Why walnuts fight Alzheimer's

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1. IOS Press BV

Walnuts fight Alzheimer's in a big way in the lab. Learn how walnuts appear to have a beneficial effect in reducing risk, delaying onset, slowing progression and preventing Alzheimer's. 

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FOLSOM, Calif. -- An important animal study published in the Journal of Alzheimer's Disease indicates that a diet including walnuts may have a beneficial effect in reducing the risk, delaying the onset, slowing the progression of, or preventing Alzheimer's disease. 

Research led by Abha Chauhan, PhD, head of the Developmental Neuroscience Laboratory at the New York State Institute for Basic Research in Developmental Disabilities (IBR), found significant improvement in learning skills, memory, reducing anxiety, and motor development in mice fed a walnut-enriched diet.

The researchers suggest that the high antioxidant content of walnuts (3.7 mmol/ounce)1 may have been a contributing factor in protecting the mouse brain from the degeneration typically seen in Alzheimer's disease. Oxidative stress and inflammation are prominent features in this disease, which affects more than five million Americans2.

"These findings are very promising and help lay the groundwork for future human studies on walnuts and Alzheimer's disease – a disease for which there is no known cure," said lead researcher Dr. Abha Chauhan, PhD. "Our study adds to the growing body of research that demonstrates the protective effects of walnuts on cognitive functioning."

The research group examined the effects of dietary supplementation on mice with 6 percent or 9 percent walnuts, which are equivalent to 1 ounce and 1.5 ounces per day, respectively, of walnuts in humans. This research stemmed from a previous cell culture study3 led by Dr. Chauhan that highlighted the protective effects of walnut extract against the oxidative damage caused by amyloid beta protein. This protein is the major component of amyloid plaques that form in the brains of those with Alzheimer's disease.

Someone in the United States develops Alzheimer's disease every 67 seconds, and the number of Americans with Alzheimer's disease and other dementias are expected to rapidly escalate in coming years as the baby boom generation ages. By 2050, the number of people age 65 and older with Alzheimer's disease may nearly triple, from five million to as many as 16 million, emphasizing the importance of determining ways to prevent, slow or stop the disease. Estimated total payments in 2014 for all individuals with Alzheimer's disease and other dementias are $214 billion2.

Walnuts have other nutritional benefits as they contain numerous vitamins and minerals and are the only nut that contains a significant source of alpha-linolenic acid (ALA) (2.5 grams per ounce), an omega-3 fatty acid with heart and brain-health benefits4,5. The researchers also suggest that ALA may have played a role in improving the behavioral symptoms seen in the study. 

MORE INFORMATION:

Reference:

1. Abha Chauhan, PhD et al. Dietary Supplementation of Walnuts Improves Memory Deficits and Learning Skills in Transgenic Mouse Model of Alzheimer's Disease. Journal of Alzheimer's Disease, Volume 42, Number 4 / 2014 DOI: 10.3233/JAD-140675

Footnotes:

1. Halvorsen BL, Carlsen MH, Phillips KM, Bohn SK, Holte K, Jacobs DR, Blomhoff R (2006) Content of redox-active compounds (ie, antioxidants) in foods consumed in the United States. Am J Clin Nutr 84, 95-135
2. 2014 Alzheimer's Disease Facts and Figures. Alzheimers Dement. 2014;2:16-17. Available from: http://www.alz.org/downloads/Facts_Figures_2014.pdf
3. Muthaiyah B, Essa MM, Chauhan V, Chauhan A (2011) Protective effects of walnut extract against amyloid beta peptide-induced cell death and oxidative stress in PC12 cells. Neurochem Res 36, 2096-2103.
4. Pan A, Chen M, Chowdhury R, HY Wu J, Sun Q, Campos H, Mozaffarian D, Hu FB (2012) Alpha linolenic acid and risk of cardiovascular disease: a systemic review and meta-analysis. Am J Clin Nutr. 96:6:1262-1273.
5. Innis SM (2007) Dietary (n-3) fatty acids and brain development. J Nutr 137, 855-859.

