Alzheimer Related News Items

News as of 2/06/01
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AD: What Once Was Lost Now Is Found - "In late-stage AD, patients generally forget -- almost immediately -- what's been said to them," says Cameron Camp, PhD, director of the Myers Research Institute in the Menorah Park Center for Senior Living in Beachwood, Ohio. "Yet, every patient has a very short 'window' during which they retain the answers. It may be two minutes, it may be 30 seconds -- then they lose access to it." Space retrieval involves widening that window, helping AD patients remember new information over longer and longer time intervals. "We've found that if we can push that window, stretch that interval up to eight-12 minutes, the information starts going into long-term memory," Camp says. "It's not improving memory per se, but makes information more accessible to them." Camp gives the example of one woman who could never remember mealtimes. He wrote the information on a card and put it in the purse she always carried. He trained her to look for the card when the question popped into her head. Other patients have been trained to look for color-coded messages on a board for answers to their frequent questions. Idleness, increasing restlessness, agitation, and depression -- all are quality-of-life issues for AD patients in long-term care. But by applying learning concepts taken from Montessori day care schools, Camp has been able to get patients engaged in all sorts of activities that improve quality of life. As in Montessori schools, the activities build skills through a series of steps, working from simple to complex -- and building self-esteem and confidence in the process, Camp says. One example involves teaching patients to eat soup. Step one: using an ice cream scoop to move golf balls from a bowl into a muffin tin. Next: using a melon scoop to move marbles. Next: moving rice grains using a spoon. "From there you go to transferring liquid, then to feeding yourself soup," Camp tells WebMD. Another therapy -- called "errorless learning" -- puts a more positive spin on traditional rehabilitation, says Leslie Gonzalez-Rothi, PhD a professor of neurology at the University of Florida, Gainesville. In a preliminary study of one patient, Gonzalez-Rothi was able to teach the patient 80 words in two weeks. "In daily half-hour sessions, we showed that the significantly impaired patient learned new words and kept those words for up to six months," Rothi says. Another group of four patients is now completing their two-week sessions and exhibiting the same progress. The therapy is effective, she speculates, because it works with the standard drug treatment, Aricept. While Aricept proves ineffective in halting the disease's decline, it does make the nervous system more receptive to learning, Rothi says. By Jeanie Davis WebMD Medical News 1/20/01

Drugs
Amelia Earhart Needed These Mice - Scientists at the University of Rochester in New York have succeeded in increasing the number and size of neurotransmitters in the brains of mice that, in turn, become much better at navigating new mazes. The gains came, in part, because researchers increased the amount of nerve growth factor, or NGF, in the mice's hippocampus, a region of the brain associated with memory and learning. NGF is believed to help with communication between cells in the central nervous system. The added NGF probably strengthened an important pathway between the hippocampus and the basal forebrain, or part of the brain linked with spatial learning, says lead researcher Dr. Howard J. Federoff. In addition, gains were registered when the mice had to really use their brains to figure their way around new mazes every day, Federoff says. "Something was triggered," he says. "The ability to access the growth factor enhanced the way the pathway worked." Dr. Leon Zacharowicz, a neurologist at the Nassau University Medical Center on Long Island, New York, commented on the study as being one of a number that currently are breaking down old beliefs about the brain. "We thought until only a few years ago that the brain was hard-wired,…but this study and others have indicated that may not be the case," Zacharowicz says. "The plasticity of the brain is greater than we expected." By Julia McNamee Neenan HealthScout Reporter 1/4/01 Proceedings of the National Academy of Science 2000 Nov 21;97(24):13378-83/ Free full copy available at http://www.pnas.org/cgi/content/full/97/24/13378

