Alzheimer Related News Items

News as of 8/11/02
For more info on these abstracts write/call Ed Cabic (edcabic@comcast.net or 410-992-7197)
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Top Items
Studies: Cholesterol Drugs May Cut AD Risk - Cholesterol-busting drugs, widely used to reduce the risk of heart attack, may also help cut the incidence of AD, scientists said on 7/23/02 at the 8th International Conference on AD and Related Disorders. Three new studies underlined an apparent link between the use of best-selling cholesterol drugs, known as statins, and a reduced risk of developing the degenerative brain disorder. Dr. Robert Green and colleagues at Boston University School of Medicine found that individuals taking statins to lower cholesterol reduced their risk of developing AD by 29 percent. The 2,378-patient study was the largest to date exploring the links between the disease and statins, use of which has grown rapidly in recent years, led by products such as Pfizer Inc.'s Lipitor and Merck & Co Inc.'s Zocor. The reason for the connection is not immediately clear, but Brain Austen of St. George's Hospital Medical School in London thinks he may have part of the answer. Using laboratory cell cultures, Austen and his colleagues found that statins dramatically lowered the production of beta-amyloid, the protein "plaque" that clumps together in the brains of AD sufferers. His work was echoed in findings presented by Tsuneo Yamazaki of the department of Neuropathology at the University Tokyo. Yamazaki's team found that statins reduced production of beta-amyloids in cell culture, with the reduction directly proportional to the statin dose. "The current generation of statin studies is very exciting in that they may give us a way to reduce the risk of developing AD," said William Thies, vice president of medical and scientific affairs for the AD Association. A major randomized clinical trial is now starting in the United States in a bid to confirm the notion that statins can reduce AD risk. Reuters 7/23/02

Blood Pressure, Cholesterol Tied to AD - Results of a large study of elderly residents of Finland have identified two important new risk factors for AD: high blood pressure and high cholesterol. If these risk factors are combined with genetic risk it makes a person eight times more likely to develop AD. Dr. Miia Kivipelto of the University of Kuopio in Finland presented the new research at the 8th International Conference on AD and Related Disorders and said that these risk factors appear to be just as important as genetic risks for AD. Researchers have previously identified a gene, apolipoprotein E-e4, that is associated with late-onset AD, meaning disease that causes loss of memory and other cognitive problems in people aged 75 or older. This is the most common type of AD and, worldwide, about one in four people carry at least one copy of the so-called AD gene. "We can't do anything to change the genetic risk," Kivipelto told Reuters Health. "But high blood pressure and high cholesterol can be controlled with medical treatments." She and her colleagues studied 1,449 individuals who had been followed by Finnish epidemiologists since 1972. Kivipelto said that individuals who carried the so-called AD gene were about twice as likely to have developed the disease than those who had no genetic predisposition. "But if they also had high blood pressure, the person is five times more likely to develop AD. When high cholesterol is added, the risk is eightfold higher than healthy people with no genetic risk," she said. She said that the association between AD and high blood pressure only relates to systolic pressure, which is the first or higher number in a blood pressure reading. Elevated systolic blood pressure is known risk factor for stroke. By Peggy Peck Reuters Health 7/23/02

Drugs
AD Drug Helps Down Patients with Dementia - A small study suggests that donepezil, a drug sold as Aricept used to slow the onset of AD, may help reverse dementia in people with Down syndrome as well. Down syndrome is a genetic disorder that causes mental retardation and certain physical abnormalities. People with the condition eventually develop two types of brain deposits--amyloid-beta plaques and tau tangles--that are also hallmarks of AD. Many, but not all, people with Down syndrome also develop AD symptoms, which generally show up decades earlier than they do in people with AD who do not have Down syndrome. The researchers gave the drug for an average of 4 months to nine people with Down syndrome who had been diagnosed with moderately advanced dementia. They were compared with a similar group of Down syndrome patients who did not get the drug. The investigators found that the Down syndrome patients on donepezil showed an improvement in brain functioning, as reflected by lower scores on tests that measure the degree of dementia in people with Down syndrome. Clinical neurological exams also found improvements in the donepezil-treated patients. Based on the positive results of their small study, Dr. Ira T. Lott of the University of California, Irvine and colleagues believe that larger, controlled trials into the use of donepezil and similar drugs in patients with Down syndrome are needed. Reuters Health 7/18/02 Archives of Neurology 2000;59:1133-1136

