheless, early and accurate diagnosis allows for treatment that might help reverse, lessen or delay the progression of symptoms.
Source:
Mayo Clinic
среда, 4 мая 2011 г.
Statins Do Not Help Prevent Alzheimer's Disease, Review Finds
An increasing number of studies show that elevated serum cholesterol levels might be part of the cause of Alzheimer disease, but a new review of studies says that, even so, the most successful class of cholesterol-lowering medicines will not stave off the condition.
Statins includes medications such as atorvastatin (Lipitor) and pravastatin (Pravachol), which are some of the best-selling drugs in the world.
The drugs lower cholesterol by inhibiting a key enzyme used by the body to make it, which decreases cholesterol formation and helps reduce the amount of low-density lipoprotein (LDL or "bad" cholesterol).
Biomedical and epidemiological studies showing the relationship between elevated cholesterol and Alzheimer disease have caused scientists to wonder if these medications could lower the risk of developing the disease, which is the most common cause of dementia. For example, in studies using animals, the expression of Alzheimer symptoms slowed with lowered cholesterol, giving hope that the same might be true for humans.
The new review appears in the latest issue of The Cochrane Library, a publication of The Cochrane Collaboration, an international organization that evaluates medical research. Systematic reviews like this one draw evidence-based conclusions about medical practice after considering both the content and quality of existing medical trials on a topic.
"From these trials, which contained very large numbers and were the gold standard ??¦ it appears that statins given in late life to individuals at risk of vascular disease do not prevent against dementia," said lead study author Bernadette McGuinness, a senior clinical research fellow in geriatric medicine at Queen's University in Belfast, Ireland. "I feel the follow-up time was sufficient to allow for an effect to appear," she added.
The review, an update to an earlier review completed in 2001, comprised 26,340 participants in two major studies. One study, the Medical Research Council/British Heart Foundation Heart Protection Study (HPS), looked at simvastatin (Zocor) use in 20,536 patients and followed them for five years. The other study, the PROSPER trial, looked at pravastatin use in 5,804 patients, with an average follow-up of 3.2 years.
Both studies were double-blind randomized, placebo-controlled studies of statin medications in individuals at risk for dementia and Alzheimer disease. Taken together, the studies comprised adults between the ages of 40 and 82.
While the review showed no evidence that statin medications were harmful to cognition, the review authors found no difference between patients receiving the medications and patients receiving placebo medications when it came to incidence of dementia, cognitive function or performance on specific neuropsychological tests, such as a picture word learning test.
"Statins have a range of mechanisms that could help or hurt cognition," said Beatrice Golomb, M.D., of the department of family and preventive medicine at the University of California, San Diego. "Regarding statins as preventive medicines, there are a number of individual cases in case reports and case series where cognition is clearly and reproducibly adversely affected by statins."
Golomb also said that some randomized trials have shown that the net effect of statin medications was significantly adverse and others that have shown it was neutral, but that none has shown statin use to be favorable for cognition.
McGuinness said that while the two large trials showed that statins given later in life do not protect against dementia, "it is unclear, however, if statins given in middle age for many years can protect against dementia in later life, as the studies did not address this."
She noted that neither study aimed to assess the prevention of dementia primarily; in fact, dementia was at most a secondary outcome in the studies. As a result, "some people with dementia may not have been picked up by the screening, especially in HPS, but it is difficult to know."
Patients taking statins might not take them reliably if they've developed cognitive problems or side effects, Golomb said. "That is, the very patients who develop cognitive problems or adverse effects as a result of statins will be less compliant on statins, the literature says, and then may be selectively excluded from the study." As a result, the study could portray unrepresentatively favorable results where cognitive function is concerned, she said. "However, the conclusion, an important one, remains largely correct."
The Cochrane Collaboration is an international nonprofit, independent organization that produces and disseminates systematic reviews of health care interventions and promotes the search for evidence in the form of clinical trials and other studies of interventions.