UK Watchdog Recommends Three AD Drugs - Britain's controversial National Institute of Clinical Excellence said on 1/19/01 three new drugs, Aricept, Exelon and Reminyl, which can improve the lives of some AD patients should be reimbursed on the state-funded National Health Service. The medicines, which can slow memory loss in cases of mild to moderate dementia, work by increasing the brain's supply of acetylcholine, a neurotransmitter that helps cells communicate. "It is clear from the evidence that some patients and their families can benefit from the provision of these medicines," said Andrew Dillon, chief executive of NICE. "However... these products will not benefit all patients and should only be used as long as they are having a worthwhile effect," said Dillon. NICE said use of the drugs should be limited to patients with early to moderate dementia and that treatment must be initiated by a specialist doctor, rather than a general practitioner, with check-ups every six months. By Ben Hirschler, European pharmaceuticals correspondent Reuters 1/19/01

AD Findings Point to Possible Treatments - The brains of AD patients contain deposits of an abnormal protein called beta-amyloid, but scientists have not been certain whether the protein is the cause or the result of the disease process. In an effort to understand beta-amyloid's role in the condition, investigators at the National Institutes of Environmental Health Sciences, National Institutes of Health, in Research Triangle Park, North Carolina studied its impact on the function of nAChR--a key receptor- located in the memory areas of rat brains. They found that beta-amyloid can significantly reduce, by as much as 39%, the ability of nAChR to transmit messages conveyed by the brain's signaling proteins, in effect preventing the key from turning the lock. The beta-amyloid specifically reduced the response of the receptors to the signaling protein acetylcholine but not to other signaling proteins, the researchers note, which may account for the benefits seen with drugs that increase the levels of acetylcholine in AD patients. Rather than being a result of AD, the scientists suggest, beta-amyloid might cause the symptoms of the disease through its interference with the nAChR receptor. Finding drugs that can prevent beta-amyloid from interfering with the function of nAChR might restore normal communications and improve the many symptoms of AD, the authors conclude. Reuters Health 1/5/01 Journal of Neuroscience 2001;21

Forest Sets New AD Trials, Eyes '03 US Launch - Forest Laboratories Inc. on 1/30/01 said it would seek U.S. marketing approval by the end of 2001 for an experimental treatment for AD but would begin new Phase III studies of its drug Memantine this spring to satisfy concerns of federal regulators. The firm said the FDA agreed that summary data from a Phase III trial conducted in the United States, if confirmed in a formal full submission, "provided evidence of efficacy" in treating afflicted AD patients. But Forest said the FDA also indicated a second study performed in Europe would likely need to be reviewed by an FDA advisory panel to verify that the specific trial goals, or endpoints, were adequate to qualify it as a second study demonstrating efficacy. Consequently, Forest said it intended to seek U.S. marketing approval by the end of 2001, but would begin several additional Phase III studies this spring that would be completed in the second half of 2002 and be used as additional evidence of efficacy. The AD drug could be launched by the second half of 2003 if any of the studies prove successful, it added. An earlier launch of the treatment is possible, Forest said, if the FDA's advisory committee recommends that the FDA accept the already completed European study, whose data will be included in the company's U.S. marketing application. By Ransdell Pierson Reuters 1/30/01

Genes & Genetic Issues
Blacks And Hispanics at Greater Risk of AD - African Americans and Hispanics may be at increased risk of developing AD, according to new study findings by researchers from Columbia University in New York, and the New York State Psychiatric Institute. They followed 1,799 elderly people living in northern Manhattan. Between the ages of 75 and 90 years, the risk of developing AD for African Americans and Caribbean-Hispanics is twice that of whites, Dr. Richard Mayeux and colleagues write. The researchers do not know what lies behind the extra burden of AD in the minority populations. Mayeux thinks genetic differences might be to blame, although which genes are involved is not clear. "Hispanics from...Caribbean nations may share some of their genetic background with individuals of African decent, which may partially explain the similarity in disease risk," the authors write. The fact that the proportion of these two groups living beyond 65 years is growing faster than the proportion of whites, "it is imperative that this disparity in the rates of disease among the elderly be understood," Mayeux and colleagues conclude. Reuters Health 1/10/01 Neurology 2001;56.