Elan Announces $802M 2Q Loss - Troubled Irish drug company Elan Corp., once a Wall Street darling because of its pioneering research into AD, on 7/31/02 announced a big second-quarter loss - - and a survival plan to slash staff and nonessential operations. Elan, based in Athlone, Ireland, said losses for the quarter ending June 30 totaled $802 million, worse than expected, compared to a $134 million profit in the same quarter last year. Revenues were flat at $459.5 million compared to $461.5 million in the same quarter of 2001. Elan said it planned to trim 1,000 jobs from its 4,700-strong work force worldwide by the end of the year. It said it would focus on developing drugs for neurological disorders, pain treatment and autoimmune diseases and would shed other research programs. By Shawn Pogatchnik, Associated Press Writer 7/31/02

Genes & Genetic Issues
Bush Bioethics Council Splits on Cloning Issue - The issue of cloning, which has stumped the U.S. Senate, also has eluded the president's top bioethics advisers, who issued a report on 7/11/02 that does not make a specific recommendation on whether to ban human cloning research. Seven top experts appointed to advise President Bush on the issue voted to allow so-called therapeutic cloning, which would use cloning technology for medical research, to proceed with strict regulation. Ten members voted for a four-year moratorium on all cloning research involving humans. "Rather than seek some kind of false consensus, we have agreed on the importance of all sides of the discussion and put them side by side in the report," Dr. Leon Kass, a bioethicist at the University of Chicago who has taken leave to head Bush's Council on Bioethics, said in a telephone interview with Reuters Health. By Maggie Fox, Health and Science Correspondent Reuters 7/11/02 The report is at http://www.bioethics.gov/cloningreport/

First Fully Human Embryonic Stem Cell Line Created - A Singapore-Australia joint venture, ES Cell International, and one of its collaborative partners, the National University of Singapore (NUS), announced the world's first published report of a human embryonic stem cell line grown entirely without exposure to mouse cells or other non-human ingredients. The research is due to be published in the September 2002 edition of Nature Biotechnology. Stem cells are immature cells capable of developing, or differentiating, into a number of different types of body cells. They offer promise for treating diseases in which a person's own cells have deteriorated, such as AD, Parkinson's disease and many more. The standard technique for creating human embryonic stem cell lines has been to extract cells from an embryo and grow them atop embryonic mouse cells, known as "feeder" cells, which excrete nutritional or growth factors that sustain the cell lines. But this close association with mouse cells raises safety questions, as the cell lines could transfer animal viruses to people. In fact, all 78 stem cell lines listed on the National Institutes of Health Stem Cell Registry have been mixed in the laboratory with mouse cells, making them xenotransplant products. This could create substantial hurdles to US Food and Drug Administration (FDA) approval for clinical trials based on these cells. Professor Ariff Bongso, who spearheaded the research at NUS, told Reuters Health that the team's early work on isolating embryonic stem cells in 1994 used human feeder cells derived from fallopian tubes. When the scientists could not sustain the cell lines for more than 2 generations, they thought the feeder cells were the problem, and so they started using mouse feeder cells. "Our recent experiments show that the feeder cells are not the issue," Bongso explained. "Embryonic stem cells are social cells that work best in a community--in the past, we grew individual cells but our latest work shows that if we maintain clusters of cells, they survive well regardless of the feeder cells they are grown on. We have created a new cell line in a totally animal-free system and maintained it for 50 generations without differentiation," said Bongso. By Pooja Vig Reuters Health 8/7/02

Stem-cell Research Gets off to Slow Start - A year after President Bush's controversial decision to allow limited federal funding for stem-cell studies, the research is proceeding slowly, and scientists are working with a fraction of the cell lines that the president said would be available. More batches of stem cells will become available in the months ahead. But many scientists say that even if they had access to all 64 of the originally promised lines -- each a colony of cells derived from an individual embryo -- it wouldn't be enough to realize the potential the cells hold to heal. By Elizabeth Weise USA TODAY 8/7/02

