Good news for Alzheimer's

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LATimes

Five million Americans have Alzheimer's, a scourge of a disease that is hard to diagnose, harder to predict and, so far, unpreventable and incurable. There is no chemotherapy for Alzheimer's. And the drugs that are prescribed are more like bandages on a bleeding wound than the powerful cocktails that tame HIV.

The greatest risk factor for the disease is simply getting old — an unsettling thought for the first wave of baby boomers turning 65 this year. One study estimates that 7,000 to 10,000 baby boomers will hit that milestone every day for the next 19 years.

But there was some heartening news last week: An advisory committee to the FDA unanimously approved the use of a chemical dye that highlights, on imaging scans, the plaque in the brain that is the telltale sign of encroaching Alzheimer's.

This might not seem like really good news. A test reveals that you'll get a disease that steals your memory and, ultimately, leaves you dysfunctional, and there's little you can do except maybe set aside some money for future caregivers. Not to mention the ethical problems: Could you lose your job if the test results become known? Or your health insurance?

Those thorny issues will all have to be dealt with. But it will be worth it. Scientists say that identifying the disease in its early stages is important in treating it. Experts think that changes in the brain start as long as 20 years before a person shows signs of Alzheimer's.

Ron Reagan claims in his new book about his father that the late president showed signs of Alzheimer's before leaving office. That has been vigorously denied by former aides. And Reagan the younger is not a doctor. But his father, who died of the disease in 2004, remains one of its most public faces.

Today, every statistic about Alzheimer's is up. Heart disease still kills more people than any other disease, but the number of deaths attributed to it went down 11.1 percent from 2000 to 2006. In that period, the number attributed to Alzheimer's went up 46.1 percent.

According to statistics from the National Institutes of Health, estimated funding for Alzheimer's in fiscal year 2011 is $480 million. For cancer, it's more than $6 billion. Only a small percentage of worthy Alzheimer's research projects receives NIH funding. That should change. Meanwhile, more people — both diagnosed and not at risk — should participate in current research studies that need more subjects so that brain-scan diagnosis won't inevitably mean a grim demise

Better Brain Scan to Detect Alzheimer's Approved by the FDA

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Daily Rosatta

U.S. Food and Drug Administration advisory panel said Thursday that it has recommended a new brain scan procedure that can detect Alzheimer’s disease, as long as doctors receive additional training to use it.

The FDA expert panel said that they have voted 16 to 0 to recommend approval of the imaging agent, known as Amyvid, made by US pharmaceutical giant Eli Lilly. The panel also revealed that the process involves injecting the Amyvid followed by an imaging scan that can detect plaque, or beta-amyloid aggregates, that indicate the presence of Alzheimer’s.

FDA suggested that a training program would be implemented to prove its usefulness and reliability in a real-world setting before it’s ready for clinical use.

“The FDA wants the company to first take a look at the data and make sure there is reliability in the data analysis. And second, to implement a training program for radiologists and technicians on how they are going to interpret the scan results in order to give a positive or a negative result,” said Alzheimer’s Association’s Maria Carrillo, who attended the FDA meeting and gave public testimony during the hearing.

Alzheimer’ disease, which has no cure, affects around five million Americans and 26 million people worldwide.

Geriatric Study Tour in Eilat

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Melabev

Melabev's Institute for the Study of Aging

Invite you to the 4th Annual Geriatric Study Tour

to be held Feb. 22-24 2011 in Eilat.

Three full days of site visits for professionals to geriatric facilities and meetings with renowned lecturers. See state of the art facilities for care of the elderly in this town best known for its tourist attractions.

Come back to work with fresh ideas.

For more information: melabev1@gmail.com

Read for program details.

Computer game dramatically helps those with Alzheimer's

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By ARIEH O’SULLIVAN
Jerusalem Post

As incidence of the incurable disease grows, experts look for new ways to slow its progress, like the Savyon computer game.

Immaculately dressed elderly men and women shuffle into the main hall and take their seats at the tables, some smiling and jabbering away, others more subdued with a vacant look in their eyes, as they begin their day at an Alzheimer’s day care center in Jerusalem.