Scientists Genetically Engineer a Monkey - Scientists said on 1/11/01 they had genetically engineered a monkey, the closest relative yet to a human to be genetically altered, in a step that could hasten the development of cures for diseases ranging from cancer to AD. Many animals have been genetically engineered such as sheep and mice, but until now no one had managed to put a new gene into a primate, the class of mammals that includes humans. The baby rhesus monkey is named ANDi, backward for "inserted DNA," and looks like any other baby monkey, said Gerald Schatten and colleagues of the Oregon Regional Primate Research Center at the Oregon Health Sciences University. "We think it's a special step," said Schatten, whose team developed the first cloned monkey in 2000, in a telephone interview with Reuters. The idea is to engineer monkeys with genes known to cause disease in humans. Perhaps these monkeys could even be cloned, so that exact copies could be used to study drugs and other potential treatments without having to factor in genetic variation, Schatten said. Mice are already used in this way but are not always similar enough to humans to be good models. "If you are a mouse with AD, there are very good vaccines available. But long before we would want to help (former) President (Ronald) Reagan, (who suffers from AD), we'd want know that those vaccines could be optimized," Schatten said. By Maggie Fox, Health and Science Correspondent Reuters 1/11//01

Root of Rare Brain Disorder Found - Scientists at the Waisman Center, University of Wisconsin-Madison tracked down a gene mutation as the definite cause of Alexander disease, a rare brain disorder that usually kills its victims before they're 6. The disorder is a cousin to AD and Parkinson's. Alexander disease affects the insulation -- called the myelin sheath -- that protects the nerve fibers in the brain. It often strikes children before their first birthday, causing catastrophic damage to the nervous system. The gene found is called glial fibrillary acidic protein (GFAP). Mutations here create an abnormal protein, which, in turn, makes fibers build up enough to damage nerves. This protein "produced a meshwork, or scarring around the nerve sheaths, damaging the nervous system," says Albee Messing, a professor at the University. When the GFAP gene is healthy, its proteins are a hallmark of a type of cell that maintains nerves and their myelin sheaths. Messing says more work needs to be done to determine whether the "protein aggregates are somehow toxic and might be compromising cell function, or whether they may be a byproduct, or a marker of the aggregates themselves." "We really know very little about normal function of GFAP. It's a black box …We're going to concentrate now on understanding how mutations in this protein cause disease." The results may have ramifications for other disorders involving protein buildups, like Parkinson's and AD, Messing says. By Fran Berger HealthScout Reporter 1/2/01 Nature Genetics 2001, 27, 117-120

Bush Opposes Federal Funds for Cell Research - President-elect Bush's spokesman Ari Fleischer said 1/4/01 he opposes federal funding for fetal tissue research that uses discarded human embryos. Although he did not say whether Bush would move to stop such research today, the president-elect has been quoted in the past as saying he favors a ban on federal funding "because of his pro-life views." It was unclear whether Bush actively plans to reverse National Institutes of Health guidelines issued in August that would allow government researchers to use such cells from discarded embryos provided by private researchers. The future of embryonic stem cell research, which scientists believe can lead to miracle treatments for Parkinson's disease and AD, is expected to be a central question in the Senate confirmation hearings of Wisconsin Gov. Tommy Thompson, Bush's nominee to head the Department of Health and Human Services, which oversees the National Institutes of Health. According to the NIH, human pluripotent stem cells are a unique scientific and medical resource. They can develop into most of the specialized cells and tissues of the body, such as muscle cells, nerve cells, liver cells, and blood cells and they can divide for indefinite periods in the laboratory, making them readily available for research, and potentially, treatment purposes. Scientists derived these unique cells from human embryos and from nonliving fetuses. The hope is to direct this development so they can be used for tissue and even organ transplants. ABCNews.com 1/4/01