Caregivers
Fear of Dementia Diagnosis Puts Patients at Risk - Britain's Alzheimer's Society said on 7/8/02 that patients with early symptoms of dementia are at risk because caregivers are too frightened to take them to a doctor to have the diagnosis confirmed. The charity said research findings showed half of all caregivers delay visiting general practitioners after first noticing something was wrong. The average delay was 3 years. The research covered 40 practices and 120 doctors, 80 nurses, 220 people with dementia and 110 caregivers. "Three years is far too long for someone to wait," Professor Murna Downs, one of the researchers, from the University of Bradford's Dementia Group, said in a statement. "We need to let people know that there are many new services and drug treatments for people with dementia. For those who may benefit from the new drug treatments, the earlier these are the prescribed, the better. There is clearly still a lot of stigma and misunderstanding attached to dementia." By Richard Woodman Reuters Health 7/8/02

Device to Track Missing People - Jennifer Durst, a single mother from Oyster Bay, N.Y., and two partners have patented a lightweight, portable G.P.S. transceiver that she says is designed to be "form-fitted into a backpack, a baseball hat or a belt," for example. Their devices can be programmed with boundaries, and if those boundaries are exceeded, the devices send messages directly to a cellphone, pager, two-way personal assistant, traditional phone or even an e-mail address. Those messages are followed by continuously updated geographic information, she said. "Up until now, a G.P.S. device could tell you where you are," Ms. Durst explained in July 2002 , just days after her latest patent was issued. "But it doesn't tell me where you are. What I've done is make it, 'Now tell me directly where you are.' " The device weighs about seven ounces, though Ms. Durst said she hoped it would become smaller as the technology advanced. It runs on a rechargeable battery and picks up its G.P.S. signals with a flat, patchlike antenna. Adults are often lost in a variety of ways: AD patients sometimes wander off, hikers and mountain climbers disappear in the wilderness, soldiers go missing in action. Ms. Durst says any of these people could be tracked with precision if only they were linked to the G.P.S. system. The system for tracking children or adults is not available for sale yet, even though Ms. Durst and her partners have a Web site at www.gpstracks.com that offers information about the dog-finding collar. Ms. Durst estimated the system would cost about $300, plus a monthly subscription fee. She and her fellow inventors, Eugene Fowler and Joseph McAlexander, have obtained three patents: the pet locator is 6, 172, 640, and the "mobile object locator: received 6,236,358 and 6,421,001. By Sabra Chartrand NY Times 8/5/02 To see U.S. Patents go to http://164.195.100.11/netahtml/srchnum.htm and type in the patent number.

Testing
Brain Changes Occur Long Before AD Symptoms - Using sophisticated scanning techniques, scientists have detected abnormalities in the brains of young people with a genetic risk for AD, decades before symptoms are likely to appear. Researchers from the Good Samaritan Regional Medical Center in Phoenix, Arizona, told an AD conference 7/23/02 that although memory lapses may not occur until 60 years or older, brain differences can be picked up in high-risk adults in their 20s and 30s. "Young adults at risk of AD have detectable brain abnormalities several decades before the possible onset of memory and thinking problems," said Dr. Eric Reiman. The scientists used a brain imaging technique called positron emission tomography (PET) to detect changes in the brains of people with ApoE-4, a gene associated with high cholesterol and AD. People with the gene have an increased risk of developing the illness but it is not a certainty, the researchers said. They compared the results of memory and cognitive tests and differences in the brain activity between 15 people with ApoE-4 and a dozen without it.The memory and cognitive results were normal for both groups but Reiman and his team found abnormally low brain activity in patients with ApoE-4 in the same region of the brain normally affected by AD.