SOURCE:

1. IOS Press BV

Is high blood sugar a dementia risk

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Group Health Research Institute.

17 out of 17 levels of people's sugar showed a direct connection between sugar & dementia. See the results and read researcher's conclusions. 

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A joint Group Health-University of Washington (UW) study in the New England Journal of Medicine has found that higher blood sugar levels are associated with higher dementia risk, even among people who do not have diabetes. (Continued below video.)

Continued below video...

Blood sugar levels averaged over a five-year period were associated with rising risks for developing dementia, in this report about more than 2,000 Group Health patients age 65 and older in the Adult Changes in Thought (ACT) study.

For example, in people without diabetes, risk for dementia was 18 percent higher for people with an average glucose level of 115 milligrams per deciliter compared to those with an average glucose level of 100 mg/dl. And in people with diabetes, whose blood sugar levels are generally higher, dementia risk was 40 percent higher for people with an average glucose level of 190 mg/dl compared to those with an average glucose level of 160 mg/dl.

"The most interesting finding was that every incrementally higher glucose level was associated with a higher risk of dementia in people who did not have diabetes," said first author Paul K. Crane, MD, MPH, an associate professor of medicine at the UW School of Medicine, adjunct associate professor of health services at the UW School of Public Health, and affiliate investigator at Group Health Research Institute. "There was no threshold value for lower glucose values where risk leveled off."

"One major strength of this research is that it is based on the ACT study, a longitudinal cohort study, where we follow people for many years as they lead their lives," said senior author Eric B. Larson, MD, MPH, a senior investigator at Group Health Research Institute who also has appointments at the UW Schools of Medicine and Public Health. "We combine information from people's research visits every other year with data from their visits to Group Health providers whenever they receive care. And this gave us an average of 17 blood sugar measurements per person: very rich data."

These measurements included blood glucose (some fasting, some not) and glycated hemoglobin (also known as HbA1c). Blood sugar levels rise and fall in peaks and valleys throughout each day, but glycated hemoglobin doesn't vary as much over short intervals.

Combining glucose and glycated hemoglobin measures into a composite measure required special statistical techniques, which Drs. Crane and Larson's co-authors Rod Walker, MS, a biostatistician, and Rebecca Hubbard, PhD, an associate investigator, both from Group Health Research Institute, had developed. (Dr. Hubbard is also an affiliate assistant professor of biostatistics at the UW School of Public Health.) These sophisticated statistical models required specialized data on the relationships between glycated hemoglobin and glucose levels, and they used data generated by co-author David M. Nathan, MD, a professor of medicine at Harvard Medical School and director of the Diabetes Center at Massachusetts General Hospital.

Journal Reference:So should people try to eat less sugar -- or foods with a lower "glycemic index"? Not necessarily, Dr. Crane said: "Your body turns your food into glucose, so your blood sugar levels depend not only on what you eat but also on your individual metabolism: how your body handles your food." But he does suggest that taking walks couldn't hurt: The ACT study has previously linked physical activity to later onset and reduced risk of dementia, including Alzheimer's disease.

Furthermore, Dr. Crane emphasized that these results come from an observational study: "What we found was that people with higher levels of glucose had a higher risk of dementia, on average, than did people with lower levels of glucose," he said. "While that is interesting and important, we have no data to suggest that people who make changes to lower their glucose improve their dementia risk. Those data would have to come from future studies with different study designs."