Stem Cell Stance Alarms Scientists - Scientists and universities are increasingly worried because the Bush administration apparently will block federal financing of promising medical research using certain master cells. "It would be tragic for many patients who now are looking to this area of work to supply some type of therapy so their lives can be vastly improved," Dr. John Gearhart of Johns Hopkins University, a co-discoverer of some of the cells, told reporters 1/30/01. "If the funding is pulled back, I think it would be devastating for the patients." Stem cells are building blocks for all human tissue, and scientists say research with them could lead to revolutionary therapies for diseases from AD to diabetes. They can be derived from aborted fetuses, fertility clinics' discarded embryos or adults. All are under study, but embryonic stem cells generate the most excitement because they appear the most flexible. Federally funded scientists can't touch human embryos, but privately funded scientists have multiplied embryonic stem cells in laboratories. The National Institutes of Health is prepared to award this spring the first federal grants for studies with just those lab-grown stem cells. Universities awaiting that money say blocking it could force researchers to work abroad or to find private sources of financing, which would remove government oversight. Baltimore's Hopkins announced 1/30/01 it had received a $58.5 million anonymous donation for a new institute studying stem cells, but said federal funding remains crucial for scientists nationwide. AP 1/30/01

Bush Won't Fund Stem Cell Research - President Bush said 1/26/01 that federal money should not be used for research on fetal tissue or on so-called stem cells derived from abortions, the week-old administration's third statement on the divisive abortion issue. "I do not support research from aborted fetuses," Bush said. He did not say whether he would move to block federal research funding - an act that many scientists say could stop promising research into therapies for numerous diseases. Aides said afterward he was signaling his intent to do so. Bush had indicated his opposition to such research during the presidential campaign, but the remarks on 1/26/01 were his first on the topic since taking over the White House a week before. "I will let you know when I decide all policy decisions, but the answer to your question is no," Bush said when asked whether he believes federal money should be spent on fetal-tissue and stem-cell research from abortions. By Ron Fournier, AP White House Correspondent 1/26/01

Judge: Univ. Must Keep DNA Samples - A judge 2/1/01 blocked Texas Tech University from destroying DNA samples and brain material collected to study AD. The university said it is must destroy the material because the school does not have proper consent forms. But six families and 168 other people sued last month, saying the material is vital to AD research. State District Judge Blair Cherry postponed a hearing Thursday until March at the request of Texas Tech lawyers. In the meantime, he instructed the university not to destroy anything. The AD DNA Bank at the university has collected samples from 2,200 families in an attempt to identify genes responsible for the mind-robbing disease. More than 10,000 blood samples, 150 brains and complete medical records of 600 patients with confirmed or probable AD are part of the bank. "These samples are ... irreplaceable," according to the lawsuit. It says "The destruction of a single DNA sample could render all other samples from that family useless for research." By Pam Easton, Associated Press Writer 2/2/01

Caregivers
Stress And Aging Affects Immune System - Stress is known to pack a punch to the immune system, and the whallop seems to hit the elderly the hardest, according to researchers at Ohio State University. After a review of several studies conducted by their own research team and others, they conclude that aging interacts with stress to lower the body's immune capabilities. "We're interested in understanding the double impact of being an elderly person and going through a chronic stressful situation, like being a caregiver for an AD patient," said Dr. Ronald Glaser, professor at Ohio State University Medical Center in Columbus. Caregivers of AD patients tend also to be elderly and experience excessive amounts of stress, leading them to become the second victims of AD, he noted. This impact to the nation's public health will increase as the population ages, Glaser told Reuters Health. For example, one study found that people caring for family members with dementia had poorer wound healing than people who were not caregivers. Those caring for relatives took an average of 9 days longer to heal a small wound (3.5 millimeters or about a tenth of an inch) than others--a 24% increase in healing time. In another study, family members caring for an AD patient an average of 5 years showed decreasing cellular immunity and significantly more days of infectious illness. This led the study authors to conclude that chronic stress might be accelerating the immune system decline that can occur with aging. The good news is that studies also suggest that there are things that people can do to reduce the impact of stress on their immune system. An important source of stress relief is a network of supportive friends and family, Glaser pointed out. By Paul D. Thacker Reuters Health 1/30/01 Current Directions in Psychological Science 2001;10

