Alzheimer's Club

But role of cholesterol in Alzheimer's disease still unclear, reports the Harvard Men’s Health Watch.

It sounds simple: The lower your cholesterol, the better your heart health. But a man’s heart and his head don’t always agree.

In fact, the relationships among cholesterol levels, psychological function, and neurologic disorders are complex and sometimes controversial, reports the March 2007 issue of Harvard Men’s Health Watch.

There are two major forms of dementia: vascular dementia and Alzheimer’s disease. Vascular dementia results when blood vessel damage deprives the brain of oxygen. Brain cells die as a result, and mental function suffers.

Some studies link high cholesterol levels to an increased risk of cognitive impairment, but others report the opposite. More research is needed to sort this out, but even now, investigations of HDL (good) cholesterol and mental function have consistently reported that high HDL levels appear to help preserve mental function in older people.

The connection between Alzheimer’s disease and cholesterol is even more complex. Scientists have learned much of the damage of Alzheimer’s comes from deposits of a sticky protein, called beta-amyloid, in vital areas of the brain.

In some studies, high cholesterol levels appear to accelerate the formation of beta-amyloid plaques. People with the genetic trait that increases the level of a particular cholesterol transport protein have a greatly increased risk of late-onset Alzheimer’s.

The urgent question is whether cholesterol-lowering drugs, such as statins, can reduce the risk of Alzheimer’s disease. In the most recent studies, people who took statins did not appear to be at lower risk for the disease. Additional research is under way.

For an in-depth information on the role of lipids in Alzheimer's disease and other neurodegenerative diseases, please see major subject journal Neurobiology of Lipids.

Source: Cholesterol May Play Part in Alzheimer's Disease. Toronto Daily News (25 Feb 2007) [FullText]

Labels: Cholesterol and AD

Ken Howard needed no research for Alzheimer's role in new TV movie
Gary Post Tribune - Gary, IN, USA
LOS ANGELES--Ken Howard required no research to play a man in the early stages of Alzheimer's disease. ''I did all my homework for this role years ago,'' he...
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MetLife Foundation Announces Major Awards to Scientists for ...
Insurance News Net - Harrisburg, PA, USA
The winners of the MetLife Foundation Awards for Medical Research in Alzheimer's Disease were announced in Washington, DC today...
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New Alzheimer's target a Notch above the rest?
DrugResearcher.com - Montpellier, France
Scientists have discovered a new potential target for Alzheimer's drugs that could reduce symptoms of the disease without interfering with...
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Man, 91, With Alzheimer's Disease Missing
WESH.com - Winter Park, FL,USA
He has Alzheimer's disease but currently isn't taking medication. Authorities said he has a heavy Polish accent and can be aggressive because of his...
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Serious memory loss and confusion are signs of possible Alzheimer's
Delmarva Daily Times - MD, USA
Forgetting names or losing car keys occasionally should be no cause for concern, said Dr. Ron Petersen, director of the Mayo Clinic Alzheimer's Disease...
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Role of Cholesterol in Alzheimer's Disease Unclear
Kansas City infoZine - Kansas City, MO, USA
There are two major forms of dementia: vascular dementia and Alzheimer's disease. Vascular dementia results when blood vessel damage deprives the brain of...
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TorreyPines Therapeutics and Eisai Co., Ltd. Extend Alzheimer's ...
PipelineReview.com (press release) - Barcelona, Spain
This collaboration, focusing on the discovery of novel, small molecules to treat Alzheimer's disease, is TorreyPines second discovery collaboration with...
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The Other Dementia
San Francisco Chronicle - San Francisco, CA, USA
"I do a lot of crying," says Dawn's mother, Emmogene, who lives in Antioch, cares for a husband with early Alzheimer's disease and regularly attends UCSF's...
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The winners of the MetLife Foundation Awards for Medical Research in Alzheimer's Disease were announced in Washington, D.C. today. Awards were made at a special scientific briefing and luncheon, to David M. Holtzman, M.D. of the Washington University School of Medicine in St. Louis, for his pioneering work in molecular biology examining the early stages of Alzheimer's, and Berislav V. Zlokovic, M.D., Ph.D. of the University of Rochester Medical Center in Rochester, New York, for his research defining the impact that blood flow plays in Alzheimer's disease.