1. Paul K. Crane, Rod Walker, Rebecca A. Hubbard, Ge Li, David M. Nathan, Hui Zheng, Sebastien Haneuse, Suzanne Craft, Thomas J. Montine, Steven E. Kahn, Wayne McCormick, Susan M. McCurry, James D. Bowen, Eric B. Larson. Glucose Levels and Risk of Dementia. New England Journal of Medicine, 2013; 369 (6): 540 DOI: 10.1056/NEJMoa1215740

Rogue researcher offers new hope for sufferers of Alzheimer's disease

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

EmaxHealth

By Robin Wulffson MD  for eMaxHealth

• Alzheimer's Disease
 
• Aging
 
• Current News

Approximately 36 million people worldwide suffer from Alzheimer's disease or dementia. Although many researchers are of the opinion that the buildup of amyloid plaques in the brain is the underlying cause of Alzheimer’s disease, Claude Wischik, MD, PhD has long backed a minority view regarding its cause. He feels that the condition is due to a protein in the brain called tau. The company he co-founded 10 years ago, TauRx Pharmaceuticals Ltd., has developed an experimental Alzheimer’s medication that it will begin testing in the coming weeks in two large clinical trials.

Dr. Wischik has been studying Alzheimer’s disease for decade. When he was a young PhD student at Cambridge University in the 1980s, he began collecting brains. It was a daunting task because few organ banks kept entire brains. In his search for an Alzheimer’s cure, he needed to examine brain tissue from Alzheimer’s patients soon after death. That required obtaining family approvals and enlisting mortuary technicians to extract the brains. In a little over a decade, Dr. Wischik collected more than 300 brains. While collecting his specimens, he embraced a concept that, if he is right, could fundamentally transform Alzheimer’s research and raise new hopes for individuals suffering from Alzheimer’s disease or dementia.

Alzheimer's experts provide strategic roadmap to tackle the disease

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The Dementia Caregiver's Little Book of Hope [Kindle Edition

Medical Xpress

This week, a strategic roadmap to help to the nation's health care system cope with the impending public health crisis caused Alzheimer's disease and related dementia will be published in Alzheimer's & Dementia: The Journal of the Alzheimer's Association. The plan aims to link the latest scientific findings with clinical care and bring together patients, families, scientists, pharmaceutical companies, regulatory agencies, and advocacy organizations behind a common set of prioritized goals. The consensus document is the outcome of a June meeting of leading Alzheimer's researchers, advocates and clinicians, who gathered as part of the Marian S. Ware Alzheimer Program at the University of Pennsylvania.

Today, 5.4 million people are living with the disease, and more than 15 million Americans are caring for persons with Alzheimer's and other dementias, according to the Alzheimer's Association. Alzheimer's disease is the sixth-leading cause of death in the United States and the only cause of death among the top 10 in the United States that cannot be prevented, cured, or even slowed. "Our plan aims to provide good quality care for affected patients and families, advance our understanding of the pathophysiology and natural history of AD and other dementias, develop effective treatments to slow or prevent these diseases, and translate scientific advances successfully into policy and practice," the authors wrote. The experts developed a prioritized and integrated set of recommendations after meeting in June at Penn. Four workgroups, focusing on Biomarkers, Clinical Care and Health Services Research, Drug Development and Health Economics, Policy and Ethics, had met separately leading up to the June conference. The document details recommendations from each group, and prioritizes the key recommendations from the paper, including: Speed the translation of research discoveries into clinical practice by revising the regulatory process and incentivize the pharmaceutical industry to develop AD drugs. Establish a diverse registry of older adults with and without dementia. Develop a risk stratification model that incorporates demographic, genetic, biologic, cognitive and environmental markers. Increase support to advance valuable care for patients affected with AD and their caregivers. Consider legislation requiring that, until the clinical value of biomarkers is fully understood, information gained through biomarker studies cannot be considered in insurance or employment decisions. "This plan addresses the needs of a truly responsive health-care system: to integrate healthcare and social services as well as research and educational programs that support people with Alzheimer's, family members, and other caregivers along an individualized and changing illness trajectory ," said lead author Mary Naylor, PhD, RN. Dr. Naylor is the Marian S. Ware Professor in Gerontology; Director of NewCourtland Center for Transitions and Health at the University of Pennsylvania School of Nursing.

