Santander Banks On Raising ??450,000 For Alzheimer's Society In 2011

Santander staff across the UK have joined forces with Alzheimer's Society to raise a national target of ??450,000 to help people with dementia and their carers.


The partnership will see Santander employees across its UK branch network carrying out national and regional fundraising initiatives in 2011 for the charity, which supports people living with dementia today and funds research to find a cure for tomorrow. The funds raised by the bank will go towards Alzheimer's Society's online forum, 'Talking Point', which provides advice, information and support for anyone affected by dementia.


Santander will mark the launch of this partnership in the New Year with a 'Go Retro' day, where staff will be able to dust off their flares or platforms and dress up for a donation. Alzheimer's Society pin badges will also be available in all Santander branches for customers to buy from February.


Other fundraising initiatives in 2011 will include a sponsored abseil in Liverpool and Milton Keynes, the Pedometer Challenge in which staff will be sponsored to walk great distances, as well as an overseas challenge to climb Mount Kilimanjaro.


Sheralee Morris, Santander Community Relations Manager said:




'We are delighted to be working with Alzheimer's Society in 2011 and have some exciting fundraising initiatives lined up in order to meet our target amount. This year more staff than ever voted for the charity they wanted to support in 2011 and Alzheimer's Society was a clear winner. It is such a worthwhile cause, one that is close to many people's hearts.'




Jeremy Hughes, Chief Executive, Alzheimer's Society said:



'Alzheimer's Society is delighted to be Santander's Charity of the Year. As a charity, we rely on voluntary donations to continue our vital work. The support of companies like Santander allows us to champion the rights of people living with dementia and the millions of people who care for them. The money raised will make a real difference to the 750,000 people living with dementia in the UK.'


Source:

Alzheimer's Society

Larger Head Size May Protect Against Alzheimer's Symptoms

New research shows that people with Alzheimer's disease who have large heads have better memory and thinking skills than those with the disease who have smaller heads, even when they have the same amount of brain cell death due to the disease. The research is published in the July 13, 2010, issue of Neurology®, the medical journal of the American Academy of Neurology.


"These results add weight to the theory of brain reserve, or the individual capacity to withstand changes in the brain," said study author Robert Perneczky, MD, of the Technical University of Munich in Germany. "Our findings also underline the importance of optimal brain development early in life, since the brain reaches 93 percent of its final size at age six."


Head size is one way to measure brain reserve and brain growth. Perneczky said that while brain growth is determined in part by genetics, it is also influenced by nutrition, infections and inflammations of the central nervous system, and brain injuries.


"Improving prenatal and early life conditions could significantly increase brain reserve, which could have an impact on the risk of developing Alzheimer's disease or the severity of symptoms of the disease," he said.


For the study, 270 people with Alzheimer's disease took tests of their memory and cognitive skills and had MRI scans of their brains to measure the amount of brain cell death. Head size was determined by the circumference measurement.


The study showed that larger head size was associated with a greater performance on memory and thinking tests, even when there was an equivalent degree of brain cell death. Specifically, for every one percent of brain cell death, an additional centimeter of head size was associated with a six percent greater performance on the memory tests.


The study was supported by the National Institute on Aging.


The American Academy of Neurology, an association of more than 22,000 neurologists and neuroscience professionals, is dedicated to promoting the highest quality patient-centered neurologic care. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as stroke, Alzheimer's disease, epilepsy, Parkinson's disease and multiple sclerosis.


Source: American Academy of Neurology (AAN)

Antihypertensive Drugs May Protect Against Alzheimer's Disease Independent From Reduction Of Blood Pressure Lowering Activities

Researchers at Mount Sinai School of Medicine have found that the drug carvedilol, currently prescribed for the treatment of hypertension, may lessen the degenerative impact of Alzheimer's disease and promote healthy memory functions. The new findings are published in two studies in the current issues of Neurobiology of Aging and the Journal of Alzheimer's Disease.


"These studies are certainly very exciting, and suggest for the first time that certain antihypertensive drugs already available to the public may independently influence memory functions while reducing degenerative pathological features of the Alzheimer's disease brain," said study author Giulio Maria Pasinetti, MD, PhD, Saunders Family Professor of Neurology and Director of the Center of Excellence for Novel Approaches to Neurotherapeutics at Mount Sinai School of Medicine.


Dr. Pasinetti's team found for the first time that carvedilol, a blood pressure lowering agent, is capable of exerting activities that significantly reduce Alzheimer's disease-type brain and memory degeneration. This benefit was achieved without blood pressure lowering activity in mice genetically modified to develop Alzheimer's disease brain degeneration and memory impairment. These data were published in Neurobiology of Aging.


In a second study published in the Journal of Alzheimer's Disease, the research team led by Dr. Pasinetti assessed how mice learned new tasks and information and recall of past information chemically stored in the brain. They found that carvedilol treatment was capable of promoting memory function, based on assessments of learning new tasks and information and recall of past information, which is already chemically stored in the brain.


In the study, one group of mice received carvedilol treatment and the other group did not. The scientists conducted behavioral and learning tests with each group of mice, and determined that it took the mice in the carvedilol significantly less time to remember tasks than the other group.


"Ongoing clinical research is in progress to test the benefits of carvedilol, which may prove to be an effective agent in the treatment of symptoms of Alzheimer's disease," said Dr. Pasinetti. "We look forward to further studying this drug in the human population."


Source:

Mount Sinai Medical Center

Alzheimer??™s Disease: Let??™s Weigh-in On The Risks

January is Alzheimer Awareness Month. Two experts from the Canadian Institutes of Health Research (CIHR) are available to comment on the effects of Alzheimer??™s Disease (AD) and ongoing research focusing on risk factors and potential cures. The availability of our experts coincides with the 2007 "Heads Up for Healthier Brains" campaign of the Alzheimer Society of Canada.


More than 280,000 Canadians aged 65 and over have AD. As populations around the world continue to age, AD will become even more prevalent. By 2031, more than 750,000 Canadians are expected to have AD and related dementias.


"Aside from its impacts on those who suffer from it, AD can be a significant burden for families and for the health care system," says Dr. Anne Martin-Matthews, based in Vancouver and Scientific Director of the CIHR Institute of Aging (CIHR-IA). "CIHR recently launched RAPID (Research to Action Program In Dementia), an initiative which seeks to accelerate the translation of research about AD and dementia by linking researchers with communities."


"Almost 25 per cent of Canadians have someone with AD in their family. Research into the causes of, or solutions to AD is significant as research may hold the key to unlocking new means of preventing, treating and curing it," says Dr. R?©mi Quirion, based in Montreal and Scientific Director of the CIHR Institute of Neurosciences, Mental Health and Addiction (CIHR-INMHA).


Recent studies have highlighted several life style risk factors for the development of AD. Does the long-term intake of caffeine reduce the risk of AD? Does physical activity have a role to play in staving off the risk of AD? What about the so-called Mediterranean diet which is high in olive oil and said to be protective against age-related memory problems? Some studies say eating fish just two to three times a week may also protect your brain as you age. And others have shown that fruits, vegetables and juices have a role to play in reducing risk.


Dr. R?©mi Quirion is available to comment in English and/or French on the neurological mechanisms underlying the disease and the science behind certain risk factors and potential cures.


Dr. Anne Martin-Matthews is available to comment in English on RAPID, as well as the social and health service-related aspects of AD and dementia.


The Canadian Institutes of Health Research (CIHR) is the Government of Canada's agency for health research. CIHR's mission is to create new scientific knowledge and to catalyze its translation into improved health, more effective health services and products, and a strengthened Canadian health care system. Composed of 13 Institutes, CIHR provides leadership and support to more than 10,000 health researchers and trainees across Canada. cihr-irsc.gc.ca.


Canadian Institutes of Health Research (CIHR)

160 Elgin St., 9th Fl.

Ottawa, Ontario K1A 0W9

Canada

Statins Have Unexpected Effect On Pool Of Powerful Brain Cells

Cholesterol-lowering drugs known as statins have a profound effect on an elite group of cells important to brain health as we age, scientists at the University of Rochester Medical Center have found. The new findings shed light on a long-debated potential role for statins in the area of dementia.



Neuroscientists found that statins, one of the most widely prescribed classes of medication ever used, have an unexpected effect on brain cells. Researchers looked at the effects of statins on glial progenitor cells, which help the brain stay healthy by serving as a crucial reservoir of cells that the brain can customize depending on its needs. The team found that the compounds spur the cells, which are very similar to stem cells, to shed their flexibility and become one particular type of cell.



The new findings come at a time of increasing awareness among neurologists and cardiologists of the possible effects of statins on the brain. Several studies have set out to show that statins provide some protection against dementia, but the evidence has been inconclusive at best. Meanwhile, there is some debate among physicians about whether statins might actually boost the risk of dementia. The new research published in the July issue of the journal Glia by Steven Goldman, M.D., Ph.D., and first author Fraser Sim, Ph.D., provides direct evidence for an effect of statins on brain cells.



"There has been a great deal of discussion about a link between statins and dementia, but evidence either way has been scant," said Goldman, a neurologist who led the team. "This new data provides a basis for further exploration.



"These findings were made through experiments done in cell culture using human brain cells and exposing them to doses of statins used widely in patients. But this research was not done in people. There are a great number of questions that need to be explored further before anyone considers changing the way statins are used," Goldman added.



Goldman's team is recognized as a leader identifying and directing the molecular signals that direct the development of stem cells and their daughter cells, known as progenitor cells. In this study, Sim ran a genomic screen to see which genes are more active in these cells compared to other brain cells. Sim and Goldman found several related to cholesterol, including the enzyme HMG-CoA reductase, which is central to making cholesterol and is the main target of statins.



"It was quite surprising that the cholesterol-signaling pathways are so active in these cells," Goldman said. "Since such signaling is blocked with compounds used literally by millions of patients every day, we decided to take a closer look."
















The team measured the effects of two widely used statins, simvastatin and pravastatin, on glial progenitor cells, which can become either astrocytes or oligodendrocytes. The team looked at progenitor cells from 16 patients who had brain tissue removed during surgery to treat epilepsy, tumors, or vascular problems.