McGuinness B, et al. Statins for the prevention of dementia. Cochrane Database of Systematic Reviews 2009, Issue 2.
Source: Health Behavior News Service
View drug information on Pravachol; Zocor.
Statins includes medications such as atorvastatin (Lipitor) and pravastatin (Pravachol), which are some of the best-selling drugs in the world.
The drugs lower cholesterol by inhibiting a key enzyme used by the body to make it, which decreases cholesterol formation and helps reduce the amount of low-density lipoprotein (LDL or "bad" cholesterol).
Biomedical and epidemiological studies showing the relationship between elevated cholesterol and Alzheimer disease have caused scientists to wonder if these medications could lower the risk of developing the disease, which is the most common cause of dementia. For example, in studies using animals, the expression of Alzheimer symptoms slowed with lowered cholesterol, giving hope that the same might be true for humans.
The new review appears in the latest issue of The Cochrane Library, a publication of The Cochrane Collaboration, an international organization that evaluates medical research. Systematic reviews like this one draw evidence-based conclusions about medical practice after considering both the content and quality of existing medical trials on a topic.
"From these trials, which contained very large numbers and were the gold standard ??¦ it appears that statins given in late life to individuals at risk of vascular disease do not prevent against dementia," said lead study author Bernadette McGuinness, a senior clinical research fellow in geriatric medicine at Queen's University in Belfast, Ireland. "I feel the follow-up time was sufficient to allow for an effect to appear," she added.
The review, an update to an earlier review completed in 2001, comprised 26,340 participants in two major studies. One study, the Medical Research Council/British Heart Foundation Heart Protection Study (HPS), looked at simvastatin (Zocor) use in 20,536 patients and followed them for five years. The other study, the PROSPER trial, looked at pravastatin use in 5,804 patients, with an average follow-up of 3.2 years.
Both studies were double-blind randomized, placebo-controlled studies of statin medications in individuals at risk for dementia and Alzheimer disease. Taken together, the studies comprised adults between the ages of 40 and 82.
While the review showed no evidence that statin medications were harmful to cognition, the review authors found no difference between patients receiving the medications and patients receiving placebo medications when it came to incidence of dementia, cognitive function or performance on specific neuropsychological tests, such as a picture word learning test.
"Statins have a range of mechanisms that could help or hurt cognition," said Beatrice Golomb, M.D., of the department of family and preventive medicine at the University of California, San Diego. "Regarding statins as preventive medicines, there are a number of individual cases in case reports and case series where cognition is clearly and reproducibly adversely affected by statins."
Golomb also said that some randomized trials have shown that the net effect of statin medications was significantly adverse and others that have shown it was neutral, but that none has shown statin use to be favorable for cognition.
McGuinness said that while the two large trials showed that statins given later in life do not protect against dementia, "it is unclear, however, if statins given in middle age for many years can protect against dementia in later life, as the studies did not address this."
She noted that neither study aimed to assess the prevention of dementia primarily; in fact, dementia was at most a secondary outcome in the studies. As a result, "some people with dementia may not have been picked up by the screening, especially in HPS, but it is difficult to know."
Patients taking statins might not take them reliably if they've developed cognitive problems or side effects, Golomb said. "That is, the very patients who develop cognitive problems or adverse effects as a result of statins will be less compliant on statins, the literature says, and then may be selectively excluded from the study." As a result, the study could portray unrepresentatively favorable results where cognitive function is concerned, she said. "However, the conclusion, an important one, remains largely correct."
The Cochrane Collaboration is an international nonprofit, independent organization that produces and disseminates systematic reviews of health care interventions and promotes the search for evidence in the form of clinical trials and other studies of interventions.
McGuinness B, et al. Statins for the prevention of dementia. Cochrane Database of Systematic Reviews 2009, Issue 2.
Source: Health Behavior News Service
View drug information on Pravachol; Zocor.
вторник, 3 мая 2011 г.