An accompanying editorial in the journal notes that the Ware Invitational Summit document may serve as an important tool for the upcoming U.S. National Plan to Address Alzheimer's Disease, as it provides concrete, achievable policy ideas, being mindful of budget constraints and cost-effectiveness. "Alzheimer's is an enormous and complex disease, and we believe that creative thinking, repurposing of existing funds, vigilance in reducing waste, and a constant focus on cost effectiveness will help make these recommendations a much-needed reality," said John Trojanowski, MD, PhD, senior author, director of the National Institute of Aging-funded Penn Alzheimer's Disease Core Center and is professor of Pathology and Laboratory Medicine in the Perelman School of Medicine at the University of Pennsylvania. "The diverse perspectives collected in this report provide constructive, ethical, cost-effective guidance for policymakers," said second author Jason Karlawish, MD, associate director of the Penn Memory Center and professor of Medicine and Medical Ethics and Health Policy in the Perelman School of Medicine. "The recommendations serve as a clear roadmap to bring caregivers, researchers, clinicians, and advocacy groups together and provide them much-needed support now and in the future." The Ware Invitational Summit brought together experts from academia; industry; government agencies and advocacy and nonprofit groups – including the meeting's co-convener, The Campaign to Prevent Alzheimer's Disease by 2020. The conference and editorial assistance were supported by the Marian S. Ware 2006 CWG Charitable Lead Annuity Trust and held at the University of Pennsylvania on June 20-21, 2012. If pieces of the plan are implemented globally - by government, private organizations and medical institutions alike - the authors' aspirations are that treatments can be developed within the next decade to improve or prevent AD; earlier diagnosis will give better options to patients ; and high-quality, effective care will be available to people with dementia throughout the course of their disease. Provided by University of Pennsylvania School of Medicine 

Autoantibodies in Alzheimer’s disease

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The Dementia Caregiver's Little Book of Hope [Kindle Edition]

ScienceDaily— New research by scientists at the University of Medicine and Dentistry of New Jersey-School of Osteopathic Medicine (UMDNJ-SOM) demonstrates how dying or damaged brain cells release debris into the bloodstream and give rise to specific autoantibodies that appear to be reliable biomarkers for early diagnosis of Alzheimer's and other neurodegenerative diseases. The researchers also identify a key mechanism in the development of Alzheimer's that mirrors a process that is common in such autoimmune disorders as rheumatoid arthritis

The study appears online in the Journal of Autoimmunity.

"Our earlier research showed that human blood contains perhaps thousands of autoantibodies for clearing cellular debris, and that some of these autoantibodies can potentially be used to accurately diagnose neurodegenerative diseases like Alzheimer's and Parkinson's," said Robert Nagele, PhD, a professor of medicine at the New Jersey Institute for Successful Aging at UMDNJ-SOM and the study's corresponding author. "Here, we found that the release of damaged proteins from dying neurons triggers the production of specific brain-reactive autoantibodies that are directed against this protein debris, a response similar to that seen in some autoimmune disorders."

The researchers focused on the role of enzymes, called PADs, in citrullination, a process that converts one type of amino acid into another (amino acids are the building blocks of proteins). After examining postmortem human brain tissue from individuals with Alzheimer's disease and healthy controls, the researchers found that neurons located in the area of the brain first affected by Alzheimer's disease accumulate both citrullinated proteins and a PAD enzyme. In addition, they demonstrated that a specific type of protein, PTCD2, which has been shown to be a potent biomarker for Alzheimer's, was present in citrullinated form in the neuron cells of the Alzheimer's disease brain samples.



Their results suggest that when neuron cells die, they release their contents into the fluid that surrounds the brain. The cellular remains then enter the bloodstream and their presence generates the production of specific autoantibodies that target this neuronal debris. This same protein citrullination process has been linked to the development of autoantibodies in rheumatoid arthritis, one of the most common forms of autoimmune disease.

"Our previous studies provided evidence that some of these autoantibodies may be able to return to the brain through breaches in the blood-brain barrier," said lead author Nimish Acharya of the UMDNJ-Graduate School of Biomedical Sciences and the New Jersey Institute for Successful Aging. "Once there, they selectively bind to the surfaces of neurons, disrupting the function of the brain cells and accelerating the accumulation of beta amyloid deposits. This chronic cycle of protein-debris-generating autoantibodies that can then seep through the blood-brain barrier helps explain the long-term, progressive degeneration that results from Alzheimer's disease."