Since 1986, major awards have been made to scientists who have demonstrated significant contributions to the understanding of Alzheimer's disease. At the heart of the awards program is a strong belief in the importance of basic research, with an emphasis on providing scientists with the opportunity to liberally pursue ideas. Each of the winners will receive a $50,000 personal award, in addition to a $200,000 research award to each of their institutions, to further their research.

"Alzheimer's is an issue of national importance. The disease is not only financially devastating to many families, but it also robs them of the person they once knew," said C. Robert Henrikson, Chairman, President and Chief Executive Officer of MetLife, Inc. "The impact of Alzheimer's on families, society, and the economy is why MetLife has been committed for over 20 years to the search for a cure."

An estimated 4.5 million Americans have Alzheimer's disease, a number that has more than doubled since 1980, and will continue to grow - by 2050 the number of individuals with Alzheimer's could range from 11.3 million to 16 million. Increasing age is the greatest risk factor for developing Alzheimer's; one in 10 individuals over 65 and nearly half of those over 85 are affected. National direct and indirect annual costs of caring for individuals with Alzheimer's disease are at least $100 billion, according to estimates used by the Alzheimer's Association and the National Institute on Aging. Alzheimer's disease costs American business $61 billion a year, according to a report commissioned by the Alzheimer's Association. Of that figure, $24.6 billion covers Alzheimer health care and $36.5 billion covers costs related to caregiving.

"The scientists we honor today are making a significant contribution to our future, by helping us better understand a disease that has an impact on so many Americans," said Sibyl Jacobson, president, MetLife Foundation. "Their hard work and dedication give us hope for the future."

Richard Hodes, M.D., director of the National Institute on Aging at the National Institutes of Health, delivered the keynote speech during the luncheon. The author of more than 200 research papers and a leading immunologist, Dr. Hodes has devoted his tenure as Director of the National Institute on Aging to improving the health and quality of life for older people and their families. He is a graduate of Yale University and received his M.D. from Harvard Medical School.

The awards program began with a research briefing, where the award recipients discussed their work. The briefing was moderated by Robert N. Butler, M.D., president and chief executive officer of the International Longevity Center - USA, and Professor of Geriatrics, Mount Sinai Medical Center in New York City, and chair of the MetLife Foundation's Research Committee. He is also the founding director of the National Institute on Aging of the National Institutes of Health.

About the Award for Medical Research Winners

Dr. Holtzman is the Andrew B. and Gretchen P. Jones Professor of Neurology and Molecular Biology & Pharmacology at Washington University School of Medicine in St. Louis, and Head of the Department of Neurology. He is also associate director of the Alzheimer's Disease Research Center at Washington University. Dr. Holtzman and the Washington University School of Medicine in St. Louis were awarded a "promising work" grant from MetLife Foundation in 2002.

Dr. Holtzman and his team recently completed landmark studies in three areas of inquiry, significantly advancing our understanding of the biology of Alzheimer's disease. The first centered on the ability of antibodies directed against amyloid-beta to decrease plaque formation in the brains of mice. Dr. Holtzman's tests of the antibody resulted in a decrease in amyloid formation in the brain and improved memory function in mice within 24 to 72 hours. A human form of this antibody is now being tested. His second area of accomplishment has been in the search for physical traits that indicate whether a person is developing amyloid plaques and will ultimately suffer dementia. The third is in the development of novel methods of assessing the formation and clearance of amyloid-beta in the central nervous systems of both animals and humans. Dr. Holtzman has also been honored with the Potamkin Prize from the American Academy of Neurology, the MERIT award from the National Institute on Aging, and the Zenith Award from the Alzheimer's Association.

Dr. Zlokovic, who is known internationally for his work on stroke as well as Alzheimer's, focuses on the crucial role of blood vessels and has shown that blood circulation plays a key role in ridding the brain of the toxic amyloid beta that attacks the brains of Alzheimer's patients. For over a decade, Dr. Zlokovic has focused his attention on the transport of amyloid beta protein in the blood that flows through the brain. He suspected that the accumulation of amyloid beta in the brain might have to do with an abnormality in a patient's ability to clear the protein through the membrane that controls the passage of substances to and from the central nervous system.

