Alzheimer Related News Items

News as of 4/07/02
For more info on these abstracts write/call Ed Cabic (edcabic@comcast.net or 410-992-7197)
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For more AD information, see Alzheimer Information at http://www.connext.net/~seniors/infoad.htm
Copies of these reports are posted there
This web page was started at the Florence Bain Senior Center in Columbia MD

Top Items
In a First, Medicare Coverage Is Authorized for AD - The Bush administration, in a major change, has authorized Medicare coverage for the treatment of AD. The new policy means that Medicare beneficiaries can no longer be denied reimbursement for the costs of mental health services, hospice care or home health care just because they have AD. In the past, many claims were automatically denied on the assumption that treatment was futile because people with AD were incapable of any medical improvement. Now, federal officials say, new studies show that people with AD can often benefit from psychotherapy, physical and occupational therapy and other services. "This is great news for people with AD and other dementias," said Stephen R. McConnell, chief executive of the Alzheimer's Association. "The new policy should eliminate a form of discrimination against millions of people." There are no estimates of the cost of the new policy. Experts said the direct cost to Medicare could be several billion dollars a year. But, they said, some of the cost could be offset by savings elsewhere in Medicare and Medicaid, because the new services will enable patients to live longer on their own, with greater ability to function. The policy is set forth in a memorandum sent late last year from the government to the companies that review and pay Medicare claims. These companies have just begun to put the change into practice. Under the policy, Medicare will pay for more therapy and outpatient services. Dr. Steven T. DeKosky, a neurologist who directs the AD Research Center at the University of Pittsburgh, said these services would "keep people out of nursing homes," avoiding costs that would otherwise be borne by the government, patients or their families. "People with AD will be able to live at home longer and avoid institutionalization," said Kim A. Warchol, an occupational therapist in Itasca, Ill., who specializes in the treatment of people with AD. "Caregivers often assume that people with AD are helpless. But we focus on their remaining physical and mental abilities, the things they can still do, and we find that many patients can perform activities of daily living if we provide appropriate cues or reminders of how to get started." By Robert Pear NY Times 3/30/02

U.S. to Rate Nursing Homes - The federal government beginning the week of April 15 will take its first step toward unveiling ratings on every nursing home in six pilot states - -Colorado, Florida, Maryland, Ohio, Rhode Island and Washington. Tom Scully, architect of the controversial project, is betting that competition will do as much, if not more, to improve the quality of long-term care as any government regulation. The market-oriented approach is built around the simple notion that information not only empowers consumers, but also forces "bad apples" in the industry up or out. "People are entitled to know more about the quality of nursing homes," said Scully, director of the federal Centers for Medicare and Medicaid Services (CMS). "My view is this is 15 years overdue." The CMS will publish the results of nine quality measurements in full-page newspaper ads and on the Internet. Although the government has collected the data for several years, this is the first attempt to translate it into user-friendly charts. A year from now, Scully hopes to publish the results nationwide. The guide, headlined "How do your local nursing homes compare," tells families which homes, for instance, have a strong record treating pain and infection. It lists where physical restraints have been used and where residents have lost an inappropriate amount of weight. Nursing homes will not be ranked, but consumers will be able to compare homes with one another and with the state average. "People looking for nursing homes have heard horror stories for many, many years," said Beth Irtz, administrator of Clear Creek Care Center in Colorado. "They'd like to have some hard data to evaluate a nursing home, and this gives them some." By Ceci Connolly Washington Post Staff Writer 4/7/02

Drugs
AD Drug Does Delay Nursing Home Move - A "real world" study of patients with suggests that drugs known as cholinesterase inhibitors do indeed help AD patients delay a move to the nursing home. The drugs are the first class of medication approved by the US Food and Drug Administration for treating the mental decline seen in patients with the memory-robbing illness. While the drugs do fight AD in the tightly controlled world of clinical trials, how they fare outside such trials is less clear. In the new study, Dr. O. L. Lopez and colleagues, from the University of Pittsburgh School of Medicine, looked at data from 135 patients with probable AD who had taken a cholinesterase inhibitor for an average of 3 years. They compared the patients with 135 people with AD never exposed to the drugs. According to the report the treated patients had a slower decline in mental status during the first year compared with untreated patients. The treated patients also retained a greater ability to take part in the activities of daily living compared with the untreated group. Overall, more than 40% of untreated patients were admitted to a nursing home during the 3-year study, compared with 6% of those taking a cholinesterase inhibitor. Mortality rates were unaffected, leading the authors to conclude that "the cholinesterase inhibitors seem to allow the patients to maintain relatively normal activities of daily living for a longer period of time, but do so without significantly prolonging life." Reuters Health 3/27/02 Journal of Neurology, Neurosurgery and Psychiatry 2002;72:310-314