Scanning May Help Detect Early AD - In research presented at an international AD meeting on 7/25/02, scientists from the University of California in Los Angeles (UCLA) said a chemical marker called FDDNP allows doctors to track early changes in the brain. They used the marker in conjunction with a brain imaging technique called positron emission tomography (PET). "We found that people with normal memory performance with a genetic risk for AD had a higher signal on the PET scan than those without the generic risk, indicating that evidence of the disease is apparent even before people have obvious memory symptoms," Dr. Gary Small said. AD is not apparent until patients develop symptoms such as memory loss and confusion. The disease is marked by the buildup of plaques and tangles in the brain, and usually occurs in people older than 60. Small and his team used FDDNP, which was developed at UCLA, and PET to pinpoint early signs of the illness. Theirs was one of several studies presented at the meeting looking into new ways to detect AD with PET scans. "What these studies are suggesting is that we can see the physical evidence of AD decades before people even reach the age at risk," Small explained. The UCLA scientists studied people with the ApoE-4 gene, which is associated with AD. It is one of several factors that may increase the risk of developing the illness. Small said the technique could have two purposes--as a potential diagnostic tool after it is developed further, and to test the effectiveness of new treatments. "What's exciting about this new invention is that it offers us a way to test new drugs that could be targeted to clearing out the plaques and tangles and to start testing them in people before they have significant brain damage from AD," he said. Reuters 7/25/02

Prevention
Vitamin E May Help Keep People Sharp in Old Age - Vitamin E intake in food and supplements may help slow decline in mental functioning among older people, according to the results of a study lead by Dr. Martha Clare Morris, a professor of internal medicine at Rush-Presbyterian-St. Luke's Medical Center in Chicago, Illinois. "High amounts of vitamin E from foods appears to be protective from cognitive decline," she told Reuters Health. The researchers theorized that vitamin E, an antioxidant, may counteract the damage done to brain cells by free radicals, which are byproducts of normal body processes that can damage tissue and have been linked to disease. Previous research has suggested that people who consume more vitamin E retain mental function and are less likely to develop AD. To investigate, the researchers studied more than 2,800 US men and women aged 65 to 102. Each was given an initial battery of mental function tests and followed for an average of 3 years, during which they were retested two or three times. They were also asked to fill out a food questionnaire assessing how much of various nutrients they received in their diets and from supplements. The findings were 61% of the study participants showed some decline in their mental function during the course of the study, while 39% had no decline or even improved. The group who reported the highest intakes of vitamin E had a slower decline in mental function than those whose vitamin E intake was lowest. "There was a 36% reduction in the rate of decline for people in the highest fifth of intake of vitamin E compared to those in lowest fifth of intake," Morris said, referring to intake of the vitamin in both food and supplements. And those with the highest intake of vitamin E in food had a 32% reduction in their rate of mental decline, compared to those with the least vitamin E in their diets, she said. For those who took vitamin E supplements, the effect on mental skill was only seen among those who received little vitamin E from their diet, but not in those who already received lots of the vitamin in their diet. "There may be a ceiling effect, and if you taking more, it's not helpful," Morris noted. However, because the number of people taking supplements during the study doubled, possibly in response to cognitive decline, it was hard for researchers to draw conclusions about whether supplement use was effective on its own in maintaining the brain. Vitamin E is found in green, leafy vegetables as well as corn, nuts, olives and vegetable oils. By Melissa Schorr Reuters Health 7/17/02 Archives of Neurology 2002;59:1125-1132