Scientists found that both compounds, when used at doses that mimic those that patients take, spur glial progenitor cells to develop into oligodendrocytes. For example, in one experiment, they found about five times as many oligodendrocytes in cultures of human progenitor cells exposed to pravastatin compared to cultures not exposed to the substance. Similarly, they found that the number of progenitor cells was just about one-sixth the level in cultures exposed to simvastatin compared to cultures not exposed to the compound.



To understand the process, think of a baseball team raising a group of great young prospects. They run fast, they throw hard, they hit well. Most teams will tailor their players to the positions the team needs - a few pitchers, for instance, and several batters. Any team that suddenly found itself with all pitchers or all hitters would be ill prepared to compete.



The Rochester team discovered that statins essentially push most of the raw talent in one direction.



Scientists don't really know the long-term effects of such a shift. Physicians are looking at statins as a possible treatment for multiple sclerosis, where the myelin coating that covers nerve cells in the central nervous system is damaged. Myelin is produced by oligodendrocytes - so spurring the development of oligodendrocytes might provide one way to reduce or repair the damage seen in M.S.



But the body maintains a pool of uncommitted glial progenitor cells for a reason. The body normally turns to that reservoir of cells when it needs to repair damage from a variety of causes, such as an infection, hemorrhage, a serious blow to the head, or inflammation within the brain, such as in patients with multiple sclerosis. No one knows the consequences if such cells weren't available when needed, though increased cognitive impairment might be one possibility.



"These are the cells ready to respond if you have a region of the brain that is damaged due to trauma, or lack of blood flow like a mini-stroke," said Sim, assistant professor of Neurology. "Researchers need to look very carefully at what happens if these cells have been depleted prematurely."



Glial progenitor cells are distributed throughout the brain and, according to Sim, make up about 3 percent of our brain cells. While true stem cells that can become any type of cell are very rare in the brain, their progeny, progenitor cells, are much more plentiful. They are slightly more specialized than stem cells but can still develop into different cell types.



The work may be relevant to drugs commonly used by diabetics as well. That's because the team discovered that a signaling molecule called PPAR gamma is central to the effect of statins on glial progenitor cells. When PPAR gamma was blocked, the statins no longer had the effect. Since PPAR gamma is the main target of diabetes medications such as Avandia and Actos, which trigger the molecule, Goldman said it's likely that those medications have the same effect on progenitor cells. He also noted that many patients are on both diabetes drugs and statins, which could increase the effect.



"Our results suggest the need for awareness of the possible toxicities accruing to long-term statin use, and identify one such potential toxicity, the premature differentiation and attendant long-term depletion of oligodendrocyte progenitor cells of the adult brain," conclude the authors in their Glia paper.







Besides Sim and Goldman, other authors include medical student Jennifer Lang, technical associate Tracy Ali, Cornell scientist Neeta Roy, and neurosurgeons Edward Vates, M.D., and Webster Pilcher, M.D. The National Institute of Neurological Disorders and Stroke and the National Multiple Sclerosis Society funded the work.



Source: Tom Rickey


University of Rochester Medical Center




View drug information on ACTOS; Avandia.

Age Related Health Conditions Affect Half Of All Seniors

A broad study of adults ages 65 and older has found that half of them have one or more conditions that can affect their ability to participate in activities of daily living, such as bathing and dressing on their own.



Researchers at the University of Michigan Health System analyzed the responses of more than 11,000 participants in the national Health and Retirement Study. They found that 50 percent of older adults had a moderate to severe form of at least one of the following conditions: cognitive impairment, falls, incontinence, low body mass index, dizziness, vision impairment or hearing impairment.



The researchers also studied whether the respondents had difficulty with activities of daily living (bathing, dressing, eating, toileting or transferring) and needed assistance to complete the tasks. They found that people with geriatric conditions had about the same level of dependency when performing activities of daily living as older patients with chronic diseases, including heart disease, chronic lung disease, diabetes, cancer, musculoskeletal conditions, stroke and psychiatric problems.



The study -- which appears in the Annals of Internal Medicine -- fills a major gap in research about older patients. Although conditions such as incontinence and falls have been studied extensively, the total impact of geriatric conditions on health and disability in the older adult population has not been investigated, notes lead author Christine Cigolle, M.D., MPH, lecturer in the U-M Health System Department of Family Medicine and a physician in the Veterans Affairs Ann Arbor Healthcare System's Geriatric Research, Education and Clinical Center (GRECC).



"The focus in medicine has long been on diseases, and how to diagnose and treat them. But that focus often isn't helpful in regard to older adults; they tend to have one or more of these geriatric conditions, which are not considered diseases and can be missed by physicians," Cigolle says.



"Our study is the first to look at all seven of these common conditions together, and we found that they are very common and increase dramatically in prevalence with age," she says. "To me, that says that clinicians need to ask patients about these issues. In many situations, they may be able to help manage the condition before it leads to disability."



In the medical world, experts have debated how to categorize conditions such as the ones in this study. Some are called geriatric syndromes, while others fall outside of categories typically used by physicians.



The lack of consistent terminology has been one obstacle to the appropriate diagnosis and treatment of these conditions, says senior author Caroline Blaum, M.D., M.S., associate professor in the Division of Geriatric Medicine at U-M and a research scientist at the Veterans Affairs Ann Arbor Healthcare System GRECC.
















Such obstacles need to be overcome so that older adults can receive the best health care possible, she says. "Geriatric conditions are integral to the health and function of older adults and should be addressed in their care," Blaum notes.



The researchers found a strong link between the conditions and dependence on others to help with activities of daily living. Just 2.6 percent of survey participants without any of the geriatric conditions were dependent on others for help with activities. That percentage jumped to 8.1 among people with one of the conditions, 19.4 among people with two conditions, and 45 among people with three or more conditions.



All conditions increased in prevalence with advancing age. Among older adults with cognitive impairment, for instance, 55 percent were 80 or older. Overall, 39 percent of people ages 65-69 were found to have one or more of the conditions. The percentage rose to 82 among people ages 90 and older.



Additionally, compared to those with no geriatric conditions, people with increasing numbers of conditions were older, female, from a minority ethnic group, unmarried, and had less education and a lower net worth.







The data used in this study are from the 2000 wave of the Health and Retirement Study (HRS), a biennial longitudinal health interview survey of adults ages 50 years and older in the United States. The HRS is sponsored by the National Institute on Aging and performed by the Institute for Social Research at U-M.



In addition to Cigolle and Blaum, authors of the study were Kenneth M. Langa, M.D., Ph.D., of the U-M Medical School Department of Internal Medicine, the U-M Institute for Social Research and the Ann Arbor VA Center for Practice Management and Outcomes Research; and Mohammed U. Kabeto, M.S., and Zhiyi Tian, M.A., M.S., of the Department of Internal Medicine.



The study was supported by grants from the John A. Hartford Foundation and the National Institute on Aging and by the Ann Arbor VA GRECC.



Reference: Annals of Internal Medicine, Aug. 7, 2007, Vol. 147, pages 156-164. "Geriatric Conditions and Disability: The Health and Retirement Study."



Source: Katie Gazella


University of Michigan Health System

Medivation To Host Conference Call To Discuss Top-Line 12-Month Results From Dimebon(TM) Alzheimer's Disease Study

Medivation, Inc.
(Nasdaq: MDVN) today announced that it will hold a teleconference at 8:30
a.m. Eastern time on Monday, June 11, to discuss top-line 12-month results
from its randomized, double-blind, placebo-controlled Phase 2 clinical
trial of Dimebon(TM), its lead product candidate, in Alzheimer's disease.



Rachelle Doody, M.D., Ph.D., lead investigator for the study, will
present the 12-month results for the first time at a scientific meeting at
the 2007 Alzheimer's Association International Conference on Prevention of
Dementia in Washington, D.C. Dr. Doody will present the data (abstract
#S3-02-03, "Results of a One-Year Randomized, Placebo-Controlled Trial of
Dimebon for the Treatment of Mild to Moderate Alzheimer's Disease") on
Tuesday, June 12, at 10:00 a.m. Eastern time during the symposium session
on "Emerging Compounds." Dr. Doody holds the Effie Marie Cain Chair in
Alzheimer's Disease Research at the Alzheimer's Disease and Memory
Disorders Center, Baylor College of Medicine in Houston.



The Alzheimer's Association, sponsor of the Prevention of Dementia
conference, has selected the Dimebon data for inclusion in a news briefing
to be held during the conference. That news briefing, which will focus on
Alzheimer's disease therapies and be open to credentialed reporters,
writers or editors from recognized external print, broadcast, syndicated or
online news organizations, will take place at 12:00 p.m. Eastern time on
Monday, June 11.




About Medivation



Medivation, Inc. is a biopharmaceutical company that acquires promising
technologies in the late preclinical development phase and develops them
quickly and cost-effectively. Medivation's current portfolio consists of
small molecule drugs in development to treat three large, unmet medical
needs -- Alzheimer's disease, Huntington's disease and hormone-refractory
prostate cancer. The Company intends to build and maintain a portfolio of
four to six development programs at all times. For more information, please
go to medivation.



This press release contains forward-looking statements, which are made
pursuant to the safe harbor provisions of the Private Securities Litigation
Reform Act of 1995. Forward-looking statements involve risks and
uncertainties that could cause actual results to differ significantly from
those projected. You are cautioned not to place undue reliance on the
forward-looking statements, which speak only as of the date of this
release. You are also cautioned that none of the Company's product
candidates has been approved for sale, that significant additional animal
and human testing is required in order to seek marketing approval for any
of its product candidates, and that Medivation cannot assure you that
marketing approval can be obtained for any of its product candidates.
Medivation's filings with the Securities and Exchange Commission, including
its Annual Report on Form 10-KSB for the year ended December 31, 2006,
include more information about factors that could affect the Company's
financial and operating results.