Novartis: Exelon Helps AD Patients Over Years - Swiss pharmaceuticals group Novartis AG said 4/5/02 that a study has showed that its Exelon drug provides relief for patients with AD for at least two years. Novartis said that the study showed that 2,010 U.S. patients treated with Exelon showed less signs of deterioration than other patients during that time frame. Exelon is currently approved for treatment of mild-to-moderate AD, a brain-altering disease that affects around 15 million people worldwide. Dow Jones 4/5/02

Statins May Prevent Damage by AD Protein, USF Study Finds - Commonly-used cholesterol-lowering drugs, known as statins, block damage by an AD-associated protein in neurons and blood vessels, a study by University of South Florida researchers found. The researchers looked at the biochemical effects of statins in reducing damage from AD. "Statins block the vasoconstrictive effect of the A-beta protein - a critical protein involved in AD pathology," said Daniel Paris, PhD, an assistant professor at the USF Roskamp Institute. "These drugs appear to have anti-inflammatory properties, independent of their benefit in lowering cholesterol, that may help protect against dementia." Recently, the risk of developing AD has been shown to be reduced in populations treated with statins, although the reason is unclear. Other studies indicate that high cholesterol or other cardiovascular conditions also increase the risk for AD. The researchers hypothesized that the same drugs that inhibit the production of cholesterol might affect A-beta protein (Aß)'s stimulation of inflammatory substances that result in blood vessel constriction. The researchers studied the effects of two statins most commonly used to treat high cholesterol - mevinolin (lovastatin) and mevastatin (compactin). Aß appears to be toxic to human neuronal cells cultured in the laboratory. But, when these same neurons were treated with mevastatin, the neurotoxicity normally induced by Aß was prevented, the researchers found. The researchers also looked at the effect of both statins mevinolin and mevastatin on the constriction of laboratory-prepared aortic arteries from rats. They observed that the statins opposed the Aß protein's propensity to cause blood vessels to constrict. Furthermore, Dr. Paris said, this prevention of vessel constriction appears to be due to the general anti-inflammatory properties of the statins, and is unrelated to the biochemical mechanism used by the drugs to reduce cholesterol production. That is, statins may protect the vessels by opposing inflammatory substances triggered by Aß. The Roskamp researchers are further testing the effectiveness of statins to prevent or slow the progression of AD in a mouse model for the neurodegenerative disease. PR 4/2/02 Atherosclerosis 2002 Apr;161(2) 293-9

Shire Pharmaceutical: Pfizer's Reminyl Trial Isn't Definitive - Shire Pharmaceuticals Group PLC on 4/4/02 said the trial data that questioned the efficiency of its Reminyl treatment for AD shouldn't be treated as definitive. Pfizer Inc. on 4/4/02 said a multinational study showed AD patients taking its Aricept treatment experienced significant improvements in cognition and their ability to perform everyday tasks when compared to other patients taking Reminyl. The three- month study included 120 patients in the U.K., Finland , Norway and Germany, with possible or probable mild-to-moderate AD. The study was primarily designed to evaluate safety and tolerability. However, Shire Pharmaceuticals said the vast majority of data available on Reminyl doesn't support these findings - five major studies on a population of 3,000 patients showed positive cognitive results. The company also said the sample size of the survey was small, with just 120 patients, and that the study took place over just three months, which it said isn't significant. Shire Pharmaceuticals also said the key advantage of Reminyl is that doses can start low and be increased gradually, and treatment shouldn't begin on a full dose of the drug. It said it is unclear from the Pfizer study which titration, or concentration, was used. Dow Jones 4/5/02

NeoTherapeutics Expects AD Results in May - NeoTherapeutics Inc. said 3/14/02 it expects results from a pivotal-stage trial of Neotrofin, its experimental drug for AD, in the first half of May. The Irvine, California-based drug developer said the F.D.A., as it has for other AD drugs, will require a second phase 3 trial of Neotrofin, but, because the first trial was extended from three months to six months, the second trial may only need to be three months long. Reuters 3/14/02