Dementia Screening In Primary Care: Is It Time? USA
Primary care physicians should focus on "dementia red flags" rather than routinely screen individuals with no dementia symptoms just because they've reached a certain age, according to Malaz Boustani, M.D., MPH, of the Indiana University School of Medicine and the Regenstrief Institute, Inc. and colleagues from the University of Kent and the University of Cambridge in the United Kingdom in a commentary published in the Nov. 28 issue of the Journal of the American Medical Association.
"To screen without symptoms, unless there is a suspicion of a problem, either by the individual, caregivers, or a physician, may led to negative consequences for the person and for society" says Dr. Boustani, who is a geriatrician.
"There currently is no accurate screening test and we would be faced with an unacceptable number of false positives and false negatives. If we focus on dementia red flags we will be identifying individuals who will have a very high probability of having dementia and be able to focus our resources, including diagnostic testing, on these people," Dr. Boustani says.
Dementia red flags include medication adherence problems, more than 7 prescribed medications, agitation, multiple falls, and more than 2 hospitalizations or emergency department visits in the past year. Dr. Boustani, who says the healthcare system in the United States misses between 60% and 80% of individuals with dementia, is currently testing ways to help physicians identify dementia red flags in their patients so these missed individuals can be helped.
Someone in the United States develops Alzheimer disease every 72 seconds, according to the Alzheimer's Association. The average primary care physician sees 2,000 patients per year of whom 300 are aged 65 or older. Of these 24 will develop dementia.
Despite this burden of disease, the benefit-harm ratio of conducting general population-based screening has not yet reached the point where the benefit outweighs the harm, the commentary maintains. Harms include possible stigma, loss of long term care insurance, emotional dislocation for both the individual and family, and resources' shifting from other health problems.
Dr. Boustani is the author of a 2003 report evaluating the wisdom of routine screening for dementia in primary care settings prepared for the U.S Preventative Services Task Force. The report found that while two-thirds of dementia cases are undetected by the patient's primary care physician, insufficient data exists to indicate whether or not it is a good idea to administer dementia screening tests to patients who do not have symptoms of memory loss or confusion.
"Pressures to institute screening of unproven benefit could divert much needed resources from the health and social care systems and have an overall negative impact on care for patients with dementia and other illnesses, ultimately delaying the point when dementia screening becomes indicated. The goal should continue to be the best possible care for the most patients, which currently does not include screening for dementia," the commentary concludes.
Indiana University School of Medicine
"To screen without symptoms, unless there is a suspicion of a problem, either by the individual, caregivers, or a physician, may led to negative consequences for the person and for society" says Dr. Boustani, who is a geriatrician.
"There currently is no accurate screening test and we would be faced with an unacceptable number of false positives and false negatives. If we focus on dementia red flags we will be identifying individuals who will have a very high probability of having dementia and be able to focus our resources, including diagnostic testing, on these people," Dr. Boustani says.
Dementia red flags include medication adherence problems, more than 7 prescribed medications, agitation, multiple falls, and more than 2 hospitalizations or emergency department visits in the past year. Dr. Boustani, who says the healthcare system in the United States misses between 60% and 80% of individuals with dementia, is currently testing ways to help physicians identify dementia red flags in their patients so these missed individuals can be helped.
Someone in the United States develops Alzheimer disease every 72 seconds, according to the Alzheimer's Association. The average primary care physician sees 2,000 patients per year of whom 300 are aged 65 or older. Of these 24 will develop dementia.
Despite this burden of disease, the benefit-harm ratio of conducting general population-based screening has not yet reached the point where the benefit outweighs the harm, the commentary maintains. Harms include possible stigma, loss of long term care insurance, emotional dislocation for both the individual and family, and resources' shifting from other health problems.