Dr. Zlokovic and his team has identified much of the molecular machinery that allows amyloid beta to sidestep the body's safeguards and enter the brain, and he has discovered the molecules that falter when the toxic protein accumulates in the brain. He has shown that a breakdown in these mechanisms may lead to the symptoms displayed in Alzheimer's and other disorders associated with accumulations of amyloid-beta in the brain or blood vessels. As a result of this work, Dr. Zlokovic has demonstrated several strategies for preventing or lowering amyloid-beta accumulation and preventing reentry from the blood stream. Dr. Zlokovic is the Dean's Professor and Professor of Neurosurgery & Neurology at the University of Rochester Medical Center. He is also director of the university's Frank P. Smith Laboratories for Neurosurgical Research and associate chairman for Neurosurgery. He holds a MERIT award from the National Institute on Aging.

Source: MetLife Foundation Announces Major Awards to Scientists for Research in Alzheimer's Disease. Business Wire (23 Feb 2007) [FullText]

Labels: Alzheimer Researchers Honored

Announced the extension of an exclusive collaboration agreement between TorreyPines and Eisai Co., Ltd. that began in February 2005.

LA JOLLA, CA, USA TorreyPines Therapeutics, Inc. (NASDAQ: TPTX) today announced the extension of an exclusive collaboration agreement between TorreyPines and Eisai Co., Ltd. that began in February 2005. This collaboration, focusing on the discovery of novel, small molecules to treat Alzheimer’s disease, is TorreyPines’ second discovery collaboration with Eisai. In a separate series of agreements, dating back to 2001, Eisai and TorreyPines are collaborating in a genetics program to discover Alzheimer’s disease targets using whole-genome family-based association screening.

The goal of the small molecule program is to discover novel Alzheimer’s disease modifying compounds based on the study of the mechanism of the disease’s pathogenesis. Under the original agreement, Eisai has exclusive rights of first negotiation and refusal for validated compounds that are discovered through the research. TorreyPines and Eisai may enter into development agreements involving the validated compounds.

“We are excited about extending this agreement with Eisai, a leader in Alzheimer’s disease research and treatment,” said Neil Kurtz, M.D., President and Chief Executive Officer of TorreyPines. “We look forward to advancing the small molecule program further with Eisai’s support, as well as to continuing to work with them on our initial research collaboration to identify genetically-validated pharmaceutical targets for Alzheimer’s disease.”

About TorreyPines Therapeutics, Inc.

TorreyPines Therapeutics is a clinical stage biopharmaceutical company that discovers and develops small molecule drugs to treat diseases and disorders of the central nervous system (CNS). Led by an accomplished management team, TorreyPines is leveraging novel drug targets and technologies to potentially deliver new CNS therapies for chronic pain, including migraine and neuropathic pain; and cognitive disorders, including cognitive impairment associated with schizophrenia and Alzheimer’s disease. TorreyPines’ common stock is traded on The NASDAQ Global Stock Market under the symbol "TPTX." For detailed company information, including copies of this and other press releases, please visit TorreyPines’website at www.torreypinestherapeutics.com...

Source: TorreyPines Therapeutics, Inc [FullText]

Labels: Alzheimer Biotech

Alzheimer's And Juice

Drinking fruit or vegetable juice may be better for you than you think. New research shows it may delay the onset of Alzheimer's disease.

Seattle researchers followed nearly 2,000 adults including for 10 years. They found drinking fruit or vegetable juice more than three times a week cuts the risk of developing Alzheimer's by 76 percent compared to drinking it less than once a week.

And having juice once or twice a week reduced the risk by 16 percent.

"The theory is that the brain accumulates damage due to oxidation as we age, and if you can protect the brain from that damage you can protect the person from Alzheimer's disease and other causes of dementia," said Dr. Eric Larson of Group Health Cooperative.

Antioxidants fight that process. And there are more in juice than in the actual fruit or vegetable.

"It's everything, the core the outside, seeds, and everything is put into it," said Dr. Larson.

Researchers saw the protective benefits from any type of juice.