Wherify Wireless Previews Breakthrough Location Services Technology at Consumer Electronics Show - Scheduled to hit the market this summer, the Wherify Personal Location System embeds a pioneering, highly miniaturized location system within a light-weight wristwatch that will allow consumers to easily determine the location of their children, elderly parents or other at-risk loved ones via the Internet or telephone. Unlike any other personal location-based service available today, the Wherify Personal Location System converges Global Positioning System (GPS) and digital PCS mobile phone technology resulting in a miniature 2-oz. safety device that delivers a fast, accurate, reliable and easy-to-use safety solution. Wherify's end-to-end solution includes the wearable device itself and is backed by a 24x7 location service that can be accessed via the Internet or by telephone to locate a child or loved one within a few feet of their exact location. The location process will typically take less than a minute. In the event of an emergency, either the child or guardian can request an emergency 911 response and local police will be dispatched. "With the Wherify Wireless Personal Location System, at-risk individuals - including the estimated 4 million Americans who currently suffer from AD - can lead more independent, empowered lives, and be protected from harm" said Timothy Neher, Wherify Wireless founder and chairman. PR 1/6/01

Hip Injury 'Terrified' Nancy Reagan - Nancy Reagan said she was "terrified, just terrified" when former President Reagan fell and broke his hip on Jan. 12 at his Los Angeles home. "It was the farthest thing from my mind that anything more could happen to him,'' Mrs. Reagan said in an interview with NBC's Tom Brokaw, a portion of which was aired 1/26/01. The following day, surgeons inserted a pin, plate and screws to repair the hip. He returned home 1/20/01. Mrs. Reagan stayed with her husband throughout his hospital stay. "I think the only time that they were able to get me out was they wouldn't let me in the operating room. But otherwise, I was there," she said. Asked how the 89-year-old Reagan was handling physical therapy, Mrs. Reagan said: "He deals with it. Ronnie is very obliging. If you ask him to do something, he'll do it. AP 1/26/01

Reagan Will Celebrate His 90th in a Quiet World - He will not have much of a celebration in the secluded house on St. Cloud Road, just a quiet dinner with his wife, some chocolate cake, maybe some physical therapy as he battles AD and painstaking recuperation from a broken hip last month. These days Mr. Reagan faces a long, twilight struggle of a more intimate kind. His office said in a statement issued in late January that he continues to make progress in his recovery from surgery to repair his right hip, which gave way in a fall at his home three and a half weeks before. Mr. Reagan's appetite has returned to normal, he sits up twice day in an orthopedic chair that helps to keep his leg straight, and he is expected to begin weight-bearing exercises this week or next. Friends say that Mrs. Reagan's inevitable response when they ask about her husband is that he is doing as well as can be expected, then she quietly reminds them that AD is a progressive disease. By Todd S. Purdum New York Times 2/6/01

Diabetes, High Blood Pressure Cause Mental Decline - People with diabetes and high blood pressure risk not only dying early, but start losing mental abilities in middle age, researchers said on 1/08/01. "Treatment of diabetes and hypertension is important even in middle age, not just in the elderly, for preventing cognitive decline in later life,'' Dr. David Knopman of the Mayo Clinic in Rochester, Minnesota, who led the study, said in an interview. Knopman and colleagues tested more than 10,000 people from across the United States who, at first visit, were aged between 47 and 70 years. Six years later they followed up. "This study showed that diabetes and hypertension were risk factors for losing cognitive function over the six years that we examined people," Knopman said. "What we saw specifically was actually not that memory declines in people with diabetes and hypertension, but rather that their speed of doing things mentally declined." Those with either or both conditions were less able to think on their feet, he said. He said that over the six years the loss was small and the patients themselves would probably not even notice it. But what was striking was how consistent the losses were -- over the whole population the decline was similar and would become noticeable after more than six years. There may be a link to AD, he added. "We feel that the cognitive loss (seen in) diabetes and hypertension might make a person more susceptible to developing AD in the future," Knopman said. "These things don't cause AD, but they might make it more likely that a person would get it later in life." By Maggie Fox, Health and Science Correspondent Reuters 1/8/01

