Alzheimer Related News Items

News as of 1/05/00
For more info on these abstracts write/call Ed Cabic (edcabic@home.net or 410-992-7197)
For more AD information, see Alzheimer Information athttp://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
Elan's Betabloc Enters Clinical Studies for Treatment of AD - Elan Corporatioon, plc announced 12/16/99 that it has initiated Phase I clinical studies with Betabloc (AN 1792), its new therapeutic agent intended for the treatment of AD. In animal studies, published in Nature in July of this year, Betabloc prevented the buildup and reduced the level of established amyloid plaque, considered by many scientists to be one of the main causes of AD. Based on these results, Elan has initiated clinical development to study the potential of this product candidate as a disease modifying agent. The Phase I studies, conducted in patients with moderate AD, are designed to study safety and tolerability of the product candidate following a single adminis- tration of the drug. The study, which will include up to 48 patients, will evaluate several dose levels of Betabloc and is expected to take one year to complete. Elan hopes to commence multidose studies in Europe in the spring of 2000. "We are delighted that we have been able to move Betabloc so quickly into the clinic," said Donal Geaney, chairman and chief executive officer of Elan. "As far as we know Betabloc is the first potential agent to be evaluated in humans as an AD plaque modifying agent." PR 12/16/99

Theory Links Brain's Repair System to AD - M.-Marsel Mesulam, director of Cognitive Neurology-Alzheimer's Disease Center at Northwestern University Medical School has a theory on the development of AD. No other animal develops AD. Human brains are susceptible to this memory-robbing disorder because they have the only brains capable of rapidly making enormous numbers of connections among brain cells during learning, a process that requires an equally enormous mechanism to maintain and repair those connections. The failure of that repair system is the key to understanding AD, according to Mesulam's theory. Scientists call the brain's remarkable ability to constantly rebuild and repair itself "plasticity." Only recently have they come to realize that plasticity may be the overriding function of the brain. Plasticity is important because evolution appears to have used the brain's facile repair process to also endow it with learning and memory. The same process that repairs brain cells can also sprout new connections among brain cells within minutes after a learning experience. "Every cause that has been described for AD turns out to interfere with plasticity," Mesulam said. "That's what we're looking at in these patients -- a brain that fails to take care of its own household repair jobs." If Mesulam's theory holds up, it could place AD in the same category as high blood pressure, heart disease and other disorders, where the risk of developing these diseases can be reduced through prevention. The risk of developing AD, for instance, could be lowered by drugs, vitamin supplements, diet or specific types of mental and physical exercises. "We need to pay more attention to the processes that promote brain plasticity," Mesulam said. "So far there is no unifying theory to explain the underlying cause of AD. Many neuroscientists have placed their bets on one of two prominent markers of AD, plaques or tangles, as the cause of the disease. The genetics favor amyloid and the clinical picture favors tangles, but nobody has been able to link the two together," Mesulam said. "The evidence suggests that the common denominator is the failure of plasticity, the failure of brain repair." The failure of the brain to make correct repairs forces the repair system to speed up. But instead of doing any good, the manic pace only makes increasing amounts of damaged goods. All of the known risk factors for AD -- head trauma, estrogen deficiency, ApoE-4, presenillin mutations, lack of education, inflammation, stroke, clogged arteries and aging -- put the repair processes into overdrive. The consequences of a dysfunctional and overheated repair process are plaques, tangles, loss of brain cells and the clinical failure of mental function. AD is not like a bullet that goes through the brain. It is a process that usually takes 40 to 50 years. The reason the destruction is so slow is that the brain has many different ways of repairing brain cells. If one repair system fails, another takes over. It is only when most of the repair systems are impaired that synaptic connections wither and brain cells die. Aging is considered to be the biggest risk factor for the disease because all repair systems eventually decline over time. "One of the most important goals will be to understand the processes that influence plasticity in the adult human brain and to determine whether their vulnerability to aging and to the other AD-causing factors can be modified," Mesulam said. By Ronald Kotulak Chicago Tribune 12/19/99