Neurochem Reports 'Promising' Phase 1 Alzhemed Results - Neurochem Inc. reported 4/4/02 "promising" results of three Phase I clinical studies with Alzhemed, its lead drug candidate for the treatment of AD. In a press release, the company said the data confirmed that the drug candidate is "orally bioavailable, with a good safety and pharmacokinetic profile in healthy young adults and elderly subjects." It said it will submit an application to regulatory authorities during the second quarter to advance Alzhemed to a Phase II clinical trial. Dow Jones 4/4/02

Gila Monster Spit May Yield AD Drug - An experimental drug derived from the saliva of the venomous Gila monster is one of a growing crop of new drugs that are being developed to

improve memory and learning. The bite of the Gila monster -- a native lizard to the southwest United States and Mexico -- can be deadly, but its saliva also contains a chemical which acts on a previously unknown receptor pathway in the brain that affects memory . The findings were presented on Thursday at the 7th

International Geneva/Springfield Symnposium on Advances in Alzheimer Therapy in Switzerland. New York-based biotechnology company Axonyx Inc., which is developing the drug, Gilatide, plans to start human trials with it as a treatment for AD later this year. By Toni Clarke and Ben Hirschler Reuters 4/5/02

Genes & Genetic Issues
Psychosis with AD May Run in Families - Many people with AD also have psychotic symptoms, and a recent study shows AD patients whose siblings have both disorders are more likely to exhibit psychosis, as well. "This paper may be the strongest evidence to date that psychotic symptoms in AD have a distinct biologic basis, with unique genetic underpinnings," said lead author Dr. Robert A. Sweet of the University of Pittsburgh, Pennsylvania. In their study Sweet and colleagues examined data from siblings of 371 people with AD. The investigators found that patients with an AD sibling with psychosis were more than twice as likely to also have psychotic behaviors. These results suggest that there may be a genetic basis to psychosis in AD, as well as to the rapid decline associated with psychotic symptoms. In an interview with Reuters Health, Sweet explained that knowing a loved one's hallucinations or delusions may come from his or her genes could help families understand and feel compassion towards such a patient. "The understanding that what the families often see as deliberate disturbing behavior may be as biological as the forgetfulness of AD may help them respond appropriately to managing these symptoms in their loved ones," he said. Further-more, Sweet recommended that all families of AD patients receive counseling on how to deal with hallucinations and delusions in these patients, since almost half will develop psychotic symptoms. "I think that general counseling about what to look for and how to react is important to all families, given how high the rate is in everyone," he said. By Alison McCook Reuters Health 3/25/02 Neurology 2002;58:907-911

In Stem-Cell Research, It's Rule Britannia - Britain is emerging as the world leader in one of the most controversial, yet promising, areas of scientific research: human embryonic stem cells. As these master cells can develop into any of the more than 200 specialized tissues in the body, they hold the key to future treatments for devastating diseases such as AD, Parkinson's and diabetes. Embryonic stem-cell research has become a hot potato in other countries, most notably in the U.S., where scientific understanding of the vast potential these cells hold has been slowed by a moral debate over when human life begins. But in Britain, home to the world's first test-tube baby and Dolly the cloned sheep, more than a decade of ongoing dialogue between scientists, government, and religious officials has resulted in the most conducive climate in the world for this important new area of scientific research. Britain is the only country on the globe with a regulatory structure in place that provides a clear road map for both public- and private-sector research on embryonic stem cells. In late February, Britain's House of Lords approved research on human embryonic stem cells cultured from surplus embryos donated by fertility clinics for scientists who receive a license from the Human Fertilization & Embryology Authority [HFEA]. The latter is a state agency that regulates fertility and embryonic stem-cell research. The House of Lords also backed the Medical Research Council's plan to create the world's first bank for newly created stem-cell lines, which are essentially a reservoir of cells derived from a single embryo. In a move that generated controversy even in Britain, the government approved the therapeutic cloning of embryos up to two weeks old under limited conditions and tightly regulated by the HFEA. The benefit, say scientists, is the ability to create a limitless supply of embryonic stem cells. Previously, British scientists had been able to use embryonic tissue only for infertility research. With the legal and regulatory stage set, Britain is attracting some of the world's top talent to its shores. By Kerry Capell EURO-TECH 4/4/02