“Staying at home kills these people,” said Motti Zelikovitch, director-general of Melabev, Israel leading organization caring for individuals with Alzheimer’s disease. “The center is better because you’re forced to get out of their home, you have to dress nicely. You come. You see your friends. Even if you don’t remember your friend from one day to the next, you see them and that helps.”

One-by-one, the men and women are led to a computer room where they sit in front of a screen and play a new game designed to maintain and improve memory in people afflicted early- and middle-stage Alzheimer’s. Alzheimer's disease causes loss of memory and other cognitive functions, and, ultimately, death.

“You’re going to build a circle with three pieces, so which piece goes over here?” an instructor asks one patient. The woman, an elderly immigrant from Switzerland, begins using the computer to assemble the circle.

While there is no cure for Alzheimer’s, Israeli researchers have developed a computer game that say can slow down the progress of the disease. It’s called Savyon, and Israel hopes to export it to treat Alzheimer’s patients around the world.

It is for innovations like these that the Alzheimer’s Foundation International (AFI) has come to Israel. The organization recently signed an agreement to include Israel’s Alzheimer’s Foundation as one of its members in an effort to boost research and share best practices related to treatment and care.

“Alzheimer’s is horrendous and it is the one thing that all nations share at this moment. It is the one situation that is causing the most turmoil for governments, for organizations and also for families all over,” Eric Hall, AFI’s chief executive officer, told The Media Line.

“Regrettably, there’s no cure, so in the meantime care becomes a priority and programs and services are really necessary. Support resources for family members are really important,” Hall said. “What the AFI hopes to do is to move from country to country and gather resources that then can be made available in a greater way to a community.”

Share / SaveEmailAdd to FavoritesStumbleUponLinkedInFacebookAOL MailGoogle GmailMySpaceTechnorati FavoritesYahoo MailDeliciousYahoo Immaculately dressed elderly men and women shuffle into the main hall and take their seats at the tables, some smiling and jabbering away, others more subdued with a vacant look in their eyes, as they begin their day at an Alzheimer’s day care center in Jerusalem.

“Staying at home kills these people,” said Motti Zelikovitch, director-general of Melabev, Israel leading organization caring for individuals with Alzheimer’s disease. “The center is better because you’re forced to get out of their home, you have to dress nicely. You come. You see your friends. Even if you don’t remember your friend from one day to the next, you see them and that helps.”

One-by-one, the men and women are led to a computer room where they sit in front of a screen and play a new game designed to maintain and improve memory in people afflicted early- and middle-stage Alzheimer’s. Alzheimer's disease causes loss of memory and other cognitive functions, and, ultimately, death.

“You’re going to build a circle with three pieces, so which piece goes over here?” an instructor asks one patient. The woman, an elderly immigrant from Switzerland, begins using the computer to assemble the circle.

While there is no cure for Alzheimer’s, Israeli researchers have developed a computer game that say can slow down the progress of the disease. It’s called Savyon, and Israel hopes to export it to treat Alzheimer’s patients around the world.

It is for innovations like these that the Alzheimer’s Foundation International (AFI) has come to Israel. The organization recently signed an agreement to include Israel’s Alzheimer’s Foundation as one of its members in an effort to boost research and share best practices related to treatment and care.

“Alzheimer’s is horrendous and it is the one thing that all nations share at this moment. It is the one situation that is causing the most turmoil for governments, for organizations and also for families all over,” Eric Hall, AFI’s chief executive officer, told The Media Line.

“Regrettably, there’s no cure, so in the meantime care becomes a priority and programs and services are really necessary. Support resources for family members are really important,” Hall said. “What the AFI hopes to do is to move from country to country and gather resources that then can be made available in a greater way to a community.”