Researchers Define Important Step In AD Progression - Researchers at the University of South Florida in Tampa reported 12/17/99 that they have identified an important cellular process in mice that contributes to the inflammation in the brain which is one of the key characteristics of AD. Drugs that block this process could potentially slow or halt the progression of the disease in humans. When a naturally occurring protein called CD40 ligand (CD40L) attaches to CD40 receptors on microglia, the microglia cells become activated. The microglia can either be in a resting state where they cause no damage, or they can become activated and cause inflammation and death to nearby cells in the brain, thus contributing to AD. Amyloid beta - a protein that is present in high amounts in AD patients - has a substance called amyloid beta peptide which is known to increase the number of receptors on microglia, giving the ligand more opportunity to bind to the cells, thereby causing damage to neurons. When researchers blocked the receptors on the microglia with an antibody, they found the antibody blocked the activation of the microglia and therefore prevented the inflammatory response and death in the adjacent neurons. Genetically engineered mice that overproduce amyloid as they aged and which produce AD-like effects were also engineered to not produce the CD40 ligand so that the microglia would not be stimulated to cause damage to other brain cells. Even with the high levels of amyloid, which would normally help injure the cells, these special mice showed a 50 percent reduction in damage to neurons, most likely due to the lack of the CD40 ligand. "The microglia weren't activated anywhere near as much, and the neurons had very little damage to them," said Dr. Michael Mullan, the study's lead author. Mullan said that he and his colleagues are currently working on refining techniques that screen various compounds to determine what would be an effective blocker of the microglia receptors and, therefore, potential treatments for the disease. "Our research indicates that the concentration of amyloid may not be as important to the development of AD as the presence of the CD40-CD40L complex," said Mullan. "Not only does AD have an inflammatory piece, but it also may have an inappropriate immune system component." The discovery that a cell receptor is involved with AD is exciting, according to Dr. Mullan, because many medications are designed to block cell receptors. Mullan said he hopes to begin testing various compounds to see if any of them block amyloid beta peptides from activating the CD40 receptor. It appears the peptides in experiments in mice begin to activate CD40 long before any symptoms of disease appear or plaques begin to accumulate. This is both good and bad news. The bad news, of course, is that AD may begin earlier in life than expected, Mullan said. But the good news is that medications that block the activation of CD40 might be able to prevent symptoms from developing in the first place. Stephen Snyder, program director with the National Institute on Aging (http://www.nih.gov/nia ) in Bethesda, Md. commented on the work as showing promise. Snyder suggested that AD may have many contributing causes and that different lines of ongoing AD research may lead to treatments that approach the disease in different ways. "It seems like there's only one disease, but in fact, it's like a syndrome - there are multiple ways to get to that end pathology," he said. "It's a complex disorder." The Medical Tribune 12/19/99; and Merritt McKinney Reuters Health 12/16/99; and Kurt Ullman, RN WebMD Medical News 12/17/99 Science 1999;286:2352-2355 (12/17/99)

Drugs
X-rays May Show the Way to Better AD Drugs - Weizmann Institute researchers in Isreal have revealed the exact nature of the 3-D interaction between galanthamine, a natural substance extracted from the common snowdrop (Galanthus nivalis), and the brain enzyme acetylcholin- esterase (AChE). Their findings may provide crucial information in designing a new family of AD drugs. One of its pathological hallmarks of AD is the deterioration of nerve cells releasing acetylcholine - a neurotransmitter that helps ferry messages in the form of nerve impulses between brain cells. The acetylcholine shortage that ensues is compounded by the action of acetylcholinesterase (AChE), the enzyme which breaks down acetylcholine in the body at an astonishing rate of 20,000 molecules per second. Using X-ray crystallography the researchers found that galanthamine acts in a similar manner to Aricept and Cognex, replenishing acetyl- choline levels by binding to AChE's active site and shutting off its "cutting machinery." In addition to its effect on AChE, galanthamine also binds to acetylcholine receptors (proteins on the surface of the nerve cell which are activated by acetylcholine) thus directly stimulating neuronal function. This dual mode of action, coupled with the evidence that galanthamine has reduced side-effects in comparison to tacrine, make it a particularly exciting candidate for designing improved potency drugs. A color image of the Galanthamine -AChE complex is posted at: http://wis-wander.weizmann.ac.il/weizmann/doa_iis.dll/Serve/level/English/1.200.html . PR 12/27/99 Federation of European Biochemical Societies (FEBS Letters) 12/17/99 issue

Apollo BioPharmaceutics Announces Issuance Of U.S. Patent On Neuroprotection With Vitamin D Analogs - Apollo BioPharmaceutics has received an exclusive license from the University of Kentucky Research Foundation to U.S. Patent No.5,939,407 (available online from the Patent Office at http://www.uspto.gov/patft/index.html ) titled "Method of Protecting Against Neuron Loss." The patent covers the prevention of neuron loss associated with neurodegenerative conditions by using molecules that interact with the vitamin D receptor. This broad technology adds to Apollo's existing patent portfolio in vitamin D mediated neuro- protection which currently includes an issued U.S. patent specifically covering the treatment of AD with vitamin D-related compounds. "Calcium dyshomeostasis at the cellular level is a seminal catastrophic event in the pathogenesis of many forms of neurodegeneration, whether by acute ischemic and traumatic causes or by slow disease progression such as that of AD," explained Dr. Katherine Gordon, CEO of Apollo. "Our growing commitment in this area reflects an increasingly deeper understanding of the interrelated events surrounding the neurodegeneration that leads to dementia." Researchers at the University of Kentucky have demonstrated in a 1998 paper that long-term treatment in rats with calcitriol, the bioactive form of vitamin D and a major calcium regulatory hormone, significantly retarded key markers for aging in a region of the brain called the hippocampus. PR 12/14/99