Antioxidant-rich Diets Improve Age-related Declines in Mental Function of Rats - Two new animal studies by researchers at the University of South Florida Center for Aging and Brain Repair bolster a growing body of evidence that certain fruits and vegetables may protect the brain against the ravages of age. "If these pre-clinical findings translate to humans, it suggests that eating a diet high in antioxidant-rich fruits and vegetables may help reverse declines in learning and memory as you get older," said Paula Bickford, PhD, lead author of both studies and a professor at the USF Center for Aging and Brain Repair. In the first study, co-authored by USF's M. Claire Cartford, PhD, older rats fed a diet rich in spinach for six weeks showed a reversal in the normal loss of learning that occurs with age. Spinach is rich in antioxidants, which scientists say can counteract free radicals generated in the body during normal metabolism and exposure to environmental insults such as pollution, ultraviolet light and radiation. An excess of free radicals can damage cellular lipids, protein and DNA. Studies suggest that a lifelong accumulation of free radicals can slow mental processes in old age and may be a factor in AD and Parkinson's disease, Dr. Bickford said. The second study found that the benefit of a diet high in fruits and vegetables depends on the levels of antioxidant nutrients in the fruits and vegetables. Furthermore, the researchers suggest, the protective effect of antioxidants may be linked to their ability to reverse age-related accumulations of potentially harmful inflammatory substances in the brain. The research has hopeful implications for the prevention of neurodegenerative disorders in an increasingly aging population, but still must be tested in humans, Dr. Bickford said. Until then, the USF neuroscientist recommends that daily diets include a variety of richly colored fruits and vegetables - - the most colorful ones tend to pack the greatest antioxidant punch. She favors spinach salads for lunch and routinely snacks on blueberries and strawberries. PR 7/15/02 Journal of Neuroscience 2002 22: 5813-5816 and 6114-6120

Mental Aerobics, Diet Stave Off 'Senior Moments' - If those "senior moments"--when you cant remember why you opened the refrigerator door or where you left your keys--are becoming more frequent, mental aerobics and a healthy brain diet may help. Just as bodies require more maintenance with the passing years, so do brains, which scientists now know show signs of aging as early as the 20s and 30s. "Brain aging starts at a very young age, younger than any of us had imagined and these processes continue gradually over the years," said Dr. Gary Small, the director of the Center on Aging at the University of California, Los Angeles. The process may be speeded up a bit by a genetic risk and pushed even faster by unhealthy lifestyle choices. But Small believes that, just as with heart disease and cancer, people can take preventive measures to keep their brains healthy and alert to stave off the ravages of the disease. "I'm convinced that it is never too early to get started on a mental or brain-fitness program," he said. In his book, "The Memory Bible," the 51-year-old neuroscientist lists what he refers to as the 10 commandments for keeping the brain young. They include training memory, building skills, minimizing stress, mental aerobics, brain food and a healthy lifestyle. By Patricia Reaney Reuters 8/6/02

Three Coffees a Day Keeps Dementia at Bay - Drinking at least three cups of coffee a day can reduce the risk of developing AD by as much as 60 per cent. New research shows that healthy elderly people, with no signs of the brain disease, had consumed an average of three to four cups a day since the age of 25. However, those with the debilitating illness drank, on average, just one cup of coffee each day. Scientists believe it is the caffeine in coffee that protects against AD. The report is from the faculty of medicine in Lisbon, Portugal, which conducted the research which compared 54 AD patients with 54 healthy people of the same age. The researchers said: "If confirmed, this finding should have a major impact on the prevention of AD." Laboratory experiments on mice have already pointed to caffeine as a potential treatment for the disease. However, this is the first study to show the link in humans. Exactly why caffeine should prevent the brain disease is not clear. The scientists found people with AD drank 74 mg of caffeine a day - the equivalent of one cup of coffee or two to three cups of tea. Those without the disease averaged 200 mg a day. The UK Alzheimers Society urged caution in interpreting the findings, saying studies examining the link between dementia and diet and lifestyle could give a clearer understanding. "All we can conclude is that long-term caffeine intake may be having a protective effect," director Dr Richard Harvey said. By Rachel Ellis News.Com.Au 7/15/02 European Journal of Neurology 2002 vol. 9, issue 4, 377-382