Medivation, Inc.

medivation

New Mechanism For Amyloid Beta Protein's Toxic Impact On The Alzheimer's Brain

Scientists have uncovered a novel mechanism linking soluble amyloid ?? protein with the synaptic injury and memory loss associated with Alzheimer's disease (AD). The research, published by Cell Press in the June 25 issue of the journal Neuron, provides critical new insight into disease pathogenesis and reveals signaling molecules that may serve as potential additional therapeutic targets for AD.



Amyloid ?? protein (A??) plays a major pathogenic role in AD, a devastating neurodegenerative disorder characterized by progressive cognitive impairment and memory loss. "Given the mounting evidence that small soluble A?? assemblies mediate synaptic impairment in AD, elucidating the precise molecular pathways by which this occurs has important implications for treating and preventing the disease," explains senior study author, Dr. Dennis Selkoe from the Center for Neurologic Diseases at Brigham and Women's Hospital and Harvard Medical School.



Dr. Selkoe, Dr. Shaomin Li, and colleagues examined regulation of a cellular communication phenomenon known as long-term synaptic depression (LTD). LTD has been linked with neuronal degeneration, but a role for A?? in the regulation of LTD has not been clearly described. The researchers found that soluble A?? facilitated LTD in the hippocampus, a region of the brain intimately associated with memory. The enhanced synaptic depression induced by soluble A?? was mediated through a decrease in glutamate recycling at hippocampal synapses.



Excess glutamate, the major excitatory neurotransmitter in the brain, is thought to contribute to the progressive neuronal loss characteristic of AD. The researchers went on to show that A??-enhanced LTD was mediated by glutamate receptor activity and that the LTD could be prevented by an extracellular glutamate scavenger system. A very similar enhancement of LTD could be induced by a pharmacological blocker of glutamate reuptake. Importantly, soluble A?? directly and significantly decreased glutamate uptake by isolated synapses.



"Our findings provide evidence that soluble A?? from several sources enhances synaptic depression through a novel mechanism involving altered glutamate uptake at hippocampal synapses," concludes Dr. Selkoe. "These results have both mechanistic and therapeutic implications for the initiation of hippocampal synaptic failure in AD and in more subtle forms of age-related A?? accumulation." Future studies are needed to determine precisely how soluble A?? protein physically interferes with glutamate transporters at the synapse.



The researchers include Shaomin Li, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; Soyon Hong, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; Nina E. Shepardson, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; Dominic M. Walsh, University College Dublin, Dublin, Ireland; Ganesh M. Shankar, Brigham and Women's Hospital, Harvard Medical School, Boston, MA; and Dennis Selkoe, Brigham and Women's Hospital, Harvard Medical School, Boston, MA.



Source:

Cathleen Genova

Cell Press

Dementia Now A National Priority: Alzheimer Scotland Welcomes Ministerial Statement

Today's Ministerial statement on dementia by Shona Robison MSP is warmly welcomed by Alzheimer Scotland. It confirms that the Scottish Government recognises the scale of the problem of dementia in Scotland, as highlighted by our recent report The Dementia Epidemic - where Scotland is now and the challenge ahead.


The programme has identified the need for changes in service provision for people with dementia across Scotland, including the integration of palliative care as promoted by Scotland's Beyond Barriers project. It also recognises the need to enhance the research into dementia, its causes and potential treatments; a need that has received much attention following the recent comments of Terry Pratchett. Awareness raising and information sharing will be promoted, increasing the understanding of dementia across Scotland. All this gievs substance to the Scottish Government's commitment to making dementia a national priority.


In addition, the announcement of joint funding of ??600,000 (over three years) between Alzheimer Scotland and the Dementia Services Development Centre in Stirling will allow the organisation to carry out invaluable work on post-diagnostic support and information initiatives for people with dementia and their carers.


Jim Jackson, Chief Executive at Alzheimer Scotland, said, "This is an important start to work which needs to be done by the Government, NHS, local authorities, voluntary and private sector services. As more people are diagnosed, Scotland will need to be better prepared to provide personalised support for people with dementia. We look forward to working with our partners in the Dementia Forum and transforming dementia services in Scotland."

Alzheimer Scotland

Possible Alzheimer's Link To Brain Organ Revealed By Purdue Findings

WEST LAFAYETTE, Ind. - Researchers have discovered that an organ in the brain called the choroid plexus apparently plays a critical role in preventing the accumulation of a protein associated with Alzheimer's disease.



The researchers found that the choroid plexus acts as a sort of "fishnet" that captures the protein, called beta-amyloid, and prevents it from building up in the cerebrospinal fluid, which surrounds and bathes the brain and spinal cord. Moreover, tissue in the organ is able to soak up large amounts of the protein and may contain enzymes capable of digesting beta-amyloid, said Wei Zheng (pronounced Way Zsheng), an associate professor in the School of Health Sciences at Purdue University.



The findings represent the first time that researchers have identified the potential existence of a natural mechanism in the brain for removing beta-amyloid.



"This newly uncovered pathway may help explain how normal brains balance this protein and how an imbalance caused by aging, genetic or environmental factors may lead to or worsen Alzheimer's disease," Zheng said.



Researchers had already known that the cerebrospinal fluid in the brains of Alzheimer's patients contains abnormally high quantities of beta-amyloid fragments. Beta-amyloid deposits accumulate over a period of years, resulting in abnormal clumps, or plaque, typical of Alzheimer's disease. Scientists do not yet know whether the disease is caused by the plaque formations or beta-amyloids themselves.



The discovery suggests that a malfunctioning choroid plexus could allow too much of the protein to build up in the brain.



Findings are detailed in a research paper written by postdoctoral research associate Janelle S. Crossgrove, postdoctoral fellow G. Jane Li and Zheng, all in the Purdue School of Health Sciences. The researchers will be honored on April 2 with a best paper award from the Society for Experimental Biology and Medicine.



Scientists do not know how beta-amyloid is deposited in the brains of Alzheimer's disease victims, but a long-held theory is that the protein is overproduced by aging brain cells, or neurons.



"We are coming from a totally different point of view," Zheng said. "We think that a balance of beta-amyloid is maintained partly by the choroid plexus, which removes beta-amyloid, and that this balance breaks down, leading to a buildup."



The majority of Alzheimer's research has historically concentrated on how the brain produces beta-amyloid protein, but the new findings point to the possibly critical importance of the "garbage-removal" process in the choroid plexus, Zheng said.



"We think the choroid plexus plays a role of removing all the garbage, including the beta-amyloid," Zheng said.



The research focused on how the choroid plexus works to clean beta-amyloid from the cerebrospinal fluid. Studies using rat brains indicated that choroidal cells removed about five times more beta-amyloid from cerebrospinal fluid compared to how much of the protein the cells allowed to pass into the fluid.
















"These results appear to tell us that a healthy choroid plexus can remove beta-amyloid from the cerebrospinal fluid, suggesting a novel pathway for the brain to maintain a normal balance," Zheng said. "Of course, much more work needs to be done to verify this theory."



The researchers also found that the choroid plexus possesses an enormous capacity to absorb beta-amyloids. The findings support the theory that the choroid plexus may possess a special enzyme that breaks beta-amyloids into smaller pieces, making it possible to soak up large quantities of the protein.



"The tissue must have a unique mechanism that is different from brain cells, something that enables it to chop up these beta-amyloids," Zheng said.



Future research may focus on efforts to isolate possible enzymes.



Zheng said the findings suggest that aging may degrade the organ's performance, and it is also possible that lead poisoning might increase the risk of Alzheimer's disease by damaging the choroid plexus and reducing its ability to filter beta-amyloids.



Alzheimer's disease affects more than 4 million Americans, and the findings might help researchers develop new methods to treat the disease. The research paper was published last November in the journal Experimental Biology and Medicine.






Writer: Emil Venere, (765) 494-4709, venerepurdue



Sources: Wei Zheng, (765) 496-6447, wzhengpurdue



Janelle S. Crossgrove, (765) 494-0737, crossgrovepurdue



Related Web sites:



Wei Zheng: people.healthsciences.purdue/~wzheng/



Society for Experimental Biology and Medicine: ebmonline/



Contact: Emil Venere

venerepurdue

Purdue University

Risk Factors For Dementia Are Different Between Men And Women

According to a study published in the Journal of Neurology
Neurosurgery and Psychiatry,
men and women have different risk factors that contribute to the
development of Alzheimer's disease and dementia. The French researchers
found
that stroke is a main risk factor for men and depression is a critical
factor for women.



The researchers analyzed a sample of almost 7000 people over age 65
from three French cities. None of the patients had dementia, but about
40% had some type of mild cognitive impairment (MCI) that affected
their
mental agility. Patients were evaluated at the start of the study, and
the researchers monitored their progress two and four years later.



Of the patients in the sample who were considered to have some type
of cognitive impairment, over 6.5% developed dementia over the next
four years. There was no change noted in about 50% of the patients, and
about 33% actually returned to normal levels of cognitive agility.



The researchers found that depressed patients and those taking
anticholinergic medications (interfering with chemical signals in the
brain) were more likely to decline from mild cognitive impairment to
dementia. In addition, people who had a particular variation in the
ApoE gene - known to be a risk factor for dementia - were more likely
to progress from mil cognitive impairment to dementia.



A key finding was that these risk factors were different for males and
females. Mild cognitive impairment in men was associated with being
overweight,
having diabetes, and having a history of stroke. Further, the
researchers found that having had a stroke increased the likelihood of
a male's progression to dementia by a factor of three.



Among the women, mild cognitive impairment was associated with
being in poorer general health, being disabled, having insomnia, and
having a poor
support network. Women who could not perform routine daily tasks were
3.5 times as likely to progress to dementia, and depressed women were
two times as likely to progress.



Although stroke occurs at a similar rate in both men and women, it was
not found to be a risk factor for dementia in women.



"Some potentially reversible risk factors for progression to dementia
were identified, which were not the same for men and women (notably
stroke in men and subclinical depression and use of anticholinergic
drugs in women). These factors should be taken into account in the
development of gender-specific clinical intervention programmes for
MCI," conclude the authors.