AD Project - Researchers at the University of British Columbia (UBC) initiated in 1992 a retrospective study on the prevalence of dementia in a group of 3000 patients, 1400 of which were treated with an existing drug for another condition. They found that the occurrence of dementia was 37% lower in the group chronically treated with this drug as compared to patients not receiving the drug. These results suggest that continuous therapy with this currently marketed drug lowers the incidence of dementia. Furthermore, there has been a great deal of evidence to support the hypothesis that inflammatory and immune mechanisms are involved in the progression of AD. From previous research it is known that this drug possesses both anti-inflammatory and anti-microbial activity, further supporting its immense potential for reducing the progression of the disease and potentially becoming a treatment for AD. On October 19, 1999, Immune Network Research Ltd. exercised its option to license the UBC technology for the treatment of AD. The Company's goal is to demonstrate that a drug (IQ200) based on the one studied by UBC is effective at slowing the progression of AD and to introduced it to market in the near future. The Company is currently finalizing plans for a Phase II, multicenter clinical trial to demonstrate that IQ200 slows the progression of AD. The Company intends to file an Investigational New Drug (IND) application with the US Food and Drug Administration (FDA) in the first quarter of 2000 with initiation of the clinical trial shortly thereafter. PR 12/9/99

One-of-a-Kind Physician's Personal Experience with AD - Dr. Leonard Breslaw, a 74-year- old physician suffering the early stages of AD, kept a diary and writes about his disease progression from what appeared to be age-related memory loss to AD. "So dramatic have been the results with Aricept," according to Breslaw, "that of all the 20 to 30 pills I take daily, I would relinquish them all before giving up this drug that I call my 'Ponce de Leon' elixir." While warning that responses to medication vary from one individual to another, Breslaw shares his experience with Aricept from his unique vantage point as a physician and patient. Dr. Breslaw believes that Aricept has had a more dramatic effect on his mood than on thinking and memory. "Some of the gloom and doom, the apprehension that goes with the knowledge of such a diagnosis, has been dispelled," writes Breslaw. He states that with Aricept he is more aware of his prior deficiencies, more attentive to grooming and appearance, and less hesitant in speech. PR 12/15/99 Article in the American Journal of Alzheimer's Disease November/December 1999 issue.

AXONYX Initiates Phase I Human Clinical Trial for AD Drug Candidate - AXONYX Inc.  announced 12/22/99 that it has initiated its Phase I human clinical trial for Phenserine, its lead AD drug. The first group of healthy, elderly volunteers received Phenserine 12/21/99.  Phenserine is a potent, brain targeted, reversible and highly selective inhibitor of the enzyme, acetylcholinesterase. In preclinical studies, inhibition of this enzyme has been shown to dramatic-ally improve memory and cognitive performance in animals. Phase I clinical studies are performed to find the appropriate dose for administering the drug to humans. The human clinical trial is taking place at a U.S. FDA approved research center in the Northwest United States. The initial study is expected to be completed before the end of the second quarter of 2000. PR 12/22/99

AstraZeneca: Medication Side Effects Make Psychosis Hard to Treat In The Elderly -  Studies presented 12/12/99 at a major U.S. psychiatry conference provide further evidence of the favorable side effect profile of the atypical antipsychotic Seroquel® (quetiapine fumarate) in elderly patients. Data indicate the medication causes fewer of the side effects that can make psychosis difficult to treat in elderly patients. "Older people are at risk for developing psychosis from a variety of fronts," said Jamie Mullen, M.D., a Medical Director at AstraZeneca. "Treating psychosis associated with AD and Parkinson's disease often calls for similar antipsychotic treat-ments that are used in treating schizophrenia and schizoaffective disorder. The data presented at the conference further support that Seroquel is an alternative to standard antipsychotic agents for use in the elderly." PR 12/13/99