Brain Reserve Capacity and its Role in Preventing Clinical Signs of AD Studied - Identifying factors that increase the reserve capacity of the brain and enable people to tolerate the pathological changes that occur in the brains of people with AD offers a new and potentially powerful approach to delaying the clinical signs of the AD and other neurodegenerative diseases, according to researchers at Rush-Presbyterian-St. Luke's Medical Center, Chicago. Research is underway at Rush to identify the factors that increase or maintain the reserve capacity of the human brain. Researchers have known for some time that education and related lifestyle experiences affect cognitive function across the lifespan. There is also evidence that these educational experiences can reduce one's risk of developing AD. "How these lifestyle experiences actually affect the brain is unknown," according to Dr. David A. Bennett, director of the Rush AD Center. "We think that education and factors related to education may affect the way the brain responds to the abnormal proteins that accumulate in the brains of people with AD. In other words, in people with similar amounts of these abnormal AD protein deposits, those with more educational experiences will be less likely to have memory loss than those with less education," he explained. "We want to understand how cognitively stimulating activities, from childhood to old age, affect brain structure," Bennett said. "Animal studies suggest that different experiences can affect the structure the brain, including the number of brain cells and the number of synapses, the connections between brain cells. The extent to which this occurs in humans is unknown. But if lifestyle affects the brain structure of humans, it is possible that education and related factors could increase neural reserve and allow the brain to tolerate pathology without manifesting memory loss and other clinical signs." PR 7/23/02

Other Items
Actor Heston May Have AD - In a declaration reminiscent of former President Reagan's 1994 "sunset of my life" letter to the American public, Oscar-winning actor Charlton Heston revealed he has symptoms consistent with AD. "I'm neither giving up nor giving in," the 78-year-old actor and National Rifle Association president said in a taped statement played 8/9/02 at a news conference at the Beverly Hills Hotel. "But it's a fight I must someday call a draw," he continued. "I must reconcile courage and surrender in equal measure. Please, feel no sympathy for me. I don't." By Eugene Tong, Associated Press Writer 8/10/02

Ron's Health Worsening - Former President Ronald Reagan is steadily slipping in his terminal battle with AD, according to close friends and former associates. Sources close to the 91-year-old 40th President report that Reagan's mental deterioration has accelerated in recent months. "He no longer knows who Nancy is," one well-placed source told the Daily News, referring to his wife of 50 years. "Some days he seems to recognize her as someone who's familiar, but most of the time she's just a blank to him." Until a few months ago, Reagan's physical condition held surprisingly steady even as his mental faculties continued to decline. But that is no longer the case. "He's becoming more difficult to deal with," a source close to the Reagan family told The News. "Both his physical and his mental problems have gotten worse." Daily News 8/10/02

US Senate Subcommittee OKs NIH Funding Increase - Under a bill approved by a US Senate subcommittee 7/16/02, the National Institutes of Health (NIH) would receive a funding increase of $3.7 billion for the fiscal year that begins October 1, completing a congressional vow to double the agency's funding over 5 years. "I believe this achievement will rank as one of the most significant health policy achievements in recent times," said Sen. Tom Harkin (D-IA), chairman of the Appropriations Committee's subcommittees on Labor, Health and Human Services, and Education. The plan will bring total NIH funding to $27.2 billion. "This investment will improve lives and save millions from cancer, AD, Parkinson's, diabetes, and many of the world's deadliest and most debilitating diseases," Harkin said. By Julie Rovner Reuters Health 7/17/02

Debate Rages over AD Research - After decades of research into this excruciatingly complex disease, there have been many inspiring advances. Potential vaccines, protease inhibitors - - like those used to treat HIV infection - - and other drugs are being developed. But most of these discoveries are based on a hypothesis that is being questioned with increasing urgency by some of the field's top scientists, who say opposing views have for too long been choked off. Now some complain that we'd be closer to a cure if the field wasn't so scientifically and politically dominated by research based on the amyloid hypothesis, as it's known, which many view as the cause of AD, but no one can say for sure. "It's the million-dollar question," says Dr. Peter St. George-Hyslop. "This is all theory and that's good, but what's the evidence it will work?" At the present time, one theory had become entrenched in the research field, in part because of the work of St. George-Hyslop. It's said that up to 80 per cent of AD scientists ascribe to it still: the amyloid hypothesis. "There are some people who say (beta-amyloid) is rubbish," St. George- Hyslop says. "I think it starts the disease process. Amyloid triggers a cascade of problems." Billions and billions of dollars have been spent in pursuit of this belief, that the buildup of amyloid causes problems, including tangles, leading to a swampy pool of dead brain cells. Stop the amyloid, the theory goes, and you'll stop the disease. Opposition to the theory is growing more urgent as time passes. There are now even organized conferences to discuss alternate possibilities because some scientists say amyloid and its proponents dominate the major world conferences. "I think the hypothesis is urgently in need of a major overhaul," says Peter Davies, of the Albert Einstein College of Medicine in New York, perhaps the world's top authority on tau tangles. "It's time to let go." "In many senses the amyloid hypothesis has been tested rigorously and the results are negative," Davies adds. But the legions of scientists still on the bandwagon are not dissuaded, he says, because of money. "There's a tremendous investment in this hypothesis, and I think that it tends to get in the way of good science." By Andrew Chung Toronto Star 8/10/02 Full copy at http://www.thestar.com search for "Chung"