Risk profiles for mild cognitive impairment and progression to
dementia are gender specific

S
Artero, M-L Ancelin, F Portet, A Dupuy, C Berr, J-F Dartigues, C
Tzourio, O Rouaud, M Poncet, F Pasquier, S Auriacombe, J
Touchon,
K Ritchie

Journal of Neurology
Neurosurgery and Psychiatry. (2008)

doi 10.1136/jnnp.2007.1369The TheWi03

Click
Here to See Article Online



Written by: Peter M Crosta

New $26 Million Study Of Alzheimer's Disease And Cognitive Decline

The University of Mississippi Medical Center and four collaborating academic medical centers have received $26 million from the National Institutes of Health to identify risk factors for Alzheimer's disease and related forms of cognitive decline, said Dr. Thomas Mosley, UMMC professor of geriatric medicine and one of the new study's lead investigators.



The new funding will pay for the ARIC Neurocognitive Study, a comprehensive examination of thousands of patients, which will include detailed neurocognitive testing and brain imaging. The project builds on the influential Atherosclerosis Risk in Communities (ARIC) study, a large epidemiologic investigation of the risk factors for heart disease and stroke.



Using the new exam data and the wealth of information collected during ARIC's 20-plus years, the ARIC Neurocognitive Study is expected to further illuminate causes of dementia, giving researchers a unique window into early physiological changes that eventually culminate in Alzheimer's.



Of particular interest is the role that vascular risk factors - including hypertension, diabetes and lifestyle - experienced during middle age play in Alzheimer's and cognitive decline later in life.



"The new ARIC Neurocognitive Study will be one for the most comprehensive investigations to date into the role of vascular and related mid-life risk factors in Alzheimer's and cognitive decline," Mosley said.



He believes Alzheimer's disease likely isn't caused by a single factor, but rather by a complex process involving multiple factors interacting and accumulating over decades.



"Understanding the risk factors involved in this complex process may lead to new targets for treatment," he said. "It could also allow us to intervene at an earlier point with people who are at high risk for dementia, a time when preventative treatments may be most effective."



Researchers at UMMC will work with four collaborating primary study sites Johns Hopkins University, receiving about $4.6 million, Wake Forest University, receiving about $3.6 million, the University of Minnesota, receiving about $4.3 million, and the University of North Carolina at Chapel Hill receiving about $4.6 million.



Funded under UMMC's $9 million portion of the grant, Mosley's team includes scientists from the Mayo Clinic, Baylor College of Medicine, the University of Texas at Houston, Boston University and Erasmus University in the Netherlands.



The ARIC study has followed a group of roughly 16,000 participants for more than 20 years, from middle age into late life. Participants were initially recruited from four communities around the U.S., including approximately 4,000 African Americans from Jackson, Miss. Through a series of medical examinations over the years, ARIC participants have been extensively evaluated for diseases and factors including heart disease, hypertension and cognitive function.
















Recent research has found African Americans may have a twofold or greater risk for Alzheimer's compared to whites. With one of the largest and most extensively evaluated African American study subgroups, the ARIC Neurocognitive Study will help illuminate the role of ethnic differences in relative risk for dementia.



Previous work by Mosley and ARIC colleagues has pointed to the importance of vascular risk factors in predicting decline in cognitive functions such as memory and processing speed. Using brain imaging, Mosley and colleagues have also shown brain changes, such as atrophy and silent strokes, are surprisingly common, even in middle-age adults and that these brain abnormalities begin to affect cognitive functions as early as middle age.



"A key question is whether brain changes we find in mid life predict dementia later in life and, if so, whether they are caused by potentially modifiable conditions, such as hypertension," Mosley said.



The ARIC Neurocognitive Study will also bring together state-of-the-art brain imaging and new genetic technology, powerful tools in the search for the causes of dementia.



"Rapidly advancing technology helps us address fundamental questions about how and why the brain ages," Mosley said. "We've put together a world-class team of leading experts representing a range of disciplines, including brain imaging, genetics, epidemiology, and neurology, to illuminate factors that increase risk as well as those that may protect against dementia."



In light of the aging U.S. population and a strong association between age and dementia risk, Mosley said it's paramount to improve clinical care and decode the factors that contribute to and protect against dementia.



"They represent some of the greatest challenges facing our medical system over the next 50 years," he said.



The ARIC Neurocognitive Study is the foundational study of UMMC's Memory Impairment and Neurodegenerative Dementia (MIND) Center, which Mosley directs.



A separate capital campaign at UMMC is under way to raise $8.9 million for the MIND Center. As the center develops, Mosley plans to recruit additional investigators to expand research in brain aging and dementia.



Due to the grant's scope, the ARIC Neurocognitive Study is co-funded by three NIH institutes: lead sponsor National Heart, Lung and Blood Institute; the National Institute of Neurological Disorders and Stroke; and the National Eye Institute.



Source:

Jack Mazurak


University of Mississippi Medical Center

Alzheimer's Society Response To The Publication Of Revised NICE Guidance On Alzheimer's treatments

Thousands of people with Alzheimer's will continue to be denied access to the only drug treatments for the disease following the publication of revised guidance by the NICE.


The original guidance recommended that only people in the moderate stages of Alzheimer's disease should have access to drugs in the NHS, denying them to people in the early stages.


Amendments were made following a Court of Appeal decision to allow consultees access to the health economic model that NICE used in the development of the guidance and a subsequent review of this model by relevant stakeholders, including Alzheimer's Society.


Despite the concerns raised by the consultees on the flaws in the economic model, the newly published and amended Final Appraisal Determination (FAD) has not altered its original recommendations and people in the early stages of dementia will still be deprived access to effective treatments.


Neil Hunt, Chief Executive, Alzheimer's Society, says,


'Alzheimer's Society has long campaigned for the thousands of people in the early stages of dementia to be given access to the effective treatments that they are currently denied because of cost. It is completely unacceptable to deny people with dementia the only treatments that could improve quality of life for them and their carers.


We are extremely disappointed to see that the NICE guidance is essentially unchanged, despite what we feel are fundamental flaws in the economic model they have used to inform their recommendations.


The glimmer of hope is that NICE has finally committed to for a full review to address these concerns, as soon as possible. This will be little consolation for the thousands of people who will develop Alzheimer's disease this year but provides hope for the future that this incomprehensible decision will be changed. We look forward to working with NICE to ensure the problems with the current economic model are overcome and people with dementia are given a fair deal.'



Notes


- Since May 2006 three Alzheimer's drugs have been denied to people in the early stages of the disease on the NHS.


- One 1 May 2008 the Court of Appeal found in favour of Eisai / Pfizer ruling NICE should have allowed public access to the health economic model that it used to make the decision.


- On 17 June 2008 NICE sought permission from the House of Lords to appeal the Court of Appeal decision.


- The health economic model has since been shared with relevant stakeholders, including Alzheimer's Society, and comments have been fed back to NICE resulting in the publication of an ammended FAD (Final Appraisal Determination) on Thursday 11 June 2009.


- One in three people over 65 will die with dementia.


- Alzheimer's Society research shows that 700,000 people in the UK have a form of dementia, more than half have Alzheimer's disease. In less than 20 years nearly a million people will be living with dementia. This will soar to 1.7 million people by 2051.


- Alzheimer's Society champions the rights of people living with dementia and the millions of people who care for them.


- Alzheimer's Society works in England, Wales and Northern Ireland


- Alzheimer's Society needs to raise money to help people live well with dementia today and for research to find a cure for tomorrow. You can donate now by calling 0845 306 0898 or visiting alzheimers.uk


- Alzheimer's Society provides a National Dementia Helpline, the number is 0845 300 0336 or visit alzheimers.uk

Source
Alzheimer's Society

Omega-3 Supplements Affect Alzheimer's Symptoms

Omega-3 supplements can, in certain cases, help combat the depression and agitation symptoms associated with Alzheimer's disease, according to a clinical study conducted at the Swedish medical university Karolinska Institutet.



A number of epidemiological studies have shown that eating fatty fish provides a certain degree of protection against Alzheimer's and other dementia diseases - an effect often thought attributable to the omega-3 fatty acids it contains. Some studies also suggest that omega-3 can have a therapeutic effect on some psychiatric conditions.



Researchers at Karolinska Institutet and Uppsala University have now examined whether omega-3 supplementation has any effect on the psychiatric symptoms associated with Alzheimer's disease. Just under 200 patients with mild Alzheimer's were divided into two groups, one of which received omega-3, and one a placebo. The study lasted for one year.



There was no observable difference in therapeutic effect between the patients receiving the omega-3 and the placebo group. However, when the researchers took into account which of the patients carried the susceptibility gene APOE ?4 and which did not, an appreciable difference appeared. Carriers of the gene who had received active treatment responded positively to the omega-3 as regards agitation symptoms, while non-bearers of the gene showed an improvement in depressive symptoms.



The team points out that no general therapeutic recommendations can be made from the results until larger studies on individuals with more pronounced neuropsychiatric symptoms are conducted.






Publication:



Omega-3 supplementation in mild to moderate Alzheimer's disease: effects on neuropsychiatric symptoms
Yvonne Freund-Levi, Hans Basun, Tommy Cederholm, Gerd Fax?©n-Irving, Anita Garlind, Mikaela Grut, Inger Vedin, Jan Palmblad, Lars-Olof Wahlund and Maria
Eriksdotter-J?¶nhagen

International Journal of Geriatric Psychiatry, doi 10.1002/gps.1857

Published online 21 June 2007; www3.interscience.wiley/cgi-bin/jissue/112161699



For further information, please contact:



Senior Physician, PhD Student Yvonne Freund-Levi

Department of Neurobiology, Care Sciences and Society



Professor Lars-Olof Wahlund

Department of Neurobiology, Care Sciences and Society



Associate Professor Maria Eriksdotter-J?¶nhagen

Department of Neurobiology, Care Sciences and Society



Contact: Sabina Bossi


Karolinska Institutet

Cell Phone Exposure May Protect Against And Reverse Alzheimer's Disease

The millions of people who spend hours every day on a cell phone may have a new excuse for yakking. A surprising new study in mice provides the first evidence that long-term exposure to electromagnetic waves associated with cell phone use may actually protect against, and even reverse, Alzheimer's disease. The study, led by University of South Florida researchers at the Florida Alzheimer's Disease Research Center (ADRC), was published today in the Journal of Alzheimer's Disease.