Caregivers
HHS to Allow Feeding Assistants for Nursing Home Residents - HHS Secretary Tommy G. Thompson announced a new proposal 3/28/02 to improve the quality of care for nursing home residents by allowing for trained assistants to help residents eat and drink. "Allowing trained feeding assistants will mean better care for residents, especially at meal times which can be the busiest times in nursing homes," Secretary Thompson said. "Trained feeding assistants will free nurses and nurse aides to focus on residents' other health care needs. The result will be that residents will receive better nutrition and care." Under the Centers for Medicare & Medicaid Services (CMS) proposal, trained feeding assistants will help residents to eat and drink, especially at meal times. Individuals would be required to complete a state-approved course to qualify as trained assistants. Currently, nursing homes rely primarily on certified nurse aides (CNAs) or other health care professionals to assist residents with eating and drinking. Volunteers and family members also may assist with these tasks. The proposed change would make it easier for nursing homes to recruit and hire enough CNAs and other appropriately trained workers to provide quality care in all areas of need. PR 3/28/02

Virginia Web Site Helps Seniors - Before he was elected governor of Virginia in November, Mark R. Warner was a millionaire venture capitalist. When his mother was diagnosed with AD and he started looking for information, he discovered it was difficult to find. So Warner put all his expertise to work and started SeniorNavigator.com, an Internet guide that links seniors, their families and caregivers with information on health and aging. "SeniorNavigator is a great example of where technology and the community intersect. It's a great resource for those people who will never touch a computer," Warner said. Warner said he intends to share the site with other governors to see if it could be replicated in other states. The site contains information such as Medicare and Medicaid availability and whether a medical provider is currently accepting new patients. Debbie Frett, executive director of SeniorNavigator, said it receives an average of 4,000 hits per week. Lois Brittell, a registered nurse at Inova Fair Oaks Hospital in Fairfax, uses the site almost daily to help patients. Her job often requires that she find nursing home placement and social service resources for the patients. She has discovered that many of the site's resources can be translated into other languages for patients who don't speak English. By Rebecca Miller, AP Writer 3/23/02

Implantable Spy Chip Gets Green Light from U.S. - Applied Digital Solutions in Florida on 4/4/02 that it will begin marketing and selling a microchip that can be implanted under the skin, after receiving the go-ahead from the U.S. Food and Drug Administration. The FDA advised the company that its biochip, called "VeriChip," is not considered a medical device and therefore is not subject to FDA regulation. FDA officials said that as long as the biochip is used for identification purposes only, it will not have to meet strict FDA guidelines. The ruling saves the product from having to undergo the agency's rigorous and lengthy safety testing procedures. Although the company has advertised the VeriChip in the past as a potential method of storing a persons complete medical history, at this stage the device will contain only a number to be used for identification. However, that ID code can be transmitted via Internet or phone to a secure data storage site, where it can be cross-referenced, allowing authorized personnel to obtain detailed medical information. By Tim McDonald NewsFactor 4/5/02

How to Comfort a Person With AD - When AD strikes someone you know, there is very little you can do other than to make them more comfortable. According to a report from the Department of Veteran Affairs Medical Center, West Roxbury, Mass., one thing that can lift the spirits of an AD patient is a telephone call from a loved one. Even if you can't call regularly, a virtual call -- a taped message played over the telephone -- can brighten the day. One of the sad facts is that one tape can be used again and again. AD patients never recall having heard the tape, so for them it's always new. HealthScoutNews 3/27/02