The study also found there are more antioxidants in juice than in vitamin C and E supplements.

Source: Juices Warding Off Alzheimer's Disease. MFTV.com (21 Feb 2007) [FullText]

Labels: Alzheimer's and diet

Alzheimer's incidence expected to grow but research not in budget

The incurable brain disease affecting more than 60,000 South Carolinians warrants more attention than it's getting on the local, state and national levels, national experts told an Orangeburg audience last week.

Without a cure, the incidence of Alzheimer's disease in the state is expected to increase by 49 percent by the year 2025, with more than 75 percent of these individuals expected to receive in-home care by an elderly spouse or adult child, according to Kate Gordon, National Alzheimer's Association associate director of grassroots advocacy.

"There are a high number of people with Alzheimer's, about 50 percent, living in nursing homes, but we know that families take on the greatest burden of care," Gordon said, speaking at Victory Tabernacle Deliverance Temple Wednesday.

The situation with federal funding for Alzheimer's research and care programs is discouraging, she said. Research funding has been on a steady decline since 2003, and funds for key Alzheimer's care program, including the 24/7 Contact Center, Safe Return and the Alzheimer's State Matching Grants Program, have been eliminated in the president's 2008 budget proposal to Congress, she said.

The FDA has over 20 drugs "in the pipeline" for Alzheimer's prevention or treatment, but money to move them forward has been declining steadily over the last 15 years, which dashes NAA's hopes for a cure within the next five to 10 years.

The reductions decrease services available for families, and Gordon encouraged such families to communicate with elected officials about what is needed.

The national association will hold its 19th Annual Public Policy Forum March 18-20.

Via "Virtual Visits," on-line users can write their personal Alzheimer's stories and voice their opinions against proposed budget cuts. State advocates will send the letters to the appropriate elected officials in Washington, D.C.

With baby-boomers approaching the highest risk age, 65, the numbers with Alzheimers will explode, Gordon said. A cure would decrease the burden on the country's overall health care system.

Alzheimer's is not "just a quiet, behind-closed-doors family issue," she said. "It's touching an entire community," said Gordon, stressing the need for caregivers.

Striking a population under 60, early-onset Alzheimer's disease is challenging for doctors specializing in older patients to diagnose, Gordon said. Ineligible for Medicare, early-onset victims don't have the resources of older patients, which offers an extra challenge to communities trying to offer services.

Hospice Care of Tri-county's Orangeburg office serves Orangeburg, Bamberg, Calhoun and Barnwell counties and a portion of Aiken County. Jerri Zeigler, community education coordinator with Hospice Care, is working to create an Alzheimer's support group with meetings likely rotating between her office and Morningside Assisted Living Center.

"My husband's grandmother died a few years ago with the disease, so it's very important to me to have a support group," she said. "I know how important it is to the community."

Hospice care can offer a critical link for those in the late, terminal stages of the disease. "People don't see hospice as a service for people with Alzheimer's disease because it's not widely known that it is a terminal disease," she said.

Family members and other caregivers experiencing burn-out can take advantage of respite care and other services that hospice provides, said Janice Harris, community education coordinator at Hospice Care of Tri-County's Columbia office. The respite program provides care for up to five days and can be used every three months, according to Zeigler.. She said the office has also helped individuals with light, taxes and other bills.

Harris, who has cared for four of her own family members with Alzheimer's, said she speaks at senior centers about how to detect the early stages of the disease. Memory loss and language problems are among the 10 warning signs of the disease.

Harris also does a 'Caring for the Caregiver' program and education programs on maintaining the brain, staying healthy, and understanding the challenging behaviors of those with Alzheimer's in nursing facilities and homes..

In book, "When Roles Reverse: A Guide To Parenting Your Parents," author Jim Comer identifies issues in families that need attention and helps them develop an action plan.

Among the 50 questions Comer said families must ask to save time, money and tears are: Who will be the primary caregiver or share responsibility when a parent becomes ill or incapacitated? What specific plans has the family made for a sudden parental illness or emergency? T

"Have a family discussion in a relaxed atmosphere, not in the middle of a holiday celebration, birthday or anniversary. These questions deserve a time slot of their own. If a family is geographically dispersed, ... arrange for a conference call," Comer says in his book.