"It surprised us to find that cell phone exposure, begun in early adulthood, protects the memory of mice otherwise destined to develop Alzheimer's symptoms," said lead author Gary Arendash, PhD, USF Research Professor at the Florida ADRC. "It was even more astonishing that the electromagnetic waves generated by cell phones actually reversed memory impairment in old Alzheimer's mice."



The researchers showed that exposing old Alzheimer's mice to electromagnetic waves generated by cell phones erased brain deposits of the harmful protein beta-amyloid, in addition to preventing the protein's build-up in younger Alzheimer's mice. The sticky brain plaques formed by the abnormal accumulation of beta amyloid are a hallmark of Alzheimer's disease. Most treatments against Alzheimer's try to target beta-amyloid.



The highly-controlled study allowed researchers to isolate the effects of cell phone exposure on memory from other lifestyle factors such as diet and exercise. It involved 96 mice, most of which were genetically altered to develop beta-amyloid plaques and memory problems mimicking Alzheimer's disease as they aged. Some mice were non-demented, without any genetic predisposition for Alzheimer's, so researchers could test the effects of electromagnetic waves on normal memory as well.



Both the Alzheimer's and normal mice were exposed to the electromagnetic field generated by standard cell phone use for two 1-hour periods each day for seven to nine months. The mice didn't wear tiny headsets or have scientists holding cell phones up to their ears; instead, their cages were arranged around a centrally-located antenna generating the cell phone signal. Each animal was housed the same distance from the antenna and exposed to electromagnetic waves typically emitted by a cell phone pressed up against a human head.



If cell phone exposure was started when the genetically-programmed mice were young adults -- before signs of memory impairment were apparent -- their cognitive ability was protected. In fact, the Alzheimer's mice performed as well on tests measuring memory and thinking skills as aged mice without dementia. If older Alzheimer's mice already exhibiting memory problems were exposed to the electromagnetic waves, their memory impairment disappeared. Months of cell phone exposure even boosted the memories of normal mice to above-normal levels. The memory benefits of cell phone exposure took months to show up, suggesting that a similar effect in humans would take years if cell phone-level electromagnetic exposure was provided.
















Based on their promising and unexpected findings in mice, the researchers concluded that electromagnetic field exposure could be an effective, non-invasive and drug-free way to prevent and treat Alzheimer's disease in humans. They are currently evaluating whether different sets of electromagnetic frequencies and strengths will produce more rapid and even greater cognitive benefits than those found in their current study.



"If we can determine the best set of electromagnetic parameters to effectively prevent beta-amyloid aggregation and remove pre-existing beta amyloid deposits from the brain, this technology could be quickly translated to human benefit against AD" said USF's Chuanhai Cao, PhD, the other major study author. "Since production and aggregation of ??-amyloid occurs in traumatic brain injury, particularly in soldiers during war, the therapeutic impact of our findings may extend beyond Alzheimer's disease."



The memory test used to evaluate the effects of cell phone exposure in mice was closely designed from a sensitive test used to determine if Alzheimer's disease, or its very early signs (mild cognitive impairment), are present in humans. "Since we selected electromagnetic parameters that were identical to human cell phone use and tested mice in a task closely analogous to a human memory test, we believe our findings could have considerable relevance to humans," Arendash said.



The researchers found a slight increase in brain temperature during the two one-hour periods when mice were exposed to electromagnetic waves each day. This increase in brain temperature was seen only in the Alzheimer's mice, and only after months of exposure. The researchers suggest the increase in brain temperature helped the Alzheimer's brain to remove newly-formed beta-amyloid by causing brain cells to release it.



The researchers were particularly surprised to discover that months of cell phone exposure actually boosted the memory of non-demented (normal mice) to above-normal levels. They suspect that the main reason for this improvement involves the ability of electromagnetic exposure to increase brain activity, promoting greater blood flow and increased energy metabolism in the brain. "Our study provides evidence that long-term cell phone use is not harmful to brain," Dr. Cao said. "To the contrary, the electromagnetic waves emitted by cell phones could actually improve normal memory and be an effective therapy against memory impairment"



"It will take some time to determine the exact mechanisms involved in these beneficial memory effects," Arendash said. "One thing is clear, however - the cognitive benefits of long-term electromagnetic exposure are real, because we saw them in both protection- and treatment-based experiments involving Alzheimer's mice, as well as in normal mice."



Previous human studies of electromagnetic waves from cell phones involved only brief exposures given to normal humans. While some studies reported small improvements in attention or memory (not enough to impact daily life), others reported no memory effects from short-term exposure. The new study by Arendash, Cao, and their colleagues is the first to investigate the effects of long-term electromagnetic exposure over many months on memory function in either humans or animals. The findings indicate that "long-term" exposure to cell phone level electromagnetic waves is needed to observe enhanced memory in normal or memory-impaired mice.



The USF researchers began investigating the effects of cell phone use on Alzheimer's disease several years ago, after several observational studies in humans linked a possible increased risk of Alzheimer's with "low-frequency" electromagnetic exposure -- like the energy waves generated by power and telephone lines. However, cell phones emit "high-frequency" electromagnetic waves, which are very different because they can have beneficial effects on brain cell function, such as increasing brain cell activity, Arendash said.



There has been recent controversy about whether electromagnetic waves from cell phones cause brain cancer. Some researchers argue that the risk of glioma (40 percent of all brain tumors) doubles after 10 or more years of cell phone use. However, others argue that since the overall lifetime risk of developing a brain tumor of any type is less than 1 percent, any doubling of this risk would still be very low. Groups such as the World Health Organization, the American Cancer Society, and the National Institutes of Health, have all concluded that scientific evidence to date does not support any adverse health effects associated with the use of cell phones. Consistent with the view of these organizations, the researchers found no autopsy evidence of abnormal growth in brains of the Alzheimer's mice following many months of exposure to cell phone-level electromagnetic waves. They also found all major peripheral organs, such as the liver and lungs, to be normal.



The research was conducted by an interdisciplinary group of neuroscientists, electrical engineers, and neurologists from universities in Japan and China as well as from the Florida ADRC at the University of South Florida. The study was supported by funds from the Florida ADRC, a statewide project sponsored by the National Institute on Aging, and the USF Health Byrd Alzheimer's Institute.



Journal citation:


Electromagnetic Field Treatment Protects Against and Reverses Cognitive Impairment in Alzheimer's Disease Mice. Gary W. Arendash, Juan Sanchez-Ramos, Takashi Mori, Malgorzata Mamcarz, Xiaoyang Lin, Melissa Runfeldt, Li Want, Guixin Zhang, Vasyl Sava, Juan Tan and Chuanhai Cao. Journal of Alzheimer's Disease, Volume 19:1 (January 2010).



Source:

Gary Arendash


University of South Florida Health

Genetic Link To Alzheimer's Disease Explored: Affected Siblings Sought

Indiana University School of Medicine researchers are looking for the tie that binds families with Alzheimer's disease together. The long-term research is seeking the gene or genes that make Alzheimer's a family disease.


Medical geneticist at IU and five other institutions are seeking genetic information from 1,000 families who have two or more living siblings with Alzheimer's disease.


"Indiana University has been involved in trying to determine the genetic links of Alzheimer's disease for a number of years," said Tatiana Foroud, Ph.D., the P. Michael Conneally Professor of Medical and Molecular Genetics at IU and the local principal investigator for the study. "Finding two living siblings afflicted with the disease will be a challenge, but one we hope will shed light on important information."


Participants will be asked to donate a blood sample which will be stored at the National Cell Repository for Alzheimer's Disease at IU, the only such repository in the nation.


For additional information or to enroll in the study, contact the IU Department of Medical and Molecular Genetics at 800-526-2839.


medicine.iu

Rethinking Alzheimer's Disease And Its Treatment Targets

The standard explanation for what causes Alzheimer's is known as the amyloid hypothesis, which posits that the disease results from of an accumulation of the peptide amyloid beta, the toxic protein fragments that deposit in the brain and become the sticky plaques that have defined Alzheimer's for more than 100 years.


Billions of dollars are spent yearly targeting this toxic peptide but what if this is the wrong target? What if the disease begins much earlier, fueled by a natural process? Reporting in the current edition of the journal Neurobiology of Aging, UCLA professor of psychiatry George Bartzokis argues just that and says that a better working hypothesis is the "myelin model."


"The greatest promise of the myelin model of the human brain is its application to the development of new therapeutic approaches," Bartzokis said.


Like insulation around wires, myelin is a fatty sheath that coats our nerve axons, allowing for efficient conduction of nerve impulses. It is key to the fast processing speeds that underlie our higher cognitive functions and encoding of memories.


But the lifelong, extensive myelination of the human brain also makes it uniquely vulnerable to damage. The myelin model's central premise is that it is the normal, routine maintenance and repair of myelin throughout life that ultimately initiates the mechanisms that produce degenerative diseases like Alzheimer's. That is, the amyloid-beta peptide and the tau peptide, which is also implicated in Alzheimer's, as well as the signature clinical signs of the disease, such as memory loss and, ultimately, dementia, are all byproducts of the myelin breakdown and repair processes.


"The pervasive myelination of our brain is the single most unique aspect in which the human brain differs from other species," said Bartzokis, who is a member of the Laboratory of Neuro Imaging in the UCLA Department of Neurology and a member of UCLA's Brain Research Institute. Myelin is produced by oligodendrocytes, specialized glial cells that themselves become more vulnerable with age.


Bartzokis notes that myelination of the brain follows an inverted U-shaped trajectory, growing strongly until our 50s, when it very slowly begins to unravel as we age. The myelin that is deposited in adulthood ensheaths increasing numbers of axons with smaller axon diameters and so spreads itself thinner and thinner, Bartzokis said. As a result, it becomes more susceptible to the ravages of age in the form of environmental and genetic insults and slowly begins to break down faster than it can be repaired.