Dr. Boustani is the author of a 2003 report evaluating the wisdom of routine screening for dementia in primary care settings prepared for the U.S Preventative Services Task Force. The report found that while two-thirds of dementia cases are undetected by the patient's primary care physician, insufficient data exists to indicate whether or not it is a good idea to administer dementia screening tests to patients who do not have symptoms of memory loss or confusion.
"Pressures to institute screening of unproven benefit could divert much needed resources from the health and social care systems and have an overall negative impact on care for patients with dementia and other illnesses, ultimately delaying the point when dementia screening becomes indicated. The goal should continue to be the best possible care for the most patients, which currently does not include screening for dementia," the commentary concludes.
Indiana University School of Medicine
воскресенье, 1 мая 2011 г.
Potential Blood Test For Alzheimer's
Researchers have revealed a direct relationship between two specific antibodies and the severity of Alzheimer's disease symptoms, raising hopes that a diagnostic blood test for the devastating disorder is within reach.
Researchers from the University of Georgia, the Charlie Norwood VA Medical Center in Augusta and the Medical College of Georgia compared antibody levels in blood samples from 118 older adults with the participant's level of dementia. The team, whose results appear in the current edition of Journal of Gerontology: Medical Sciences, found that the concentration of two specific proteins that are involved in the immune response increases as the severity of dementia increases.
"We found a strong and consistent relationship between two particular antibodies and the level of impairment," said study co-author L. Stephen Miller, professor and director of clinical psychology training in the UGA Franklin College of Arts and Sciences. "The finding brings us closer to our ultimate goal of developing a blood test that can diagnose Alzheimer's disease or potentially identify if someone is at higher risk for the disease."
Miller's co-authors include Jennifer S. Wilson, a former undergraduate student in the UGA Honors program who is now pursing graduate studies at Emory University; Shyamala Mruthinti, research pharmacologist at the VA Medical Center and adjunct professor at MCG; and Jerry Buccafusco, director of the MCG Alzheimer's Research Center. The team focused on antibodies that the body creates in response to two proteins that are associated with Alzheimer's disease. One protein, known as amyloid-beta, forms the plaques that are evident in the brains of people with Alzheimer's upon autopsy. The other protein, known as RAGE, is involved in the normal aging process but is expressed at higher levels in the brains of people with Alzheimer's.
In a previous study that compared a group of people with Alzheimer's disease to a healthy control group, Mruthinti and her colleagues found that anti-amyloid beta and anti-RAGE antibodies are significantly higher in the group with Alzheimer's. The team's latest study expands on that finding to reveal a direct relationship between severity of Alzheimer's disease and levels of the two antibodies in the blood.
"Alzheimer's is an inflammatory disease of the brain, and these two antibodies give us a way to measure that inflammation," Mruthinti said. "Using them as an early diagnostic marker may allow us to start drug treatment early, when it's most effective, to increase the patient's quality of life."
While optimistic about their findings, the researchers caution that it could still be years before a diagnostic test based on their work is clinically available. The study found that the relationship between the two antibodies and Alzheimer's severity persists even after controlling for patient age and total antibody levels. To further test the strength of the relationship, the researchers are now working with a sample that controls for other factors that have the potential to influence levels of the two antibodies, such as diabetes and heart disease. Buccafusco and his colleagues are also working to decrease the cost and time involved in the test.
"We're in the process of trying to reduce the test to a one-day procedure, whereas right now it takes three to four days," Buccafusco said. "But even now, our test is orders of magnitude cheaper than having people come in every few months to get a functional MRI or PET scan to try to discern brain plaques."
The team is targeting the two proteins themselves as a possible treatment for Alzheimer's disease. Mruthinti explains that, individually, amyloid-beta and RAGE proteins don't provoke an immune response. The trouble begins when the two bind and the immune system attacks, resulting in constant state of inflammation that damages the brain. The researchers recently developed a way to measure levels of amyloid beta-RAGE complex, and preliminary data using transgenic mice that express Alzheimer's symptoms suggest that an antigen they created to boost the body's natural immune response to the complex can reduce the formation of the brain plaques.