Drugs That May Delay AD Face Test - The hope that some common pain drugs may prevent or delay the ravages of AD has prompted a massive, seven-year clinical trial at four U.S. medical centers. The National Institute on Aging is funding the new study, called the AD Anti-inflammatory Prevention Trial, or ADAPT. The ADAPT trial is testing the drugs naproxen and celecoxib, which are often taken for arthritis and other inflammatory conditions. Naproxen is sold under the names Aleve, Naprosyn and Anaprox, and celecoxib, one of a new class of drugs called COX-2 inhibitors, is sold as Celebrex. Nationwide, the study aims to recruit 2,600 volunteers aged 70 or older, with a family history of AD, who will be randomly assigned to take the anti-inflammatory drugs or a placebo for seven years. No one knows for sure what causes AD, but Dr. Robert Green, a neurologist at Boston University who heads the Boston study, said there is growing evidence that inflammation damages or kills nerve cells in AD patients. It is thought that anti-inflammatory drugs might help by dampening the inflammatory attack which is associated with the buildup of deposits of amyloid, a sticky protein, that dot the brains of victims. The researchers do not claim that anti-inflammatory drugs can work miracles, but research in the 1990s showed "modest but consistent" benefits in warding off the disease, said Green. However, the findings, discovered only in retrospect, are not scientifically sound enough to validate the drugs' benefits. Anti-inflammatories have failed in recent tests to benefit patients who already have AD, said Dr. John Breitner at Johns Hopkins School of Public Health in Baltimore who heads the national trial, but still might delay the onset of symptoms. "If these things work, they probably work by retarding a process that's been going on in the brain for years or decades before the development of symptoms," he said. By Richard Saltus New York Times Syndicate 1/31/01

Other Items
Study Uncovers Mystery Cell's Role - Stanford University scientists have filled an important gap in understanding how the brain works. They discovered that glial cells, long thought to be just some passive scaffolding for the brain's all-important neurons, are directly responsible for how many connections neurons form so they can talk to each other. Glial cells make up most of the brain's cells - for every one neuron there are 10 glia, says Stanford lead researcher Dr. Ben Barres. The scientific dogma was that they only supported neurons, perhaps by providing nutrition, but nobody really knew. His team set out to uncover the function of a main glial cell called an astrocyte. Neurons are nerve cells that send and receive messages by swapping chemical signals, such as signals that say you're suffering pain or move that leg to walk or retrieve that memory. To do that communicating, neurons first must form synapses. Scientists once thought neurons were wired to simply build as many synapses as needed. Not so, Barres' team discovered - young neurons form only a few immature synapses when there are no astrocytes nearby, he said. But add astrocytes to neurons in laboratory dishes and suddenly they form seven times more synapses, and strong, healthy ones, Barres said.The finding was confirmed with another experiment in which they took astrocytes away and the synapses promptly started shriveling. What does it mean for brain research? "We're very interested in the possible disease implications," he said. Under the microscope, numerous brain diseases show "gliosis," an abnormal accumulation of glia in the brain-injured area. Perhaps glia overreact to an injury, causing neurons to form too many synapses and thus triggering the overfiring that means an epileptic seizure, Barres theorized. Or consider degenerative diseases like Lou Gehrig's, in which neurons initially die in just one area before the disease spreads. Could overreacting glia kill those additional neurons by overstimulating them? Then there's the question of memory. Many scientists believe memories are stored by building or strengthening synapses. Astrocytes signal neurons to build synapses by secreting a protein. If Barres could identify that protein - he has experiments under way to try - then scientists could test both the disease and memory theories. By Lauran Neergaard, AP Medical Writer 1/25/01 Science 2001 291 (5504) 657-661