Gordon is particularly excited about the creation of a local support group which she said will empower the community to fight Alzheimer's more effectively.

Because there is no cure, NAA advocates families getting involved in the fight for a world without the brain disease.

"People are suffering in our communities, and we need help," Gordon said.

Source: Dionne Gleaton, T&D Staff Writer. Alzheimer's incidence expected to grow but research not in budget (19 Feb 2007) [FullText]

T&D Staff Writer Dionne Gleaton can be reached by e-mail at dgleaton [at] timesanddemocrat.com

Labels: Alzheimer's funding, Alzheimer's grant

A completely new approach to the study of Alzheimer's disease, initiated by a professor at the University of California, Santa Barbara, may solve a critical piece in the puzzle of the disease. This tragic neurological illness progressively erases memory in its millions of victims. The key to the new approach is understanding the way certain proteins in the brain fold, or rather "misfold."

Michael Bowers, a professor in the Department of Chemistry and Biochemistry, developed this project, which is being funded by the National Institutes of Health. Bowers's laboratory will receive $1.3 million of the total $9 million project grant, plus biological samples worth an additional $500,000. The grant covers a five-year period. Four institutions are involved.

Bowers is using specialized chemical research methods and applying them to biology. His research will depend upon the study of rare peptides, or strings of amino acids, that are difficult to produce. These will be provided by co-investigator David Teplow, a professor at UCLA's David Geffen School of Medicine, who has been involved in Alzheimer's research for over 10 years. Joan-Emma Shea, also a professor in UCSB's Department of Chemistry and Biochemistry, heads the theoretical modeling aspect of the project.

"Until about five or six years ago, everyone assumed that the large amyloid plaques, or neurofibrillary tangles, that were found in the brains of Alzheimer's victims were the cause of the disease," said Bowers. "However, recent scientific discoveries indicate that these large, insoluble aggregates might merely be markers of the disease ---- they do not cause the disease. Rather, smaller soluble oligomers, or peptide complexes, are now felt to be the causative agents, and I find that very interesting."

He explained that now the hunt is on for the "small stuff." Because of their expertise in certain chemical methodologies, Bowers and his research group are able to track down the molecular level changes that lead to development of the disease.

The process of aggregation of proteins that cause the plaque begins in a way that Bowers has begun to clarify. The goal is to find non-toxic drugs that will interrupt the aggregation process. "If we can do that, we can stop the disease," said Bowers. "However, once you start losing neurons, things become very difficult, because the body doesn't readily replace them due to their very large size. If we could find a marker, early on, to indicate when the patient first has the disease, then the new drug or drugs that we hope to develop could prevent further damage."

Bowers described his approach as a whole new way to determine the structure and composition of the Abeta 42 peptide and its oligomers that are primarily responsible for Alzheimer's disease. The research team is analyzing the way this peptide folds, causing it to aggregate and disrupt neuronal function.

"In biology, structure and function are tightly coupled," said Bowers. "When it became clear that small soluble oligomers were most probably the toxic agents, I realized our ion mobility methods could contribute, since we could measure the oligomer distribution and shapes of these peptides for the first time."

Three years of preliminary work convinced the National Institutes of Health to provide funding. "In the last several months, I believe we have uncovered the identity and shape of the primary toxic oligomer," said Bowers. "Our results are consistent with findings on transgenic mice, recently published in the journal Nature, indicating that soluble oligomers with masses matching those we have identified have been extracted from the brains of the diseased animals."

The transgenic mice that Bowers refers to are laboratory mice that have had the gene that creates the Abeta 42 precursor protein spliced into their genome. This process has been shown experimentally to produce memory loss in the animals.

The key aspect of ion mobility is its ability to measure accurate cross sections of complex aggregations of proteins and obtain information on their three-dimensional shape. When coupled with mass spectrometry, electrospray ionization, and high-level molecular modeling, it becomes a very powerful technique.

The experiment starts with electrospray ionization, a method of spraying the solution containing the peptides of interest into fine droplets and then letting the droplets evaporate. Following evaporation, mass spectrometry is employed to determine the mass or weight of the species that were in the solution, and from that to determine the composition. Finally ion mobility is used to show the shape of the Abeta 42 peptide and its oligomers.