The Alzheimer’s population is growing in developed countries as baby boomers enter old age and the elderly population grows, according to Hall,. Some11,000 Americans turn 65 everyday, and one in eight will be afflicted by Alzheimer’s. It is estimated that 35.6 million people worldwide have dementia, and the incidence is expected to increase to 115 million by 2050. An estimated five million Americans suffer from the disease while in Israel there are some 200,000 diagnosed patients. Zelikovitch estimates that another 200,000 cases are undetected.

“Alzheimer’s is truly going to be a pandemic in most countries, where mortality occurs in peoples’ seventies, eighties and nineties,” Hall said. “It‘s a disease that doesn’t discriminate. It’s a crisis. And, with the absence of a cure, we really need to figure out how we are going to recognize its impact. AFI’s vision is simply that no one country, no one government can do this by themselves and that perhaps a unified international effort is the most beneficial.”

The AFI has a vision to boost awareness of the disease and to scour the world to look for better treatment and innovations that can be shared. From Jerusalem, Hall was to travel to France to examine their treatment practices and possible innovations.

The Israeli Savyon computer program is currently available in Hebrew, English, Spanish, French and Greek. Developed over a decade at Ben Gurion University of the Negev, the program looks much like a child’s mathematical tutorial. But, researchers say, it is specifically designed to spark the brains of Alzheimer’s patients.

“If a patient works with this computer program two or three times a week for half an hour at a time, Alzheimer’s can be stabilized or slowed down. It’ not going to go away, but it can be stabilized or slowed,” Zelikovitch told The Media Line.

Too much iron, too much Alzheimer's

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FoodConsumer

Too much iron may increase risk of Alzheimer's disease, according to studies.


Iron deficiency may result in low production of hemoglobin and myoglobin that are involved in the transport and storage of oxygen. Iron is also involved in electron transport and energy metabolism, antioxidant and beneficial pro-oxidant functions, oxygen sensing and DNA synthesis as an enzyme known as ribonucleotide reductase needs iron.


But high intake of iron can be risky. Excess iron has been associated with cardiovascular disease, cancer, type 2 diabetes and metabolic syndrome, neurodegenerative disease and drug interactions.


Salvador GA and colleagues from Biochemical Research Institute of Bahía Blanca in Argentina reported in the Dec 2010 issue of international Journal of Alzheimer's disease that accumulation of transition metals copper, zinc, and iron is linked with the pathogenesis of several neurodegenerative disease.


The authors said high iron concentration was consistently found in the brains of patients with Alzheimer's disease or Parkinson's disease.


Animal-based foods high in iron include beef, children dark meat, oysters, shrimp, and tuna. Plant-based foods high in iron include black-strap molasses, raisin bran cereal, and prune juice, potato with skin, kidney beans, lentils, tofu and cashew nuts.


David Liu

Promising treatment for Alzheimer's

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WVU finds promising treatment for Alzheimer's

Researchers take potential first step to cure brain degeneration

By Veronica Nett

The Charleston Gazette

CHARLESTON, W.Va.-- West Virginia researchers have found a promising treatment that might reverse the debilitating effects of Alzheimer's disease, and offer the first step toward a potential cure for the more than 5 million Americans who suffer from it.



In a study published this month in the Journal of Neuroscience, researchers at the Blanchette Rockefeller Neuroscience Institute have found the potential root cause of Alzheimer's, and a way to treat the symptoms of the disease.





The degeneration of synapses -- the point of connection between two nerve cells -- in the brain plays a critical role in the development of dementia in Alzheimer's patients, said Dr. Daniel Alkon, co-author of the study and scientific director of the BRNI at the West Virginia University Robert C. Byrd Health Sciences Center.





For decades, though, the thrust of research and pharmaceutical development has not been toward synapses loss but trying to reduce the amyloid plaques and neurofibrillary tangles - twisted fibers found inside the brain's cells - that form in the brain after the loss of synapses, Alkon said.





"Alzheimer's disease is not primarily a disease of plaques and tangles, as many had previously concluded," Alkon said. "It is most importantly a disease of synapses."





Alkon and his team are the first to achieve a fundamental molecular understanding of how synapses are lost in Alzheimer's patients before the plaques and tangles develop.