The exclusive targeting of the amyloid-beta peptide for many years is understandable because the same genes and enzymes involved in controlling myelination and myelin repair are, ironically, also involved in the production of amyloid-beta proteins. Bartzokis' point is that the amyloid beta may actually develop as a result of the natural process of the repair and maintenance of myelin.















"So the breakdown that leads to Alzheimer's and other age-related brain diseases, such as Parkinson's, may begin much earlier, before the formation of the protein deposits that are used to define these diseases," Bartzokis said.


Most drugs being developed for Alzheimer's are targeting amyloid beta, but little if any clinical improvement is being seen. This is, according to Bartzokis, "similar to cleaning up a house that's been flooded by water but never repairing the actual pipe that created the flood.


"For drug development then, the targets should be much further upstream, earlier in the process before the AB plaques even develop," he said.


Instead of focusing on reducing amyloid beta, Bartzokis argues, the myelin model suggests entirely different approaches to treatment and prevention of Alzheimer's disease that precede plaque formation. With modern brain imaging technology, clinicians could track the dynamic changes taking place in the brain and intercede well before any signs of Alzheimer's are seen.


"With earlier intervention," Bartzokis said, "we could reduce and potentially eliminate the increasingly catastrophic burden of dementia on the individual and their family, the health care system, and our society."


The research was supported by the National Institutes of Health, the RCS Alzheimer's Foundation and the U.S. Department of Veterans Affairs. The author reports no conflicts of interest.


The UCLA Department of Psychiatry and Biobehavioral Sciences is part of the Semel Institute for Neuroscience and Human Behavior at UCLA, an interdisciplinary research and education institute devoted to the understanding of complex human behavior, including the genetic, biological, behavioral and sociocultural underpinnings of normal behavior, and the causes and consequences of neuropsychiatric disorders. In addition to conducting fundamental research, the institute faculty seeks to develop effective treatments for neurological and psychiatric disorders, improve access to mental health services, and shape national health policy regarding neuropsychiatric disorders.


Source: University of California, Los Angeles

Cancer Drug Model Could Be A Potential Treatment For Alzheimer's - Alzheimer's Society Comment

Treatments modelled on the cancer drug Gleevec could potentially prevent the formation of amyloid plaques - one of the major hallmarks of Alzheimer's disease according to a study.


Treatments modelled on the cancer drug Gleevec could potentially prevent the formation of amyloid plaques - one of the major hallmarks of Alzheimer's disease according to a study published in the journal Nature.


Researchers at the Laboratory of Molecular and Cellular Neuroscience in the U.S. tested the drug on mice and found that Gleevec has the ability to attach itself to a protein (GSAP). GSAP promotes the production of plaques in the brain and is therefore a potential target for anti-amyloid treatments.


Alzheimer's Society comment:


'This study provides us with exciting new information about a protein that has been found to promote the production of amyloid plaques - a major hallmark of Alzheimer's disease. Although the drug highlighted in the report targets this protein and is available and safety tested, this research is in the early stages and we are some way from this being a viable treatment for Alzheimer's.


'A million people will develop dementia in the next ten years yet dementia research receives eight times less investment than cancer research. We must invest now if we are to move forward in the development of effective Alzheimer's treatments.'


Dr Susanne Sorensen

Head of Research


Ref: Gen He et al., 'Gamma-secretase activating protein is a therapeutic target for Alzheimer's disease', Nature, 2 September 2010


Source:

Alzheimer's Society


View drug information on Gleevec.

A Drug Could Improve The Memory Of Those With Alzheimer's Disease

A drug used in a type of hereditary metabolic disorder improved the memory of laboratory animals with Alzheimer's disease. The results of the project, developed by researchers of the Center for Applied Medical Research (CIMA) of the University of Navarra have been published in the journal Neuropsychopharmacology.



The research project showed that the drug sodium phenylbutyrate, prescribed until now for patients with alterations in the urea cycle, eases the fusion of proteins responsible for neuron connections, thus increasing the learning capacity of the mice involved. As a result, these discoveries offer new, promising perspectives for the treatment of Alzheimer's Disease and other related dementias.



In addition, these findings provide a new alternative to the drugs that are currently available for fighting this devastating disease, explained Dr. Ana Garc?­a-Osta. Dr. Garc?­a-Osta is a researcher from the Department of Neurosciences and the principal author of this project.



The research team is currently focused on discovering the acting mechanism in this drug. As the drug is now clinically available and well tolerated, the confirmation of its therapeutic affectivity in humans could be applied to Alzheimer's in a shorter period of time than other drugs being studied.



Alzheimer's disease is a neurodegenerative disorder associated with age and characterized by the progressive deterioration of cognitive and intellectual abilities. "Cognitive deficit is associated with a loss of neuron connections. For the memory to develop, it is necessary for a series of cellular and molecular mechanisms to be activated. The interruption of these processes affects the capacity to assimilate and store new memories, explained Dr. Garc?­a-Osta.







Source: Oihane Lakar


Elhuyar Fundazioa

Sleep Disorder May Be Early Sign Of Dementia Or Parkinson's Disease

People with a sleep disorder that causes them to kick or cry out during their sleep may be at greater risk of developing dementia or Parkinson's disease, according to a study published in the December 24, 2008, online issue of Neurology®, the medical journal of the American Academy of Neurology.


The sleep disorder is called REM sleep behavior disorder. People with the disorder do not have the normal lack of muscle tone that occurs during REM sleep, often known as the dream stage of sleep. Instead, they have excessive muscle activity such as punching, kicking, or crying out, essentially acting out their dreams.


The study involved 93 people with this type of sleep disorder who had no signs of a neurodegenerative disease, such as dementia or Parkinson's disease. The participants were followed for an average of five years. During that time, 26 of the people developed a neurodegenerative disease. Fourteen developed Parkinson's disease, 11 developed dementia and were diagnosed with either Alzheimer's disease or Lewy body dementia. One person developed multiple system atrophy, a rare disorder that affects movement, blood pressure and other body functions.


The estimated five-year risk of developing a neurodegenerative disease was 18 percent, with the 10-year risk at 41 percent and the 12-year risk at 52 percent.


"These results are obviously of great interest to people who have this sleep disorder and their physicians and families," said study author Ronald B. Postuma, MD of McGill University in Montreal, Canada, who carried out the studies at the sleep disorders center at the Sacre Coeur hospital, University of Montreal. Postuma is also a member of the American Academy of Neurology. "The results may help us better understand how these neurodegenerative diseases develop. They also suggest that there may be an opportunity for protecting against the progression to disease, perhaps even preventing it before the symptoms can appear."


Postuma noted that the study involved only people with no known cause for the REM sleep behavior disorder. The disorder can also be caused by narcolepsy or rare brainstem abnormalities. REM sleep disorder from these causes does not necessarily carry the risk of developing a neurodegenerative disease, he said.


The study was supported by grants from the Canadian Institutes of Health Research and the FRSQ (Fonds de la recherch?© en sant?© du Quebec) in Montreal, Canada.


The American Academy of Neurology, an association of more than 21,000 neurologists and neuroscience professionals, is dedicated to improving patient care through education and research. A neurologist is a doctor with specialized training in diagnosing, treating and managing disorders of the brain and nervous system such as Parkinson's disease, ALS (Lou Gehrig's disease), dementia, West Nile virus, and ataxia. For more information about the American Academy of Neurology, visit aan.

Lipogen Food Additive Approved By FDA - Natural Ingredient Improves Brain Functions In Children And Adults

Americans looking for a natural way to improve memory and mood now have a powerful tool at their disposal. The FDA has authorized an Israeli-made product called Lipogen to be used as a food additive.


A natural functional food ingredient that improves brain functions in both children and adults, Lipogen contains phosphatidylserine (PS), a nutrient found in fish, green leafy vegetables, soybeans and rice, which goes to the brain and regulates metabolic processes such as neuronal signaling. Studies have associated the nutrient to improvements in memory and mood, and specifically linked it to delaying symptoms of early-onset Alzheimer's.


"PS is a naturally occurring material within the membranes of the cells in the brain. Generally the brain produces the required amount of the material, but age as well as the stress of modern life slows down its production," explained David Rutenberg, the founder and CEO of the Galilee-based company Lipogen which developed and produces the product.


"When it's lacking, the neurochemistry of the cells in the brain malfunction, leading to potential memory loss," he told ISRAEL21c.


According to a report issued last week, more than five million Americans are living with Alzheimer's disease, a 10 percent increase since the last Alzheimer's Association estimate five years ago - and a count that supports the long-forecast dementia epidemic as the population grays. Unless scientists discover a way to delay Alzheimer's brain attack, some 7.7 million people are expected to have the disease by 2030, the report says. By 2050, that toll could reach 16 million.


"Lipogen PS simply recuperated the loss of the material in the brain. It's effective for memory functions. Memory degradation with age isn't considered a disease but a natural process of getting older. Therefore, it's not regarded as medicine. We regard Lipogen PS as the brain vitamin," said Rutenberg.


Lipogen began developing its vegetarian and kosher PS products in 1992, focusing on natural mental health solutions for dietary supplements or for enhancing foods and beverages. Rutenberg explained that prior to the company's start; the difficulty that has existed in bringing PS substance to the market has primarily been due to supply source. The only commercially available PS was derived from cow's brain (BCPS - Bovine Corte Phosphatidylserine). However, Lipogen introduced soy lecithin PS, whose enzymatic reaction process utilizes cabbage enzyme.


"We were the first to produce Lipogen PS from soya lecithin in substantial amounts at competitive prices. It's administered orally, in tablet or capsule," he said.


Lipogen PS has been clinically tested in double-blind, placebo-controlled studies. The research showed significant memory and mental improvements in comparison to the placebo groups. The results also showed that dietary supplementation with PS can play a vital role in supporting human cognitive functions as we age. Among the numerous studies conducted with PS, most were concerned with subjects already experiencing noticeable declines in judgment, abstract thought, memory, behavior, and personality


In Israel, where Lipogen PS is marketed under the brand name L-Telect, no side effects or any adverse events were reported. "Israelis have been using Lipogen for several years - we're popular in health food stores and pharmacies," said Rutenberg. "But the market is not in Israel, it's in America."