Agent Lights Up Alzheimer's Tangles

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By MedPage Today Staff2

Lighting Up the Tangles

Several contrast agents are in development for imaging beta-amyloid plaques in patients with incipient Alzheimer's disease, but what about the disorder's other major pathology, neurofibrillary tangles? Nothing suitable has yet come along for measuring these abnormalities in live patients.

That may now be changing, thanks to efforts by Masahiro Ono, PhD, and colleagues at Japan's Kyoto University. In ACS Medicinal Chemistry Letters, they say they have identified a new agent that binds both to beta-amyloid plaques and to neurofibratory tangles made of rogue tau proteins.

Studies in mice showed that the compound, based on fluorine-18, is stable enough in vivo to serve as a useful contrast agent. And, when applied to brain sections from deceased Alzheimer's disease patients, tangles as well as plaques lit up brightly in PET and SPECT scans.

-- J.G.

New Study Challenges Accepted Approaches to Research in Senile Dementia

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Health canal

Amsterdam, NL – Impacting millions of families and devouring billions of dollars globally, Alzheimer’s disease is the focus of exhaustive research to find a cure.

Although intensely investigated over the last three decades using cutting-edge technologies, the “pathogenic cause” of Alzheimer’s disease has not been found. While many research “breakthroughs” have been claimed and high-profile drugs trials carried out, why does the promised “cure” still seem to elude scientists?

In an effort to address this question, Ming Chen, PhD, Huey T. Nguyen, BS, and Darrell R. Sawmiller, PhD, Aging Research Laboratory, R&D Service, Bay Pines VA Healthcare System and University of South Florida, undertook an independent and systematic analysis of the underlying research assumptions against the established scientific principles. This analysis led them to hypothesize that perhaps the main problem is the research community’s perception of the disease.

In an article scheduled for publication in the December issue of the Journal of Alzheimer’s Disease the authors suggest that when the National Institutes of Health separated out dementia from other senile conditions and redefined it as a distinct and “curable” disease — Alzheimer’s – in the 1970s, it opened a Pandora’s box and may have misdirected research for decades. It triggered the search for pathogenic factors and cures, and disregarded the role of demographic change and its diverse end results in the elderly.

The authors argue that senile disorders – diseases occurring after age 60 and eventually affecting the majority of the elderly, such as tooth, hearing or memory loss – are caused by aging, thus differ fundamentally from distinct diseases by origin, study paradigm and intervention strategy.

Moreover, the authors contend that a central regulator in cognition − the Ca2+ signaling system − has been misconceived by institutional thinking that favors a “cure” for senile dementia. The dominant hypothesis, although unproven, is that Ca2+ levels rise throughout the aging process, leading to cell death, and thus research has focused on calcium antagonists to lower those levels. This viewpoint has been promoted by policy makers, and the subject of a number of high profile clinical trials, but to date no positive results have emerged.

In contrast, the authors propose that declining functionality of Ca2+ signaling as a result of the aging process, among a myriad of other age-related changes, leads to cognitive decline. Therefore interventions for senile dementia could activate Ca2+ function by promoting energy metabolism and also by Ca2+ agonists such as caffeine and nicotine. At the same time, risk factors play a key role. “Aging and Ca2+ deficits set the stage for senile dementia, but do not always lead to senile dementia in real life,” explains Dr. Chen. “Lifestyles and other risk factors are the key. So we think that senile dementia may be explained by ‘advanced aging plus risk factors.’ This model points to a new direction for prevention. This means we must support the elderly in healthy lifestyles. And we should develop medications to extend the lifespan of old neurons, rather than looking for ways to inhibit far-fetched ‘pathogenic’ factors.”