"In a way, I think we have the first comprehensive picture of the cause of this disease," Alkon said. "We're virtually looking at the entire picture. We're not looking at one aspect, not the plaques or the tangles or the synapses, we're looking at all of it, and by treating the target, we treat everything at once."

By targeting synapses loss, researchers have found a potential way to stop the development of plaques and tangles in the brain that contribute to dementia and other hallmarks of Alzheimer's, "virtually eliminating all other elements of the disease," Alkon said.

Researchers found that the use of Bryostatin and similar compounds target the enzyme PKCe, which controls the creation of synapses at the molecular level, Alkon said.






The compounds promoted the growth of new synapses and preserved existing synapses in the brain, Alkon said. They also stopped the decrease of PKCe and the increase of soluble Beta amyloid, meaning that the treatments could be used to prevent formation of plaques and tangles in the brain, he said.





The neuroscience institute has received approval to begin clinical testing of Bryostatin to treat the symptoms of Alzheimer's, and will begin testing in the next several months.





Researchers at the institute also are developing a skin test to identify Alzheimer's in patients during the early stages of the disease.





"Detection early and a vaccine to stop degeneration -- it's a potential cure, Alkon said."





The synaptogenic drugs designed by researchers at the institute also have potential in the treatment of traumatic brain injury and stroke, Alkon said.





"The potential is great," Alkon said. "We need to get clinical trials going. We feel the sooner we can get this to the patients, the better."

Neuroscientist says spatial strategies can reduce risk of dementia

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Véronique Bohbot, PhD., neuroscientist at the Douglas Mental Health University Institute and associate professor at McGill University, leads studies on navigational strategies. She presented her findings at the recent meeting of the Society for Neuroscience in San Diego, which could bring light into how we can make better use of our hippocampus in order to reduce the risk of dementia.

Why it is better to use a spatial strategy - Summary of findings

In her lab, Bohbot and her team used virtual navigation to conduct a series of studies. It was shown that, in healthy older adults:

1) Participants using spatial strategies had reduced risk of dementia as assessed with the MoCA© (The Montreal Cognitive Assessment is a cognitive screening test designed to assist Health Professionals for detection of mild cognitive impairment)

2) Spatial strategies significantly correlated with grey matter in the hippocampus.




3) Only the people who used spatial strategies showed significant fMRI activity in the hippocampus during a virtual navigation task that allowed for both spatial and response strategies.



Two strategies used by our brain



When we find our way in the world, we rely on one of two strategies. One is spatial strategy, in which we build cognitive maps using relationships between landmarks to help us determine where we are but also help us plan where we want to go (for instance, you will memorize the spatial relationship between the market, home and school such that you can take shortcuts when going to novel destinations). The other one is a stimulus-response strategy, which is kind of an auto-pilot mode (after some repetition, you make a series of right and left turns out of habit like going to work every day using the same route. Sometimes you get there out of habit without knowing what you saw on the way). When you use a GPS, you don't necessarily use your spatial memory.



Significant results



"These results are in agreement with the literature showing that the first symptoms of Alzheimer's disease involve problems with spatial orientation as well as the literature that shows that decreased volume in the hippocampus is a risk factor for conversion from mild cognitive impairment to Alzheimer's disease." adds Bohbot.



Source: DOUGLAS MENTAL HEALTH UNIVERSITY INSTITUTE

Bad teeth, bad memory

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US News and World Report

Healthday News--Elderly people who lose their teeth may be at increased risk for dementia, researchers have found.




The new study included more than 4,000 Japanese participants, 65 and older, who underwent a dental examination and a psychiatric assessment. Compared with participants who still had many of their natural teeth, those with fewer or no teeth were much more likely to have experienced some memory loss or have early-stage Alzheimer's disease.





The findings were published online Dec. 31 in Behavioral and Brain Functions.



Participants with symptoms of memory loss tended to report that they had visited the dentist rarely, if at all. Dr. Nozomi Okamoto, the study's principal investigator, said that this may be one explanation for the study's findings but suggested that there may be other links between tooth loss and memory problems.