"The amyloid beta-RAGE complex cuts off the connections between neurons," Mruthinti explained, "but our hope is that we can protect those connections by preventing those plaques from forming."
Notes:
The research was funded by a Merit Review Award from the Veterans Administration to principal investigator Mruthinti and by the Medical College of Georgia Alzheimer's Research Center.
Source: Sam Fahmy
University of Georgia
Researchers from the University of Georgia, the Charlie Norwood VA Medical Center in Augusta and the Medical College of Georgia compared antibody levels in blood samples from 118 older adults with the participant's level of dementia. The team, whose results appear in the current edition of Journal of Gerontology: Medical Sciences, found that the concentration of two specific proteins that are involved in the immune response increases as the severity of dementia increases.
"We found a strong and consistent relationship between two particular antibodies and the level of impairment," said study co-author L. Stephen Miller, professor and director of clinical psychology training in the UGA Franklin College of Arts and Sciences. "The finding brings us closer to our ultimate goal of developing a blood test that can diagnose Alzheimer's disease or potentially identify if someone is at higher risk for the disease."
Miller's co-authors include Jennifer S. Wilson, a former undergraduate student in the UGA Honors program who is now pursing graduate studies at Emory University; Shyamala Mruthinti, research pharmacologist at the VA Medical Center and adjunct professor at MCG; and Jerry Buccafusco, director of the MCG Alzheimer's Research Center. The team focused on antibodies that the body creates in response to two proteins that are associated with Alzheimer's disease. One protein, known as amyloid-beta, forms the plaques that are evident in the brains of people with Alzheimer's upon autopsy. The other protein, known as RAGE, is involved in the normal aging process but is expressed at higher levels in the brains of people with Alzheimer's.
In a previous study that compared a group of people with Alzheimer's disease to a healthy control group, Mruthinti and her colleagues found that anti-amyloid beta and anti-RAGE antibodies are significantly higher in the group with Alzheimer's. The team's latest study expands on that finding to reveal a direct relationship between severity of Alzheimer's disease and levels of the two antibodies in the blood.
"Alzheimer's is an inflammatory disease of the brain, and these two antibodies give us a way to measure that inflammation," Mruthinti said. "Using them as an early diagnostic marker may allow us to start drug treatment early, when it's most effective, to increase the patient's quality of life."
While optimistic about their findings, the researchers caution that it could still be years before a diagnostic test based on their work is clinically available. The study found that the relationship between the two antibodies and Alzheimer's severity persists even after controlling for patient age and total antibody levels. To further test the strength of the relationship, the researchers are now working with a sample that controls for other factors that have the potential to influence levels of the two antibodies, such as diabetes and heart disease. Buccafusco and his colleagues are also working to decrease the cost and time involved in the test.
"We're in the process of trying to reduce the test to a one-day procedure, whereas right now it takes three to four days," Buccafusco said. "But even now, our test is orders of magnitude cheaper than having people come in every few months to get a functional MRI or PET scan to try to discern brain plaques."
The team is targeting the two proteins themselves as a possible treatment for Alzheimer's disease. Mruthinti explains that, individually, amyloid-beta and RAGE proteins don't provoke an immune response. The trouble begins when the two bind and the immune system attacks, resulting in constant state of inflammation that damages the brain. The researchers recently developed a way to measure levels of amyloid beta-RAGE complex, and preliminary data using transgenic mice that express Alzheimer's symptoms suggest that an antigen they created to boost the body's natural immune response to the complex can reduce the formation of the brain plaques.
"The amyloid beta-RAGE complex cuts off the connections between neurons," Mruthinti explained, "but our hope is that we can protect those connections by preventing those plaques from forming."
Notes:
The research was funded by a Merit Review Award from the Veterans Administration to principal investigator Mruthinti and by the Medical College of Georgia Alzheimer's Research Center.
Source: Sam Fahmy
University of Georgia
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