Testing
Scans Show Brain Loss Before AD Symptoms - The brain appears to undergo a predictable pattern of degeneration with AD, with certain areas shrinking and being replaced with the fluid that normally cushions the brain, study findings suggest. What's more, the results of the small study indicate that such changes can be picked up with brain scans--at least in people with an inherited form of the disease--before the symptoms of the memory-robbing disorder begin. The researchers found that the memory center of the brain undergoes a rapid rate of decline before symptoms begin, and as the disease progresses, other regions of the brain show a faster rate of decline. Eventually, there is shrinking of the brain across the board, with lost tissue being progressively replaced by cerebrospinal fluid, which normally cushions the brain. "This study provides further evidence that AD manifests progressive losses in the brain earlier than we had thought, and that increased rate of loss may occur even before symptoms are noticeable," said co-author Dr. Nick C. Fox of University College London, in an interview with Reuters Health. Regions of the brain used for memory underwent the most rapid tissue loss very early in the disease, according to the report. In contrast, degeneration of tissue involved in brain areas associated with functions such as speech and perception increased as the disease progressed. Fox told Reuters Health that the technique of using serial MRI scans to detect changes in the brain of patients may help in early diagnosis. Currently, there is no good way to diagnose a patient with AD, besides ruling out other conditions as the cause of symptoms. Only examining the brain of a patient after death can determine if brain plaques typical of the disease are present. Ultimately, Fox explained, if doctors know more about how patterns of atrophy spread as the disease progresses they may be able to use this information to develop ways of tracking the disease either to improve diagnosis or to improve therapeutic monitoring. It's a study that someday could be used to help treat AD, says Dr. Donald L. Price, professor of neurology, pathology and neuroscience at the Johns Hopkins School of Medicine. Treatments for this once unstoppable condition are starting to emerge, he notes. "If a therapy has some downside, you want to be sure you are treating only AD patients," Price says. "It would be critical to enhance the early diagnosis of AD as differentiated from other forms of dementia." By Keith Mulvihill Reuters Health 4/3/02 and Ed Edelson HealthScout News Reporter 4/4/02 Proceedings of the National Academy of Sciences 2002;99:4703-4707

Mild Memory Loss Could Signal AD Risk - Mild but persistent memory impairment, like always forgetting appointments you used to remember, could mean you're at increased risk of developing AD. However, it doesn't mean you'll automatically get the debilitating disease, according to scientists at the University of Kentucky. Their study of 130 nuns, aged 75 to 102, found those who had mild memory or other cognitive impairment were more likely to have higher levels of abnormal protein deposits in their brains, a physiological condition associated with AD. However, not all the nuns who had high levels of the protein went on to develop AD. "Just because you have mild cognitive impairment doesn't mean you're going to have dementia," says Kathryn P. Riley, a psychologist at the university's Sanders-Brown Center on Aging and lead author of the study. Riley's study is one of several that have used data from a long-term study of 678 School Sisters of Notre Dame to find evidence of physiological changes in the brain that could be associated with AD. The nuns she studied were tested for cognitive abilities four times over six years. Following their deaths, brain autopsies revealed a close correlation between the degree of cognitive impairment and levels of the protein, called "neurofibrillary tangles." However, a little less than half of the nuns who had mild cognitive dysfunction and whose brains showed the presence of the neurofibrillary tangles never went on to develop AD. By Janice Billingsley HealthScoutNews Reporter 3/22/02 It appears in the May 2002 Annals of Neurology, and it is already available online as DOI 10.1002/ana.10161

Relatives Can Help Doctors Diagnose Mental Decline - Comparing an elderly patient's report of his or her own mental ability with information from a close relative could help doctors identify those who are at high risk of developing AD according to researchers. Patients with mild mental impairment who reported having no difficulties with daily function--even though a spouse, adult child or other close relative said they did--were the most likely to develop AD within 2 years, Dr. Matthias Tabert of Columbia University in New York City and colleagues found. "Numerous studies have demonstrated that a large proportion of patients diagnosed with mild to moderate AD lack full awareness of this progressive decline." "Less is known about the functional status of elderly patients with mild cognitive impairment," they add. Tabert and his team used the term "mild cognitive impairment," which has varying definitions and criteria, to broadly define older individuals whose cognitive deficits are worse than those typical of normal aging but not severe enough to warrant a diagnosis of dementia. "Our findings suggest the importance of obtaining a statement regarding an older patient's cognitive functioning from an objective individual, such as a close relative, as well as the patient," Tabert said in a prepared statement. "Patients in whom the informant reports considerable functional deficits while the patient denies having these deficits should trigger a high index of suspicion for AD," he added. "This additional history-taking would be highly beneficial to the primary care physician and ultimately to the patient for whom AD poses a significant risk," Tabert concluded. Reuters Health 3/20/02 Neurology 2002;58:758-764.