“The model implies that senile dementia is, by and large, a lifestyle disease,” says Dr. Chen. “This view, in fact, has been shared by many in the medical and clinical community, but contrasts sharply with current dominant theories in the Alzheimer research field, which assume a linear and ‘cause and effect’ mechanism. Since they have not taken into account the fundamental roles of aging and risk factors, it is clear that these theories, though highly appealing to the public and researchers alike, are of little relevance to the scientific nature of senile dementia.”

“The two overwhelming concepts, senile dementia as a distinct disease and the Ca2+ overload hypothesis, have effectively blocked any meaningful progress in senile dementia research, and have inhibited the self-correcting mechanism of science,” concludes Dr. Chen. “An independent scrutiny on the field may be helpful.”

“Although incurable”, Dr. Chen is optimistic. “Our research, if guided by correct theories, will produce medications to help delay dementia to a certain extent − similar to the drugs that delay or ameliorate atherosclerosis and osteoporosis today.”

Blood Test Predicts Course of Alzheimer's

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By Crystal Phend, Senior Staff Writer, MedPage Today

Reviewed by Robert Jasmer, MD; Associate Clinical Professor of Medicine, University of California, San Francisco and
Dorothy Caputo, MA, RN, BC-ADM, CDE, Nurse Planne

Plasma levels of sphingolipid compounds can predict progression of Alzheimer's disease, a small, early, observational study showed.

Higher ratios of sphingomyelins to ceramide and of dihydrosphingomyelin to dihydroceramides predicted significantly slower clinical progression, Michelle M. Mielke, PhD, of Johns Hopkins University, and colleagues found. Mielke is now at Mayo Clinic in Rochester, Minn.

If validated, sphingolipids could be "a sensitive, and easily accessible, biomarker" for Alzheimer's progression, they reported online in the Journal of Alzheimer's Disease.

That would be a big advantage for families and caregivers and also may help in development of better treatments for Alzheimer's, the group suggested.

Sphingolipids play a critical role in cellular signaling as major components of cell membranes, particularly in the central nervous system, where the proper balance of different species of these fats is essential for normal function of neurons.

The researchers correlated sphingolipid levels measured in 120 patients with probable Alzheimer's disease, predominantly of mild to moderate severity, at a single center. They were followed for progression over 2.3 years on average.

Higher levels of the various sphingolipids didn't predict more severe dementia at baseline, but they did predict rate of decline.

Higher dihydroceramides predicted significantly greater decline on the Mini-Mental State Exam (MMSE, P=0.050 as a continuous variable), while ceramides showed a similar but nonsignificant trend.

On the other hand, plasma sphingomyelins at higher levels predicted less progression on the MMSE (1.15 points difference for highest versus lowest tertile, P=0.006).

The same was true for dihydrosphingomyelin, with the top tertile progressing by 0.84 fewer points than those in the bottom tertile (P=0.046).

But the strongest predictors were ratios of metabolically-linked pairs of these lipids.

Ceramides are both a precursor for sphingomyelins and can be formed by their catabolism, and the same is true for the dihydro form of both.

The ratio of sphingomyelins to ceramides was associated with 1.19-points less decline on the MMSE (P=0.004) and 2.42-points less worsening on the Alzheimer's Disease Assessment Scale-Cognitive Subscale for the top versus bottom tertile (P=0.016).

The ratio of dihydrosphingomyelins to dihydroceramides correlated with a decline of 1.35 fewer points on the MMSE and an increase of 3.18 fewer points on the cognitive scale (both P=0.001).

"Together, these results suggest a shift in the metabolic pathways from ceramide to sphingomyelins over the course of Alzheimer's disease," such that the ratios may be useful predictors of clinical progression in later stages of the disease, Mielke's group suggested in the paper.

Total cholesterol and triglycerides didn't predict progression of Alzheimer's disease.

The researchers also looked at correlation of all the factors with functional decline measured on the Clinical Dementia Rating-Sum of Boxes but found no significant predictors.

They cautioned that the lipid levels measured at baseline weren't taken while fasting, which may have affected levels of some plasma sphingolipids.