In 2003, the FDA recognized the validity of Lipogen and allowed it to have a certified health claim that it 'may reduce the risk of cognitive dysfunction in the elderly', said Rutenberg. "It was sold over the counter as a dietary supplement."


Now, the FDA has issued a 'no questions' approval following Lipogen's self-affirmed generally recognized as safe (GRAS) status notification for PS.


"With this new ruling by the FDA, Lipogen can now be introduced into food as a functional ingredient. It's a major breakthrough," said Rutenberg.


As a result, Lipogen has announced it is increasing production of its Lipogen PS patented product line for the food and beverage fortification, and dietary supplement markets in the US.


"We're looking forward to cooperating with food companies to introduce Lipogen as a functional ingredient in order to make the food more beneficial for children and adults alike," said Rutenberg who's been traveling back and forth to the US meeting with major food companies. "We have a lot of interest."


lipogen.co.il


News Source: israel21c

Preliminary New Blood Test To Detect Alzheimer's Disease Uncovered

UT Southwestern Medical Center scientists have helped develop a novel technology to diagnose Alzheimer's disease from blood samples long before symptoms appear.


This preliminary technology, which uses synthetic molecules to seek out and identify disease-specific antibodies, also could be used eventually in the development of specific biomarkers for a range of other hard-to-diagnose diseases and conditions, including Parkinson's disease and immune system-related diseases like multiple sclerosis and lupus, the researchers predict.


"One of the great challenges in treating patients with Alzheimer's disease is that once symptoms appear, it's too late. You can't un-ring the bell," said Dr. Dwight German, professor of psychiatry and an author of the paper published in the Jan. 7 edition of Cell. "If we can find a way to detect the disease in its earliest stages before cognitive impairment begins we might be able to stop it in its tracks by developing new treatment strategies."


Because patients with Alzheimer's disease (AD) exhibit immune system activation and neurodegeneration in several brain regions, researchers in the study hypothesized that there may be numerous antibodies in the serum of affected patients that are specific to the disease and can serve as a biomarker.


Antigens substances such as protein from a virus or bacteria that triggers an immune response traditionally have been necessary for the discovery of antibody biomarkers. It has been impossible previously to identify an antibody (a type of targeted immune molecule) without first knowing the antigen that triggers its production.


The new study, however, challenges conventional wisdom and uses synthetic molecules (peptoids) rather than antigens to successfully detect signs of disease in patients' blood samples. These peptoids have many advantages; they can be modified easily and can be produced quickly in relatively large amounts at lower cost.


The adaptive immune system is thought to be a rich source of protein biomarkers, but diagnostically useful antibodies remain undiscovered for a large number of diseases, Dr. German said. This is, in part, because the antigens that trigger an immune response in many diseases are unknown. The technology behind this discovery is essentially an immune-system reader, which is designed to pick out antibodies without knowing in advance which ones to look for.


The researchers used a combination library of several thousand peptoids to screen serum samples from mice with multiple sclerosis-like symptoms as well as from healthy control mice. The particular peptoids that retained more antibodies from the blood samples of the diseased animals were identified as potential agents for capturing diagnostically useful molecules.


The investigators then examined serum samples from six AD patients, six healthy patients and six patients with Parkinson's. Three peptoids were identified that captured six times the IgG antibody levels in all of the Alzheimer's patients when compared to the control group or to the Parkinson's patients. Two of the peptoids were found to bind the same IgG antibody, while the third was shown to bind to different antibodies meaning there are at least two candidate biomarkers for AD. Using an additional set of 16 normal control subjects and 10 subjects at the very early state of AD, the three candidate biomarkers identified AD with 90 percent accuracy.


"The results of this study, though preliminary, show great potential for becoming a landmark," said Dr. German.


Other UT Southwestern researchers involved in the study were Dr. Ramon Diaz-Arrastia, professor of neurology and neurotherapeutics; Steven Connell, research technician; and Dr. Linda Hynan, professor of clinical sciences. Others include senior author and former UT Southwestern faculty member Dr. Thomas Kodadek, now at Scripps Florida Research Institute; Dr. Anne Gocke, former postdoctoral fellow in translational medicine; and researchers with Opko Health Laboratories.


Source: UT Southwestern Medical Center

Alzheimer's Society Comment On Research Linking High Blood Pressure To Memory Problems

Data in a recent study published in Neurology, the medical journal of the American Academy of Neurology links elevated diastolic blood pressure to the cognitive impairment of people over 45


The study of nearly 20,000 people aged 45 (average age 65) found that people with high diastolic blood pressure, the bottom number of a blood pressure reading, were more likely to have cognitive impairment or problems with their memory than people with normal readings.


Previous research has demonstrated that people with high blood pressure have an increased risk of developing dementia later in life.


High blood pressure affects one in three adults in the UK with a quarter of people not aware that they have it.


'This large study adds weight to the growing body of evidence that high blood pressure can be linked to cognitive impairment. Now further study is needed to establish why these two factors could be linked.


'Alzheimer's Society recommends that you can reduce your blood pressure by exercising regularly, eating healthily and not smoking. High blood pressure can often also be controlled by medication so if you're not sure what your blood pressure is or haven't had it checked recently you should visit your GP to have it measured.'


Dr Susanne Sorensen

Head of Research

Alzheimer's Society


Reference: 'Association of higher diastolic blood pressure levels with cognitive impairment' G Tsivgoulis, MD, A.V Alexandrov, MD et al (Neurology, 25 August 2009)



Source

Alzheimer's Society

Cocoa Flavanols Linked To Improved Brain Blood Flow

Cocoa flavanols, the unique compounds found naturally in cocoa, may increase blood flow to the brain, according to new research published in the Neuropsychiatric Disease and Treatment journal. The researchers suggest that long-term improvements in brain blood flow could impact cognitive behavior, offering future potential for debilitating brain conditions including dementia and stroke.



In a scientific study of healthy, older adults ages 59 to 83, Harvard medical scientists found that study participants who regularly drank a cocoa flavanol-rich beverage made using the Mars, Incorporated Cocoapro® process had an eight percent increase in brain blood flow after one week, and 10 percent increase after two weeks.



In this first-of-its-kind study, the researchers found both short and long-term benefits of cocoa flavanols for brain blood flow, offering future potential for the one in seven older Americans currently living with dementia. When the flow of blood to the brain slows over time, the result may be structural damage and dementia. Scientists speculate that maintaining an increased blood flow to the brain could slow this cognitive decline.



"The totality of the research on cocoa flavanols is impressive. This is just one more study adding to an increasing body of literature connecting regular cocoa flavanol consumption to blood flow and vascular health improvements throughout the body," said Harold Schmitz, Ph.D., chief science officer at Mars, Incorporated, which has supported research on cocoa flavanols for more than 15 years. "Though more research is needed, these findings raise the possibility that flavanol-rich cocoa products could be developed to help slow brain decline in older age."



The Body of Evidence



Contrary to statements often made in the popular media, the collective research demonstrates that the vascular effects of cocoa flavanols are independent of general "antioxidant" effects that cocoa flavanols exhibit in a test tube, outside of the body. While research aimed at studying the potential role of cocoa flavanols in the context of blood vessel and circulatory function continues, a number of previously published studies already suggest that the consumption of cocoa flavanols can have important beneficial effects on the function of the body's network of blood vessels. The body of research not only suggests that cocoa flavanols may provide a dietary approach to maintaining cardiovascular function and health, but also points at new possibilities for cocoa flavanol-based interventions for vascular complications associated with cognitive performance, skin health and age-related blood vessel dysfunction.



Future Cocoa Flavanol Research Directions



For more than 15 years, Mars, Incorporated has conducted and/or supported a significant portion of the research undertaken in the field of cocoa flavanols and reported new insights in peer-reviewed scientific literature. Working in collaboration with top research institutions around the world, Mars, Incorporated continues to lead the way in exploring the nutritional and medical potential of cocoa flavanols. Mars' commitment to rigorous scientific research of cocoa and flavanols is evidenced by more than 100 peer-reviewed research publications and more than 80 patents held by the company. Mars also developed and patented the breakthrough process called Cocoapro® that helps retain more of the naturally occurring flavanols in cocoa. The high-flavanol cocoa powders made using the Mars Cocoapro® process are thoroughly characterized in terms of nutrient content, as well as standardized with respect to flavanol level and flavanol profile. Through the newly created Mars Botanical division, Mars will continue to develop and apply industry-leading analytical techniques and standards to further investigate the biomedical potential of cocoa flavanols. For more information on the many research studies on cocoa flavanols, click here.
















Source: Sorond FA, Lipsitz LA, Hollenberg NK, Fisher NDL. Cerebral blood flow response to flavanol-rich cocoa in healthy elderly humans. Neuropsychiatric Disease and Treatment. 2008;4:433-440.






About Mars, Incorporated



Mars, Incorporated, headquartered in McLean, Virginia is a family-owned company with a strong commitment to science-based research. With more than 15 years of research into the health effects of cocoa flavanols, and decades of research invested into improving the cocoa plant and farming techniques, Mars, Incorporated has become the global leader in cocoa research. For more information, visit cocoapro. For more information about the Mars, Incorporated cocoa sustainability program, click here.



About Mars Botanical



Mars Botanical, headquartered in Rockville, Maryland, is a newly-established division of Mars, Incorporated. The mission of Mars Botanical is to further develop leading edge science and technologies in the field of phytonutrients with the goal of creating new plant-derived products aimed at improving human health, and do so in a sustainable way that helps both farming communities and their local environment. Mars, Incorporated scientists and colleagues at leading research institutions are dedicated to unlocking the full nutritional and medical potential of cocoa flavanols. For more information, click here.



Source: Lori Fromm


Weber Shandwick Worldwide

Alzheimer's And Intelligence

"Fish oil brain boost," is the headline in the Daily Mail . The paper says that a "breakthrough in the battle against Alzheimer's is being claimed by British scientists who believe it can be fought with omega-3 oils". The newspaper adds that "older people whose diets are rich in omega-3 oils do better in mental tests than those without the oils in their diets".