"Our experimental and theoretical methods allow us to investigate structure, aggregation, and energetics in a variety of protein systems," said Bowers. "In addition, we are able to explore correlations between solution and gas phase protein structures, learning that in many critical cases, these structures are very similar."

The experimental methodology for the Alzheimer's study was developed at UCSB 15 years ago, in studies involving "buckyballs." Buckyball is the nickname for the versatile carbon molecule known as C60, which scientists named "buckminsterfullerene" after American architect R. Buckminster Fuller, who designed geodesic domes in a soccer-ball shape. "Our ion mobility and mass spectrometry methods provide a new way to attack the molecular basis of neurological diseases that has not been explored until now," said Bowers.

Bowers and his group are currently investigating proteins involved in the study of several neurological diseases. Besides Alzheimer's disease, they are studying Parkinson's disease and the various transmissible spongiform encephalopathies or "prion" diseases. In this latter case Bowers is receiving funding from the British government to find an ante-mortem test for the bovine prion disease usually called "mad cow" disease. The same test, if successful, should also work on deer and elk; an epidemic in the Midwestern United States now affects these animals.

Besides Teplow and Shea, co-investigators on the Alzheimer's project include Gal Bitan, assistant professor at UCLA's David Geffen School of Medicine; Eugene Stanley, physics professor at Boston University; and, George Benedek, physics professor at MIT.

Source: Innovative Alzheimer's Research May Solve Critical Piece In Disease's Puzzle. Science Daily (15 Feb 07) [FullText] Note: This story has been adapted from a news release issued by University of California - Santa Barbara.

Labels: Alzheimer's funding, Alzheimer's grant

What you don't know about Alzheimer's disease could hurt you. That's why it's important to seek medical attention if you experience any of these warning signs:

Increasing and persistent forgetfulness.

Difficulty performing familiar tasks.

Problems with finding the right words to express your thoughts.

Disorientation with time and place.

Poor or impaired judgment.

Problems with abstract thinking.

Putting everyday items in illogical places.

Changes in mood, behavior or personality.

Forgetfulness and confusion can also be caused by diabetes, thyroid disease, depression, drug interaction and vitamin deficiencies. These symptoms may also indicate the presence of another form of dementia.

If you have Alzheimer's or another form of dementia, the sooner you're evaluated and diagnosed, the more options you're likely to have in improving your symptoms.

Although Alzheimer's is a progressive disease with no known cure, drugs may temporarily slow the progression of the disease or improve symptoms. An early diagnosis may give you the opportunity to be involved in making important legal, financial, social and medical decisions that will affect you and your family.

Source: Mayo Foundation for Medical Education and Research

Labels: Alzheimer's symptoms

Scientists at the University of Virginia have identified what appears to be a major missing link in the process that destroys nerve cells in Alzheimer’s disease, an incurable disease that slowly destroys memory and cognitive abilities.

In Alzheimer’s disease, two kinds of abnormal structures accumulate in the brain: amyloid plaques and neurofibrillary tangles. The plaques contain fibrils that are made from protein fragments called “beta-amyloid peptides.” The tangles also are fibrous, but they are made from a different substance, a protein called “tau.” In the new U.Va. study, the researchers found a deadly connection between beta-amyloid and tau, one that occurs before they form plaques and tangles, respectively.

According to George Bloom, the senior author of the study and a professor of biology and cell biology at U.Va., this connection causes the swiftest, most sensitive and most dramatic toxic effect of beta-amyloid found so far. What makes it most remarkable, though, is that it requires a form of amyloid that represents the building blocks of plaques, so called “pre-fibrillar beta-amyloid,” and it only happens in cells that contain tau. Even though they account for just ~10 percent of the cells in the brain, nerve cells are the major source of tau, which likely explains why they are specifically attacked in Alzheimer’s disease.