Blood Test May Identify AD - A blood test may be able to identify AD long before there are symptoms of the brain-destroying disorder, say researchers who hope early knowledge can help in developing treatment. In their study researchers at Washington University School of Medicine in St. Louis say that injecting an antibody into mice causes a sudden flood in the bloodstream of a protein that forms neuron-destroying plaques in the brain. The level of the protein, amyloid- beta, after the injection was an indication of the amount of plaque, said David M. Holtzman, a Washington University neurologist and co-author of the study. He emphasized that although the technique works in a strain of mice that develop AD, it is still not known if the test would work in humans. Because the disease progresses so slowly, Holtzman said it would take at least five years of studies before the test's value could be proven in human patients. Holtzman said the study is a part of a major effort by AD researchers to find a way to identify people who will develop the disease before they have obvious symptoms. Right now, AD can be proven only at autopsy, although some clinical tests can diagnose the disease to a high degree of accuracy after profound symptoms have appeared. "One of the hottest thing now is to figure out a diagnostic tool for AD," said Holtzman. Amyloid-beta is a normal substance in the body, but starting at about age 50 it can accumulate in plaques in the brain. These plaques are linked to the death of neurons, causing a gradual loss of memory and control of body function and leading eventually to death. "By the time a patient has the earliest clinical symptoms of AD, there already is a massive amount of amyloid in the brain," said Holtzman. "It is a very slow process over 10 to 20 years." He said the study in mice suggests that the blood test could identify the tendency to form amyloid-beta plaques at a very early point in the disease. By Paul Recer, AP Science Writer 3/21/02 Science Mar 22 2002:2264-2267

Prevention
Cholesterol-Lowering Drugs May Cut Dementia Risk - Women with high cholesterol levels are at increased risk of developing memory problems and other signs of dementia as they age, according to a report released 3/14/02. However, those who took cholesterol-lowering drugs appeared to reduce their risk. In the study of more 1,000 women in their 60s and 70s who had heart disease, those with the highest levels of total cholesterol and LDL ("bad") cholesterol were nearly twice as likely to develop symptoms of dementia over 4 years, compared with their peers with the lowest cholesterol levels. However, women who lowered their cholesterol levels during the study cut their risk of developing symptoms of dementia by about 40%, according to the report. Women whose cholesterol levels fell in the lowest 25% were more likely to be taking a statin drug, a common type of cholesterol-lowering medication. Among all women, those who reported using a statin drug scored higher on tests of mental ability regardless of their cholesterol level. The findings support previous studies suggesting a link between elevated cholesterol and impaired mental functioning, including the development of AD, among older women. The study also points to a potential way to lower the risk of developing dementia, conclude Dr. Kristine Yaffe from the University of California, San Francisco, and colleagues. Reuters Health 3/15/02

Other Items
Studies Shed Light on Degenerative Brain Diseases - Two sets of scientists have zeroed in on a process called protein folding that is believed to go awry in several illnesses including AD and Creutzfeldt-Jakob disease (CJD), the human form of "mad cow" disease. To make proteins, cell structures called ribosomes arrange amino acids into long chains. For a protein to perform its normal function, the chains of amino acids must be looped around each other, or folded, in a particular way. Deposits in the brain called plaques are hallmarks of AD, in which protein misfolding is thought to play a role. These plaques are made up of abnormal proteins called amyloid-beta proteins. In one of two papers in the April 4th issue of the journal Nature, Dr. Christopher M. Dobson at the University of Cambridge in the UK and colleagues report that even proteins that are not linked to disease can be harmful when protein folding goes awry. Dobson and his colleagues took proteins that are not connected with neurological diseases and coaxed them to misfold to form the thread-like structures. These so-called protein aggregates were toxic to cells. The present study suggests that the early stages of the misfolding process that gives rise to the thread-like formations could be the "real culprits" in protein misfolding diseases, Dobson said. "These early aggregates expose 'sticky' patches on their surfaces that can result in their inappropriate interactions with cells and cellular components," he said. In the second study, Dr. Dennis J. Selkoe of Harvard Medical School, and associates also found that molecules formed early in protein misfolding can be harmful. Previous research had linked the amyloid-beta protein to the interruption of synapses, the brain's memory switches, but scientists did not know precisely which form of amyloid-beta was to blame and how the interruption occurred, Selkoe told Reuters Health. "We now identify a specific form of amyloid-beta and show directly in living, anesthetized rats how it interrupts memory circuits in the brain," he said. This form of amyloid-beta is known as an oligomer. "This work thus provides a missing link for the amyloid hypothesis of AD." Once they identified the form of amyloid-beta that is to blame for interrupting the brain's memory circuits, the researchers used a compound called a gamma-secretase inhibitor to keep the oligomers from forming. This treatment lowered levels enough to keep the rats' memory circuits from being disrupted. "It is this approach that we believe now needs to be tried in AD patients," Selkoe said. Taken together, the results of both studies "suggest that damage to cells can be caused by misfolded intermediates generated during the production of amyloid fibrils, whether or not the fibrils--or the normal proteins from which they are derived--are also toxic," Drs. R. John Ellis and Teresa Pinheiro, of the University of Warwick in Coventry, UK, note in a related editorial. "These ideas highlight the importance of understanding the cellular mechanisms that combat these potentially lethal mistakes, and identifying the precise cellular targets of aggregates that escape such surveillance," they write. Ellis and Pinheiro point out that some strains of E. coli bacteria also produce amyloid fibrils, so scientists may be able to use E. coli to study protein misfolding. By Merritt McKinney Reuters Health 4/3/02 Nature 2002; 416: 483- 484, 507-511, 535-539.