Scientists Create Big-brained Mice - A single gene change that boosts the amount of a certain protein in early brain cells causes mice to develop abnormally large brains, new research shows.Normal mice have smooth, flat brains, but the genetically engineered mice developed brains that were so big they folded in on themselves, forming wrinkles and ridges--structures also found in the human brain. According to study author Dr. Anjen Chenn of Brigham and Women's Hospital and Harvard University in Boston, this finding may help researchers understand how humans came to develop brains that dwarf those of other mammals. During the study, Chenn and Dr. Christopher A. Walsh engineered mouse embryos that contained a single gene change, which resulted in early nerve cells that produced an excess amount of the protein beta-catenin. In normal cells throughout the body, this protein is involved in helping cells stick together and in regulating the expression of proteins. The brains of the mouse embryos with abnormal levels of beta-catenin grew abnormally large, the researchers report. In an interview with Reuters Health, Chenn explained that during brain development, early nerve cells --known as precursor cells - - divide and thereby generate more precursors, then eventually stop dividing and form nerve cells. In these situations where cells contain large amounts of beta-catenin, however, Chenn speculated the cells are simply triggered to keep dividing. These findings may have future implications for people who need extra brain cells, such as after disease or injury, Chenn said. Furthermore, understanding the growth process may help explain why some people develop mental retardation as a result of too few brain cells, he noted. In an interview with Health Scout News Dr. James Grisolia, a neurologist with Scripps Mercy Hospital in San Diego, said that beta catenin isn't the only key to brain growth. However, it could be useful in a variety of treatments. "Maybe adding catenin to retarded infants will improve their brain growth and make them smarter," he suggests. "Maybe it will help prevent atrophy of the brain in old age and keep away the ravages of AD, or at least normal aging." "The chances that beta catenin itself could be used as a treatment are small, but once we understand how it works, the avenues may open to devising drugs that increase its effects or stimulate its production within the brain cells," he says. By Alison McCook Reuters Health 7/18/02 and Randy Dotinga Health Scout News 7/16/02 Science Jul 19 2002;365-369

US AD Cases to Triple by 2050 - Recent US census figures suggest that by 2050, the number of people with AD will triple, researchers reported at the 8th International Conference on AD and Related Disorders on 7/24/02. Currently, there are about 4.6 million people with AD living in the US, according to Dr. Denis Evans of the Rush Institute in Chicago, Illinois. Based on 1990 and 2000 census data the researchers estimate that there will be 11 million to 16 million people with AD by 2050. The disease will be most common among those aged 85 and older. Jed Levine, program director of the New York City chapter of the Alzheimer's Association, told Reuters Health that he is not surprised by the estimates. "The number of people over 85 has increased and is going to increase. (The figures) have a demographic explanation." Levine added, "AD is going to be one of the major health crises in the future. We are currently spending $100 billion on caring for AD patients." He warned that the growing epidemic will further stress the country's already-stretched healthcare system and put an "enormous burden" on Medicare and Medicaid. "We are not ready, not adequately prepared to handle the AD patients we have now. The system is fragmented," Levine said. "As the numbers (of patients) grow, the problem will grow." He stressed that more research funding is needed to develop strategies for preventing and treating the disease. Reuters Health 7/24/02