The researchers used cultured mammalian cells that either did or did not make tau to study how cells respond to beta-amyloid. They found that pre-fibrillar, but not fibrillar beta-amyloid works together with tau to break apart microtubules — highways along which “synapse” replacement parts move rapidly in the nerve cell from where they are made to where they are needed. Synapses are connections between nerve cells, and in the brain they are the structural basis of memory and cognition. When nerve cells in the brain lose their microtubules they also lose the ability to replace worn out synapse parts, and synapses therefore disappear. The loss of synapses, and consequent loss of memories and cognitive ski lls, cannot be reversed, and can lead directly to nerve cell de ath.

“We think we’ve found one of the seminal cell biological events in the pathogenesis of Alzheimer’s and if we can figure out all of the steps in the process and understand each player at every step, it will represent many potential new drug targets for Alzheimer’s therapy,” Bloom said. “Our paper defines one of the earliest events that causes neurons to die in both early-onset familial Alzheimer’s and late-onset Alzheimer’s disease. We believe this is the first evidence for the long elusive ‘missing link’ between amyloid and tau in Alzheimer’s disease.”

“This is a very significant finding that greatly improves our understanding of the mechanisms within the cell that ultimately lead to Alzheimer’s disease,” said Lester Binder, professor of cell and molecular biology at Northwestern University and a leading researcher on Alzheimer’s. Binder said he has already incorporated the U.Va. study into classes he teaches on the pathogenesis of Alzheimer’s disease and dementia.

The study’s first author and lead investigator is Michelle King, a U.Va. research assistant professor of biology. Other investigators include Bloom, Ho-Man Kan and Alev Erisir of U.Va., Peter W. Baas of Drexel University and Charles G. Glabe of the University of California at Irvine.

Source: (10 Feb 2006) Alzheimer's Disease : Missing link in process leading to Alzheimer's disease. SpiritIndia [FullText]

Labels: Alzheimer hypothesis

By Melissa Beattie-Moss, Research Penn State

Most of us have had the experience of forgetting where we've parked our car or have struggled to recall an acquaintance's name. But once we hit our 50s, said James R. Connor, these incidents might cause us to worry that we're showing early signs of Alzheimer's disease.

Fortunately, that's not usually the case, says Connor, professor of neurosurgery in Penn State's College of Medicine, Penn State Milton S. Hershey Medical Center. "If forgetting something now and then was a good indicator of dementia, we'd all be in trouble," he added with a laugh.

This dreaded condition was first classified as a disease 100 years ago by German psychiatrist Alois Alzheimer and is the "leading cause of dementia in the elderly," explained Connor. In fact, four million Americans now suffer from this progressive disease, including up to 50 percent of seniors over age 85 and up to 15 percent of those over 65.

The aging of baby boomers will swell those numbers in the coming years. "At the present time, Alzheimer's disease (AD) costs the nation $100 billion a year, with an average $174,000 lifetime cost per patient," Connor said. "By the year 2050, there will be an estimated 14 million Americans with the disease. The human and economic toll is devastating, so it's imperative that we learn more about prevention, early diagnosis and treatment."

Is it possible to prevent Alzheimer's? For those who already have signs of persistent memory decline, there are some neurosurgical procedures and therapeutic drugs available that may help slow the disease's ravages, Connor noted. But for the millions of "worried well," science has not yet found any definitive ways to prevent the disease.

Although recent research suggests that genes may play a role in contracting the disease, "the No. 1 risk factor for Alzheimer's is aging," said Connor. "You have to live long enough to develop this disease," which researchers believe to be caused, in part, by a sticky protein called "amyloid plaque" that accumulates on brain cells, disrupting the transmission of their signals. "Neurofibrillary tangles" -- protein threads that strangle and eventually kill nerve cells -- are also present in the brains of AD patients. "If we have a computer with cables that are broken and tangled, it won't work right, and it's the same with our brains," added Connor.

Scientists speculate that the protein coatings and tangles within the brain could be the body's inflammatory response to long-term toxin exposure, as well as damage from "free radicals," unstable molecules that attack and harm the body's cells by stealing their electrons through a process called oxidation.

Although some studies suggest that anti-inflammatory drugs (including common painkillers such as ibuprofen and naproxen) may help to dissolve amyloid plaques, "we need to proceed with caution in this area," Connor believes. One paradox of the disease, he says, is that "there may be a positive function to the plaques. They may be the body's way of sealing off leaky blood vessels in the brain."