But controlling for body mass index, diabetes and cardiovascular disease status, as well as other factors in the individuals in whom they were known didn't appear to impact the results.

The study was funded by a grant from George P. Mitchell and the late Cynthia W. Mitchell and by the National Institute of Aging.

The researchers reported having no conflicts of interest to disclose.



Primary source: Journal of Alzheimer's Disease
Source reference:
Mielke MM, et al "Plasma sphingomyelins are associated with cognitive progression in Alzheimer's disease" J Alzheimers Dis 2011; DOI: 10.3233/JAD-2011-110405.

Walking to Save Your Brain

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AC Content

Kirk Erickson, PhD, at the University of Pittsburgh in Pennsylvania, and his colleagues reported these findings in the October 13 issue of the journal, Neurology.

Dr Erickson found the results quite astounding. He said that other studies have shown that exercise is related to brain function, but what amazed him was the fact that he and his colleagues found that walking as little
as one mile a day is related to brain volume nine years later, and dementia 13 years later.

According to these researchers, the volume of gray matter in your brain decreases in late adulthood and usually precedes cognitive impairment. It has been hypothesized that participation in physical exercise will protect brain tissue against deterioration. "This hypothesis has not been tested in longitudinal study", Dr. Erickson and colleagues wrote.

In the Cardiovascular Health Cognition Study, 299 people free of dementia, whose mean age was 78 years were assessed for physical activity, which was measured by the number of blocks they walked in one week.

Nine years later after the physical activity assessment, MRI scans were used to measure brain size. Four years later, the participants were tested for cognitive impairment and dementia.

Those participating were classified into four groups depending on the number of blocks they walked. MRI scan measurements nine years later showed that gray matter volume in the highest quarter differed from the other three quarters significantly.

Those participants who walked at least six miles per week had more gray matter than people who walked less, but walking more than nine miles did not increase gray matter volume any more.

In the four year follow-up, 116 of the participants, or 40%, had developed cognitive impairment or dementia.

"Based on our results, we can conclude....read all of Walking to Save Your Brain

Another promising finding in the fight against Alzheimer's

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Scientists have discovered a new target for the prevention of adverse immune responses, which have been identified as factors in the development of Alzheimer's disease (AD).

The discovery was made by researchers at the University of South Florida's Department of Psychiatry and the Center of Excellence for Aging and Brain Repair.

The CD45 molecule is a receptor on the surface of the brain's microglia cells, cells that support the brain's neurons and also participate in brain immune responses.

Previous studies by the USF researchers showed that triggering CD45 was beneficial because it blocked a very early step in the development of Alzheimer's disease. In the present study, the researchers demonstrated in Alzheimer's mouse models that a loss of CD45 led to dramatically increased microglial inflammation.

Although the brain's immune response is involved in Alzheimer's disease pathology, "this finding suggests that CD45 on brain immune cells appears critically involved in dampening harmful inflammation," said study senior author Jun Tan, a professor of psychiatry and Robert A. Silver chair at the Rashid Laboratory for Developmental Neurobiology, USF Silver Child Development Center and research biologist for Research and Development Service at the James A. Haley Veteran's Hospital.

The investigators also found an increase in harmful neurotoxins, such as A beta peptides, as well as neuron loss in the brains of the test mice.

"In short, CD45 deficiency leads to increased accumulation of neurotoxic A beta in the brains of old Alzheimer's mice, demonstrating the involvement of CD45 in clearing those toxins and protecting neurons," Dr. Tan said. "These findings are quite significant, because many in the field have long considered CD45 to be an indicator of harmful inflammation. So, researchers assumed that CD45 was part of the problem, not a potential protective factor."

The next step is to apply these findings to develop new Alzheimer's disease treatments, said Paula Bickford, PhD, a professor in the USF Department of Neurosurgery and senior career research scientist at the James A. Haley Veteran's Hospital.

"We are already working with Natura Therapeutics, Inc. to screen for natural compounds that will target CD45 activation in the brain's immune cells," Dr. Bickford said.