Brain's Cleaning Crew May Aid Learning, Memory Formation - In the brain, several chemicals called neurotransmitters carry messages in the spaces connecting one nerve cell, or neuron, to the next, allowing the brain to function properly. Scientists believe that the strengthening of these connections by the neurotransmitter glutamate - a process called long-term potentiation - is one mechanism responsible for the storage of some memories. Now, for the first time, researchers at the University of Houston have determined that levels of transport molecules for glutamate - chemicals that latch on to and "sweep away" glutamate - increase during learning, suggesting that this molecular cleaning crew has an important role in the process. UH biochemist Arnold Eskin says their "results suggest that the regulation of glutamate uptake by the transport molecules may be important for maintaining the strength of connections among the neurons in the area of the brain associated with memory." "Maybe there are people who can't learn as well because their transporters are out of whack, or have memory problems because there are deficiencies in their glutamate transporters. Before we did these studies no one was even asking these questions. Now we have a fundamental reason to investigate this mechanism further. "We knew that glutamate is involved in learning, but our study is the first to investigate the role of glutamate transporters and glutamate uptake in the learning and memory formation process," Eskin said. The job of glutamate transporters in the brain is two-fold. "Clearing away neurotransmitters allows the next batch of chemical messengers to deliver a 'clean' signal between neurons" he said. "Also, in the case of glutamate, which desensitizes its receptors and kills nerve cells if too much hangs around too long, transport molecules are essential to maintaining effective transmission and a non-toxic environment in the brain." Other studies have suggested that deficiencies in glutamate transporters may be responsible for neuron damage and death associated with neurodegenerative diseases such as amyotrophic lateral sclerosis, or Lou Gherig's disease. PR 3/12/02 Nature Neuroscience 2002;5:155-161

US Lawmakers Want Exemptions From Gene Patents - A bill introduced in the US Congress Thursday could suspend federal patent laws for some doctors and medical researchers working with disease-causing genes. The bipartisan proposal would prevent entities owning patents on human genes from barring the use of those genes in non-commercial genetics research or diagnostic disease testing. Supporters contended that a rapidly growing number of patent owners - - usually companies or universities - - are stifling research and patient care by strictly enforcing their exclusive rights on human genes. "There is little doubt that most of the significant claims on our genetic code will be tied up as private property within a few years," said Rep. Lynn Rivers (D-MI), who sponsored the bill with GOP Rep. David Weldon of Florida. The proposal applies only to diagnostic tests and academic research and does not exempt the development of drugs or other treatments. Dr. Debra Leonard, a past president of the American Association of Molecular Pathology, said that her lab at the University of Pennsylvania has been barred from testing patients for the genetic underpinnings of AD and a variety of rarer disorders. "Right now gene patent holders control part of every individual's genetic information more than the individual or their physician. Gene patents are not good for the public health when used to prevent the broad availability of genetic testing services," she said. By Todd Zwillich Reuters Health 3/14/02

Jim Broadbent Wins Best Supporting Actor Oscar - Jim Broadbent won the best supporting actor Oscar on 3/24/02 at the 74th Annual Academy Awards for playing the husband of British writer Iris Murdoch, whose painful decline into AD was depicted in the movie "Iris." It was Broadbent's first Oscar and his first nomination. Broadbent was considered one of the front-runners for the supporting actor award for "Iris" after he won a Golden Globe in that category in January. Known for his comic skills, Broadbent showed his versatility with his performance in "Iris," a love story based on a memoir by Murdoch's husband, author John Bayley. In his acceptance speech he thanked Bayley for allowing the moviemakers "to plunder, and I'm sure misrepresent, his life with Iris." Reuters 3/24/02

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