Many researchers believe that metals (chiefly iron, copper and zinc) may play a role in Alzheimer's, since these substances are abundant within the folds of plaque in diseased brains. When free radicals bump into metal atoms in the body, they unleash a chain reaction that can wreak havoc on healthy cells, prematurely aging them and potentially leading to a variety of serious health conditions. MRIs and autopsies of patients with advanced Alzheimer's often reveal massive iron accumulation, Connor noted.

Although excess metals may damage the brain, he adds, another paradox is that small amounts of these micronutrients are absolutely essential to healthy brain function.

Research on the exact link between metals and memory processing is inconclusive at this point. "Is there too much copper or too little in the brains of AD patients? Studies are unclear," Connor remarked. So, too, is the role of zinc, he added. Though there's high zinc content in the healthy hippocampus -- the part of the brain responsible for short-term memory -- the jury is still out on the connection, so there's no reason to recommend zinc supplements at this point. Too much might cause a problem as well. It's all about the right balance.

Nor should one completely avoid dietary iron or copper, suggested Connor, although some physicians recommend "decreasing your iron burden" through occasional blood donation, particularly for men and post-menopausal women, who are at higher risk for accumulating iron and for developing neurodegenerative diseases.

Other recommendations made by some physicians (particularly for patients noticing subtle cognitive decline) include taking antioxidants such as vitamins E and C, going for chelation therapy and making dietary changes.

"Remember," said Connor, "that if you flip the statistics, at least half of those over 85 don't have Alzheimer's. In addition to studying those with the disease, we're also studying seniors with good short-term memories, looking for predictors of healthy neurocognitive aging."

Full Text at Psychorg.com

Chicago, IL (AHN)-A new study published in the February issue of the Journal Archives of General Psychiatry finds that loneliness may increase the risk of developing Alzheimer's disease later in life.

For the study, researchers at Rush University Medical Center in Chicago examined 823 participants, at an average age of 81, over a period of four years. Using a scale from 1 (lowest) to 5 (highest), researchers assessed the participants' level of loneliness at the start of the study and each subsequent year after over a period of 4 years. Participants were also screened for signs of dementia by testing a range of cognitive functions.

According to the study, the mean loneliness score at the start of the study was 2.3 on a scale of 1 to 5. Over the course of the study, seventy-six people developed Alzheimer's disease, with researchers determining that each point of increase on the loneliness score was associated with about a 51 percent increased risk of developing Alzheimer's.

While, the actual physiological mechanism linking loneliness and Alzheimer's remains unclear, researchers found that people who described themselves as most lonely were twice as likely to develop Alzheimer's as the ones who described themselves as least lonely.

But, the researchers' say that it is unlikely that Alzheimer's actually causes the loneliness, with the study authors writing, "In human beings, loneliness has been associated with impaired social skills. Thus, neural systems underlying social behavior might be less elaborated in lonely persons and, as a result, be less able to compensate for other neural systems compromised by age-related neuropathy."

Source: Julie Farby. Study Finds Loneliness May Increase Risk Of Alzheimer's Disease. allheadlinenews.com (6 Feb 2007) [FullText]

Labels: Alzheimer's and lifestyle

The UK government's drug watchdog NICE has received a lot of publicity recently after publishing guidelines restricting the prescription of certain cognitive enhancers for Alzheimer's disease for reasons of cost. However, a recent survey of 181 neurologists by Datamonitor indicates that the NICE cost-benefit methodology may not reflect how the drug is actually used in the clinical setting.

'Content Cognitive enhancers do not treat the cause of Alzheimer's, rather they seek to prevent the cognitive decline associated with it, and fall into two categories: acetycholinesterase inhibitors (AChEIs) including Aricept (donepezil), Exelon (rivastigmine) and Razadyne (galantamine), or the NMDA antagonist memantine, which is branded as Namenda and Ebixa in the US and Europe respectively.

Source: PBR Staff Writer. Alzheimer's disease: physicians do not always practice what NICE preaches (5 Feb 2007) [FullText]

Labels: Alzheimer's watchdog