The findings are published online in the Journal of Neuroscience. (ANI)

Dementia in Later Years an Independent Risk Factor for Death

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Medscape Today
Fran Lowry

Having dementia in later life more than doubles the risk of death, and this risk is independent of known midlife sociodemographic and cardiovascular risk factors, according to a new prospective historical study published in the January issue of the American Journal of Geriatric Psychiatry.




"This study is suggesting that dementia per se kills," lead author Michal Beeri, PhD, from Mount Sinai School of Medicine in New York City, told Medscape Medical News.



"Our original hypothesis was that one of the reasons why demented people die more and faster is because they have a bunch of other risk factors that increase their mortality, but we are finding that that is not the case."



The aim of the study was to compare the mortality rates of elderly patients with and without dementia and the differential association of midlife risk factors with mortality according to dementia status.



Study participants were drawn from a large study of 10,059 male Jewish civil servants who participated in the Israel Ischemic Heart Disease study, which began in 1963. In 1999 and 2000, 1713 of the surviving participants were evaluated for dementia and for midlife sociodemographic and cardiovascular risk factors, late-life dementia (dementia occurring older than age 65 years), and mortality.



During a period of 6 years, 718 of the participants died (42%); of the 307 participants with dementia, 71.8% died, and of the 1407 patients without dementia, 35.4% died.



On multivariate survival analysis, patients with dementia had a hazard ratio (HR) for mortality of 2.27 compared with patients without dementia (95% confidence interval [CI], 1.92 - 2.68). The study also found that other risk factors associated with mortality were socioeconomic status (HR, 0.94; 95% CI, 0.88 - 1.00), higher systolic blood pressure (HR, 1.16 per 20 mm Hg; 95% CI, 1.06 - 1.28 mm Hg), higher diastolic blood pressure (HR, 1.15 per 10 mm Hg, 95% CI, 1.06 - 1.25 mm Hg), and ever smoking (HR, 1.38; 95% CI, 1.18 - 1.61).



However, midlife total cholesterol was not associated with mortality.



Moreover, none of the interactions of the risk factors with dementia was significant.



"You would assume that those cardiovascular risk factors that were measured in midlife would be associated with mortality 35 years later, so people who had high blood pressure, higher systolic, low sociodemographic status, higher diastolic, and having ever smoked had higher mortality in this study, which is what everybody else has shown too," Dr. Beeri said.



"But when you try and see an interaction, whether the fact that you have high blood pressure and dementia is what is increasing your risk of death, you don't find that."



Dr. Beeri also emphasized that her study does not have information on the cause of death. She hopes that this information will be forthcoming in another upcoming study.



However, she added, this research demonstrates that "midlife risk factors associated with increasing mortality, including in our study, were not the explanation for the increased death of demented people," she said.



Confirmatory Findings



The fact that people with dementia are at increased risk for mortality is something that is well known and has been well known for a long time, said David Knopman, MD, professor of medicine at the Mayo Clinic in Rochester, Minnesota, who was asked by Medscape Medical News to comment on the findings.



"The diagnosis of dementia definitely has a large impact on survival. That's well known. It roughly halves survival rate in older people. The issue about this paper is that these researchers looked at midlife cardiovascular risk factors and found that there was not an interaction between the presence of the cardiovascular risk factors and dementia — that having had hypertension or diabetes or smoking in midlife didn't make the mortality rate rise or reduce the survival for dementia additionally," said Dr. Knopman, who is also deputy editor of Neurology and a fellow of the American Academy of Neurology.



The fact that dementia in and of itself is associated with a greater mortality risk has been repeatedly demonstrated in many studies.



"A clinical diagnosis of Alzheimer's disease is associated with about a halving of the survival rate. If you have vascular dementia from a stroke, and have cognitive impairment or meet criteria for vascular dementia, that's even worse in terms of survival, so this is pretty well known. I would say that this study confirms what we already know," Dr. Knopman said.



Dr. Beeri and Dr. Knopman have disclosed no relevant financial relationships