"Infections in the gums that can lead to tooth loss may release inflammatory substances, which in turn will enhance the brain inflammation that cause neuronal death and hasten memory loss," she said in a news release from the journal's publisher. "The loss of sensory receptors around the teeth is linked to some of the dying neurons."



This may lead to a vicious cycle, Okamoto explained. The loss of these brain connections can cause more teeth to fall out, further contributing to cognitive decline.

Long-Term Pesticide Exposure Linked to Cognitive Decline

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Medscape Today
Megan Brooks

Individuals exposed to pesticides on the job are more likely than their unexposed peers to experience a decline in cognitive function as they grow older, new research shows.




"The mild impairment we observed raises the question of...possible evolution towards neurodegenerative diseases such as Alzheimer's disease or other dementias," write Isabelle Baldi, MD, from the Université Victor Ségalen Bordeaux 2 in Bordeaux, France, and colleagues.



The study was published online December 2 in Occupational and Environmental Medicine.



Despite growing evidence linking pesticide exposure to neurological diseases, epidemiological data on neurobehavioral effects of chronic pesticide exposure are limited, the study team notes.



The PHYTONER study is monitoring the neurobehavioral effects of long-term exposure to pesticides in vineyard workers in southwest France. A total of 929 workers aged between 42 and 57 years enrolled in the study between 1997 and 1998.



Dr. Baldi's team followed-up with 614 study participants between 2001 and 2003. On both occasions, the workers completed a questionnaire and 9 neurobehavioral tests that measured memory and recall skills, language retrieval skills, verbal skills, and reaction time.



All of the participants have worked in agriculture for at least 20 years. They were grouped into 4 categories of on-the-job pesticide exposure: directly exposed (mixing or applying pesticides, cleaning or repairing spraying equipment; n = 336), certainly indirectly exposed (contact with treated plants; n = 107), possibly indirectly exposed (work in building, offices, cellars; n = 52), and not exposed (none of the above; n = 119). The analysis did not focus on specific pesticides.



On both testing occasions, lower scores in some or all of the cognitive tests were associated with older age, lower education levels, excessive alcohol intake, depression, and drug use, which was not unexpected, the researchers note.



In follow-up testing, the risk for scoring low on a cognitive test was higher in exposed subjects, with odds ratios ranging from 1.35 to 5.60.



In addition, when the authors compared baseline test scores with follow-up test scores 4 to 5 years later, they found that exposed workers had the greatest decrease in performance with time.



In all but 2 of the tests, those who had been exposed to pesticides were most likely to perform worse the second time around compared with nonexposed workers.



In multivariate analysis taking into account the type of exposure, the odds ratio for a 2-point drop on the Mini-Mental State Examination between baseline and follow-up was 1.97 (95% confidence interval, 1.09 - 3.59) in the directly exposed workers compared with the nonexposed workers.



"This result is particularly striking in view of the short duration of follow-up and the relatively young age of the participants," Dr. Baldi and colleagues write.



They point out that no decline in MMSE scores was seen over the course of 5 years in a separate longitudinal study of cognitive test performance in a general, dementia-free French population aged 65 years and older.



"The observed decline in pesticide-exposed subjects on the MMSE, a composite measure reflecting global cognitive deterioration, cannot therefore be considered a sole effect of ageing, especially since the subjects were relatively young," they say.



The current findings, Dr. Baldi and colleagues say, are consistent with several previous studies in pesticide-exposed farm workers. In addition, in a recent review of 21 relevant studies on the cognitive effects of chronic pesticide exposure, 76% found positive associations with some tests, and 82% found a relationship with psychomotor function (Kamel et al. Environ Health Perspect. 2004).



In correspondence with Medscape Medical News, Dr. Baldi said the second follow-up of the PHYTONER cohort began this year, a full 12 years after baseline. This time lag, she said, should provide a better understanding of cognitive impairment and its evolution in pesticide-exposed vineyard workers. It is also possible that the first cases of Alzheimer's disease among the study group will be identified, as they will be close to 65 years old.