AD Drug Ups Memory in Healthy Pilots - Airplane pilots who took a drug normally used to enhance memory in AD patients performed better during a flight simulator test than their unmedicated peers, new study findings show. However, the investigators caution that the effect of the drug on the pilots' performance was relatively small. Furthermore, the results are based on only a small number of pilots, 18--and many legal and ethical aspects of the use of this drug, called donepezil, would have to be worked out before it ever could be used as a memory enhancer in healthy people. During the study, 18 pilots, who were an average of 52 years old, took seven turns on a flight simulator to practice complex tasks, such as handling emergency situations and responding to frequent control commands. Nine pilots then took donepezil for 30 days, while the rest took an inactive placebo. At the end of the treatment period, the pilots took two more turns on the flight simulator, to see how much of their earlier training they had absorbed. Dr. Jerome Yesavage of Stanford University in California and his team found that pilots treated with donepezil performed slightly better during the post-treatment flight simulations than those who were not given any memory-enhancing medications. The donepezil- treated pilots especially excelled during emergency situations, and when preparing the plane for a landing. In an interview with Reuters Health, Yesavage explained that donepezil achieves its effects by inhibiting the enzyme acetylcholinesterase, which breaks down the substance acetylcholine. Reduced levels of acetylcholine have been associated with impairments in memory function, he noted. By Alison McCook Reuters Health 7/8/02 Neurology 2002;59:123-125

Stroke Stories
Dementia - Before or after Stroke - Increases Risk of Death - Stroke survivors who have symptoms of dementia before or after a stroke have a significantly greater risk for stroke-related death, according to new research reported from the Fundación Hospital Alcorcón, Madrid, Spain. An analysis of data from a stroke registry compiled in Spain indicates that patients who have post-stroke dementia have a more than eight-fold increase in risk of death within two years of stroke than patients who have no signs of dementia after stroke. When dementia was diagnosed before the stroke, the risk for death was twice as high as the death risk for patients who had no dementia before or after stroke. When dementia is related to stroke, the risk for death within two years increased more than six-fold. Researchers found that dementia - declines in memory, cognitive function and capacity to perform daily living activities - is an independent risk factor for death after stroke and one of the most important determinants of death in stroke patients, explains the study's lead author Raquel Barba, M.D., Ph.D., a clinical investigator in the department of medicine at the hospital. Possible explanation for the poor survival rate among stroke survivors with dementia is that these patients may not receive the same treatment as stroke survivors who have no cognitive impairment, says Barba. For example, the study found that a patient with dementia was less likely to be treated with oral anticoagulants than one without dementia, even if atrial fibrillation was diagnosed. Atrial fibrillation is an abnormal heart rhythm associated with increased risk for blood clots. It's often treated with anticoagulants to prevent stroke. But these drugs require careful compliance with dosing guidelines and patients with dementia are less likely to comply with medication regimens. PR 8/1/02 Stroke: Journal of the American Heart Association 2002;33:1993

Bypass Surgery Linked to Increased Stroke Risk - Coronary bypass surgery for heart disease could increase the risk of stroke and memory problems in some patients, doctors said 7/24/02. In the surgery, a blood vessel from elsewhere in the body is attached to the heart to bypass a blocked artery. Patients who undergo the surgery generally need to be on a heart-lung machine for a certain amount of time. Researchers from Johns Hopkins School of Medicine told an international conference in Sweden that patients with high blood pressure, diabetes or who have had a previous stroke may be more likely to experience the ill effects of the surgery. "There appears to be a sub-population of patients undergoing coronary bypass surgery, with risk factors for stroke, cognitive decline and long-term cognitive changes," Dr. Guy McKhann told attendees of a meeting on AD. Reuters 7/24/02

Lingering Cognitive Impairment May Be Linked to Coronary Bypass Surgery - North Carolina neuropsychologists at the University of North Carolina at Wilmington believe they have gathered reliable evidence linking cardiopulmonary bypass surgery to impaired memory and attention. Claims about this relationship have been made before, but the current team used statistical methods that they consider to be more sound, less biased and less likely to over- estimate occurrence than those used in previous research. The researchers also, for the first time, documented that the cognitive declines persist beyond the first couple of weeks. The study appears in the July issue of Neuropsychology. PR 7/4/02 Neuropsychology 2002, Vol. 16, No. 3, 411-421