Area of Brain Found to Play Key Role in Initiating Memory Storage - Flee, freeze or fight. A response to a threat is based on experience and memory. Now scientists have discovered that an area of the brain, the amygdala, which was thought to store painful and emotion-related memories, also initiates memory storage in other brain regions. There has been a growing debate on the function of the amygdala [pronounced uh-MIG duh-luh], an almond-shaped sub-cortical structure in the temporal lobe. It receives electrical signals carrying auditory information through axons traveling one way from the medial geniculate (MG) nucleus in the thalamus. New research at the University of Illinois Beckman Institute for Advanced Science and Technology suggests that the amygdala plays a pivotal role in the initial process of storing memory elsewhere in the brain. The amygdala appears to decide which experiences are important enough to store -- a decision based on the emotional significance of the events in a decoding process that affects both learning and memory. "Our data show that a disabled amygdala leads to a breakdown of learning-related changes in other parts of the brain," said Michael Gabriel, a professor at the University. "Specifically, disabling the amygdala blocks learning-related changes in the sensory pathway, the media geniculate nucleus. These changes are essential for the ability to discriminate between important and unimportant sounds." PR 2/2/01 The Journal of Neuroscience, January 1, 2001, 21(1): 270-278

University of Kentucky Center Probes Chemical Communication in the Brain - Research at the Center for Sensor Technology at the U of K is centered on the development and use of high-tech sensors and other state-of-the-art equipment, such as tiny microelectrodes, for studies of brain function. The microelectrodes can be implanted in various regions of the brain to measure tiny amounts of chemicals such as dopamine, norepinephrine, serotonin, glutamate and nitric oxide. "We design and build these very small sensors to understand how cells in the brain, called neurons, actually communicate with one another," said Greg Gerhardt, a professor at the University who also serves as director of the University's Morris K. Udall Parkinson's Disease Research Center. "These cells are very small, about a third of the size of a human hair. So in order to go into that environment and listen to how neurons speak, we have to develop by hand these very tiny sensors that are even smaller than the neurons themselves. In fact, with Harvard we are working on a procedure to actually use the sensors during neurosurgery as a tool to understand more of what's wrong with the brain of a person that has Parkinson's or epilepsy." The sensors measure lightning-quick chemical interactions that nerve cells use to exchange signals. These molecules are recorded by the tiny sensors and transmitted to a computer program where researchers can monitor the reactions in real time. Studies are under way using sensors implanted into the brains of laboratory rats, which allow researchers to monitor what is going on in the animals' brains while they are in motion and at rest. Gerhardt hopes that a better understanding of the communication process will lead to breakthroughs in the treatment of such neurological disorders as Parkinson's disease, Huntington's disease and AD. AP 1/1/01

Largest Gift to U.S. Public University Announced - A Silicon Valley couple on 1/16/01 donated $250 million to the University of Colorado, the largest gift ever to a public university in the United States. Bill Coleman, founder and chairman of BEA Systems of San Jose, Calif. and his wife, Claudia, will finance the University of Colorado Coleman Institute for Cognitive Disabilities. The institute aims to help people who are mentally retarded, have AD or who have suffered traumatic brain injury or a stroke. The Colemans said they were inspired by their niece, Suzanne, who had learning problems, after they saw her make progress using a computer they had given her in the mid-1980s. "It helped her with motor skills and dexterity. Computers also provide a great way to stay focused,'' said Mr. Coleman. In October 2000, the Colemans donated $2 million to the university to sponsor a forum on treating cognitive disabilities. Out of that effort grew a desire to bring together professionals with diverse backgrounds, such as engineers and geneticists, to work on solutions. Reuters 1/16/01

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