The study is supported by the Ministère de l'Environnement, Agence Nationale pour l'Amélioration des Conditions de Travail, Conseil Régional d'Aquitaine, Recherche et Partage. The authors have disclosed no relevant financial relationships.

CME Education online

Rosemary for Alzheimers

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Rosemary and Alzheimer's disease. Dr. James Duke, former U.S. Department of Agriculture chief of medicinal plant research, and one of the world's leading authorities on medicinal plants, is convinced that rosemary may retard the progression of Alzheimer's disease. He explains that Alzheimer's has been blamed on oxidative and inflammatory processes and on the breakdown or deficiency of choline and acetylcholine in in the brain.


"Rosemary contains more than a dozen antioxidants and a half-dozen compounds reported to prevent the breakdown of acetylcholine. It's fabulous that the classical herb of remembrance has so many compounds that might help people suffering from this disease," Duke says.

President Obama signs National Alzheimer's Project Act

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Alzheimer's Association

President Obama signed the National Alzheimer’s Project Act (NAPA) into law. NAPA will provide a coordinated national strategy to confront one of America’s most feared and costly diseases, one that will only plague more baby boomers as they age. NAPA is a victory for you and more than 300,000 other Alzheimer advocates who stood up and demanded that our nation's leaders create a plan for combating this disease. Please continue to stand with us in the fight against Alzheimer's.

Dementia in Later Years an Independent Risk Factor for Death

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Medscape Today
Fran Lowry

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




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



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



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



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



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



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



However, midlife total cholesterol was not associated with mortality.



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



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



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



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



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



Confirmatory Findings



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



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



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



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



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

Role of Clotting Mechanism in Alzheimer's Disease

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Science Daily

The aggregated proteins strewn about the brain are the hallmark of one of the most common neurodegenerative disorders: Alzheimer's disease. But while these irregular, gunky proteins, called amyloid-β, are believed to contribute to the deterioration of memory and cognitive ability in Alzheimer's patients, no one knows how they lead to these symptoms, and the severity of the dementia doesn't directly depend on the amount of amyloid-β plaques found in diseased brains.


New experiments from The Rockefeller University, building on a paper published earlier this year, show how amyloid-β interacts with a clotting agent in the blood, increasing blood clots that are harder than usual to break down and starving neurons of their regular supply of oxygen. The research suggests that the effects of amyloid-β on the blood vessels feeding the brain could be an important aspect of the havoc they wreak on the brain.




"There has been a suggestion that vascular dementia and Alzheimer's disease might be related, and our current work provides a possible connection between the two," says Sidney Strickland, head of the Laboratory of Neurobiology and Genetics at Rockefeller.



Led by Hyung Jin Ahn, a postdoctoral associate in Strickland's lab, researchers used biochemical tests to home in on exactly how a particularly nasty form of amyloid-β, called Aβ42, interacts with the blood clotting agent fibrinogen, causing fibrinogen to grow into unusual clot structures that are hard to degrade. Ahn and colleagues show, by incubating Aβ42 and fibrinogen and studying the effects, exactly what pieces of the molecules interact and what happens when they do. The results indicate that the interaction between Aβ42 and fibrinogen may induce abnormal fibrinogen structures prior to fibrin clot formation and that this oligomeric fibrinogen plays an important role in Alzheimer's disease pathogenesis, Ahn says.



The findings could suggest a drug target for disrupting this interaction, thereby preventing the downstream consequences, which could include decreased blood flow, cognitive dysfunction and inflammation of the neurons.



In June, researchers from the same lab published a report in Neuron demonstrating that amyloid-β leads to the formation of tougher blood clots, and that decreasing the level of fibrinogen could reduce the pathology of Alzheimer's disease. The latest work, published November 22 in Proceedings of the National Academy of Sciences, shows how those tougher blood clots are formed.

Ahn and colleagues are now in the process of identifying small molecules that can inhibit the Aβ42-fibrinogen interaction and hope these inhibitors could become an effective drug therapy for patients with Alzheimer's disease.