The story is based on a study that investigated people aged about 66 to 68 years who had taken an intelligence test at school when they were 11. The researchers looked at whether there was any link between the fatty-acid content of some of these people's red blood cells and their performance in that intelligence test and in later assessments of cognition. The study was not set up to establish whether there was any effect of dietary fatty acids on improved intelligence or brain activity. The only way to address this particular question is through further randomised controlled trials.


Where did the story come from?

Dr Lawrence Whalley and colleagues from the University of Aberdeen, the University of Edinburgh, Robert Gordon University, the University of Dundee and the Rowett Research Institutes carried out this research. The study was funded by the Wellcome Trust and the Alzheimer's Research Trust. It was published in the American Journal of Clinical Nutrition, a peer-reviewed medical journal.


What kind of scientific study was this?

The study was a retrospective cohort study of Scottish people who had taken an intelligence test called the Moray House Test at school in 1947 when they were 10 to 11 years old. Those people who were still alive and were living independently in the community in good general health between November 1999 and February 2002 were identified from local health registers. They were then invited to participate in this follow-up study. Of the original 660 people who were invited to take part, 506 (76%) agreed to, and data was available for 478 participants. These people were interviewed and demographic and dietary information (including the use of fish-oil supplements) was recorded. The participants were invited for further assessment when they were aged between 66 and 68 years old (i.e. about two years later); overall, 289 people participated in all three assessments.


At each follow up assessment, cognitive testing was performed (to screen for dementia), as well as tests of verbal memory and non-verbal reasoning as well as executive function, psychomotor performance and constructional ability. Blood was taken and the DNA was analysed to determine whether a gene that is known to increase susceptibility to Alzheimer's - APOE ?µ4 - was present.


The fatty acid content of blood cells (n-3 PUFA - a type of fatty acid found in fish oils) was measured in a subgroup of participants (120 people, equal numbers of fish-oil supplement users and non-users). The researchers looked at whether there was an association between the n-3 PUFA content of cells and ability at both 11 years old and at 63 to 65 years. They also looked at whether carrying the APOE ?µ4 gene had any effect on the relationship between the level of fatty acids in the cells and general ability. Genetic data was only available for 113 people.















What were the results of the study?

The researchers found that in people who were carrying the gene variant APOE ?µ4, total fatty acid concentrations were not linked to general intelligence at age 11 or at age 64 years. In people who did not have the APOE ?µ4 gene, the high total fatty acid content and "intelligence" at age 11 and 63-65 were significantly linked. When they analysed the components of 'total' fatty acid separately, they found that both n-3 PUFA and DHA (another fatty acid which is found in fish oils) were significantly associated with higher scores. However, the link with DHA was no longer significant when researchers took into account other factors that might be responsible such as gender and gene variant status.


What interpretations did the researchers draw from these results?

The researchers conclude that cognitive testing at age 11 and at follow up were linked to total fatty acid content in the cells (of n-3 PUFA and DHA - both of which can come from fish oils).


What does the NHS Knowledge Service make of this study?

It is difficult to interpret this study. There are several points to keep in mind:


- The researchers say that people with better functioning are more likely to have stayed in the study. This would mean that the people available for analysis at the end of the study aren't truly balanced and don't represent the distribution of characteristics in the starting population. The researchers believe this didn't have much of an effect on their results. For measures of fatty acid, this imbalance may have less of an effect because their sample for this aspect of the testing was not random (i.e. they selected equal numbers of people who took fish oil supplements and those who didn't).


- The researchers found a link between cognitive benefits and the concentration of the fatty acid n-3 PUFA in the red blood cells only in the absence of a gene variant that is associated with increased risk of Alzheimer's disease (APOE ?µ4). The researchers put forward some theories for why this might be the case, all of which need to be assessed in further studies. The researchers acknowledge that as they only had genetic data from 38 carriers of this gene variant, their study is not large enough to detect any real differences if they are there. This again suggests that more research is needed to clarify this issue.


- Importantly, though the researchers say that they collected information on diet, they do not set out to establish any link between consumption of fish oils or any element of diet and cognitive performance or intelligence. Their focus is on the link between the content of fatty acids in red blood cells and these outcomes. Although other studies may explore the relationship between fish oil intake and the concentration of these fats in the cells, this one did not. In fact, in their discussion, the researchers state clearly that though the association they found between better cognitive performance in later midlife and higher concentration of fatty acids in red blood cells may be explained by "a life-long healthier lifestyle that includes a diet rich in marine oils or supplementation with n-3 PUFAs and many other micronutrients, or both". Though they conclude that this seems an unlikely explanation of the results reported here, it isn't clear whether this is a valid explanation.


- When assessing "cognitive benefits", the researchers combined the results from all six tests they performed during the follow ups. The appropriateness of assuming that a single "general cognitive trait" (common to each of the tests) was being measured and combining all these test results into a single representative score is unclear.


Overall, this study provides some evidence of an interaction between a gene and the environment that affects cognition during advancing age. It isn't clear how the study's weaknesses should affect the interpretation of the results, but perhaps the most important point is that this study was not looking directly on the effect that dietary fish oils could have on cognition.


Links to the headlines


Fish oils offer Alzheimer's disease hope. The Scotsman, April 7 2008

Fish oil brain boost. Daily Mail, April 7 2008


Links to the science


n-3 Fatty acid erythrocyte membrane content, APOE ?µ4, and cognitive variation: an observational follow-up study in late adulthood.
Whalley LJ, Deary IJ, Starr JM, et al.
Am J Clinical Nutrition2008; 87:449-454

This news comes from NHS Choices

What Celebrity Names Can Reveal About The Onset Of Alzheimer's Disease

Research that is targeting the early diagnosis of Alzheimer disease has drawn national attention to the work of Michael Seidenberg, PhD, a faculty member at Rosalind Franklin University of Medicine and Science.


Dr. Seidenberg, a professor in the university's Department of Psychology, is the lead author of an article in the journal Neurology detailing a study that maps the brain activity of 69 healthy senior men and women, aged 65-85, including some at higher risk for Alzheimer's disease, as they distinguish between famous and unfamiliar names.


Participants were divided into three groups: those with no risk factors for Alzheimer's disease, those with a family history of the disease but no genetic risk factors and those who not only have relatives diagnosed with Alzheimer's, but who also carry the apolipoprotein e4 gene, which studies have shown increases the risk of developing the disease.


Published in late August, the two-year study created a flurry of interest among national media outlets including online editions of Time and Newsweek, for its use of celebrity names in gauging how much effort brains expend in retrieving information stored in the brain areas associated with memory.


Researchers used functional magnetic resonance imaging, or fMRI, which offers a view of brain activity related to a specific task or neural region. While lying in the scanner, participants signaled recognition as they listened to a list of 60 names, half of them well known - people like Albert Einstein, Britney Spears, George Clooney and Marilyn Monroe ??" and half of them obscure or unfamiliar.


The results were compelling. The control group, which had no risk factors, exhibited increased brain activity when confronted with unfamiliar names. But it was the opposite for those at high risk. They showed higher levels of activation when recognizing famous names.


"Even though they are getting to the information as accurately as people with no risk factors, their brains are doing something differently," Dr. Seidenberg said. "The way we're beginning to view this is it's a compensatory mechanism to allow them to perform the task. More activity reflects that different brain areas are contributing."


That hypothesis will be tested by Dr. Seidenberg and his research partners, scientists from the Cleveland Clinic, Wayne State University and the Medical College of Wisconsin, when they study another group of subjects who will react to a new list of names. The research team will examine the changes in brain activity which has taken place since the original fMRI session.


Funded by the National Institutes of Health, the study is one of a series begun approximately seven years ago, according to Dr. Seidenberg. "We have hypothesized that you do get different patterns of activity on fMRI as you look at people at risk for developing dementia," Dr. Seidenberg said. "Bringing this group back allows us to look at people who are becoming symptomatic ??" that are experiencing day-to-day memory problems ??" and see what happens over time to their brain activity."















A future phase of the research will include a clinical drug trial in which at-risk subjects will take a medication which has been shown to have some success in alleviating symptoms of Alzheimer's. Researchers will again administer fMRI to measure brain activity during a name recognition task.


This research is at the frontier of treatment for a disease that poses an increasing threat to the world's aging population. The Alzheimer's Association estimates that 5.3 million people in the U.S. and 35 million people worldwide are living with Alzheimer's disease and dementia. According to the 2009 World Alzheimer Report, released by Alzheimer's Disease International, the number of people with Alzheimer's is expected to nearly double every 20 years, to 65.7 million in 2030 and 115.4 million in 2050.


"It's a very important topic given the escalating costs both to society and the individual," Dr. Seidenberg said. "We've learned so much in the last 10 years but we have a great deal still to learn. The advent of new technologies like fMRI has provided a new avenue to pursue the issue."


Dr. Seidenberg hopes the "name game" will ultimately help delay the onset of Alzheimer's by identifying people well before they manifest symptoms including confusion or memory loss.


"There's the notion that people are in some pre-Alzheimer dementia state for several years before they actually become symptomatic in terms of overt memory problems," Dr. Seidenberg said. "If we can get people before they become symptomatic using these techniques, we will be in a better position to successfully treat them and to delay the onset of the disease."


A nationally respected researcher in clinical neuropsychology, Dr. Seidenberg teaches courses in brain behavior relationships and neuropsychological assessment. He notes the connection between the genetic component of his team's research and British researcher Dr. Rosalind Franklin's work to identify the double-helix structure of DNA, which ultimately revolutionized medical and genetics research. "Among the risk variables we're looking at is people who have a certain genetic susceptibility," Seidenberg said.


The scientist is pleased that his research is bringing enhanced national visibility to Rosalind Franklin University of Medicine and Science. "I feel very fortunate to be collaborating with other researchers from major institutions around the country on work that is really remarkable," he said.


Source

Rosalind Franklin University of Medicine and Science