Genes & Genetic Issues
Nature and Science Articles Report Success Employing Sequitur's Functional Genomics Technology for AD Target Validation - Sequitur, Inc. announced 12/10/99 that two major pharmaceutical clients have independently employed Sequitur's functional genomics technology to validate targets in AD. Pharmacia & Upjohn of Peapack, New Jersey reported positive results in Nature (Yan, et al., Nature (1999) 402:533-537) and another group reported its success in a recent Science research article (Vassar, et al., Science (1999) 286:735-740). Results of this research may lead to the development of drugs that will halt or slow the progression of AD. Mark Gurney, the leader of the Pharmacia & Upjohn research team, noted, "Use of Sequitur antisense reagents were critical to our success. Antisense provides a high through-put, cost effective means of linking genes to function." Tod Woolf, Sequitur's Vice President of Technology Development, said "We are pleased that our technology has now been validated by two corporate drug develop-ment leaders in their research targeting AD." Sequitur's proprietary antisense functional genomics technology accelerates drug discovery by helping to identify disease triggers. Sequitur's technol-ogy is a tool for determining the function of the human genetic code, now being decoded as part of the international human genome project. Antisense determines gene function and validates small molecule drug targets by specifically inhibiting gene expression. Sequitur's Antisense Functional Genomics Program offers highly potent and specific second generation antisense compounds, target site selection, collaborative research and cell transfection optimization. PR 12/10/99

Y2K to Herald a Medical Revolution: Three Thousand Physicians and Scientists Proclaim That Immortality Is Within Our Grasp - By the close of 2001, humankind will realize numerous scientific and medical phenomena that will revolutionize the delivery of healthcare in the next five years. As a result, the quantity, as well as quality, of the human lifespan will forever be changed for the better. According to Dr. Ronald M. Klatz, President of the American Academy of Anti-Aging Medicine, author, medical futurist, and founding physician of the anti-aging movement, the next two years hold enormous promise for the realization of boundless youth and vitality. He contends AD will be halted -- genetic therapies, including manipulation of the predisposing Apolipoprotein-E factor, will become available to battle this life-draining disease within the next eighteen months. PR 12/21/99

Caregivers
Health Risk Tied to Stress of Caregiving Is Measured - Caring for an elderly loved one can be hazardous - even fatal - researchers warned 12/14/99 in the first study conducted by University of Pittsburgh scientists to document higher death rates among family caregivers. Elderly caregivers who reported feeling stressed by attending to a disabled spouse were 63 percent more likely to die over the next four years, compared to elders without such a burden. The study followed 392 elders who cared for their spouses and another 427 elders who lived with their spouses, but did not provide care. When the researchers took into account the levels of underlying disease among the different groups of elders, they found that something about the stress of caregiving imposes an additional risk of death, irrespective of whatever underlying disease the caregiver suffers. "We have evidence that this group of strained caregivers had higher levels of depression and anxiety, and reported higher rates of not getting enough rest, not having time to exercise, not having time to rest when they get sick, said Scott R. Beach, who did the study with Richard Schulz. "We think being in this stressful situation prevents people from being able to take care of themselves," Beach said in an interview. After adjusting for differing levels of underlying disease and other factors, the stressed caregivers were 63 percent more likely to die in four years compared to those not providing care for a family member. The risk of death was not significantly higher among care-givers who reported little stress, or those who had a disabled spouse, but were not providing care. Peter Vitaliano of the University of Washington said elders are not equally vulnerable to the health-destroying effects of constant caregiving. "It's not enough to be a caregiver," Vitaliano said. "You have to be vulnerable, and you have to have poor social supports" to suffer ill effects. "We need to find out which types of caregivers are at risk," so additional resources can be targeted to them, he said. An accompanying editorial noted that physicians should question caregivers about their health and stress levels. By Richard A. Knox, Boston Globe 12/15/99 A03 Journal of the American Medical Association 1999;282:2214-2219

AD Patients Patterns Eyed - Researchers are working to determine behavior patterns among those with AD who wander from their homes and disappear. About 32,000 AD patients escape U.S. homes or care facilities each year, said Robert Koester, a Virginia researcher who studies the habits of AD patients. Searches for those with dementia make up 12 percent of search and rescue operations in the Mid-Atlantic states, he said. If AD patients aren't found within 24 hours, their survival rate drops to 46 percent. Among the similarities Koester's study found among 100 disappearances: The AD patients didn't call out for help or respond to shouts. About 67 % of them crossed over roads or paths, and continued in a straight line until they couldn't go any further. When wandering patients died, it was usually because they couldn't go any farther. Many were found in creek or drainage areas, or deeply entangled in briars or bushes. Searchers some-times find bodies in areas so densely packed that dogs can pass within feet of them without find-ing a scent, said Gerald Flaherty, of the state's AD Association chapter. "They're very, very frightened and they're trying to find a place to hide and they go into places that are terribly dangerous," he told The Boston Globe. AP 12/25/99

Adult Children Of AD Patients Unnecessarily Worry About Getting AD - A study of 25 adults with a parent with probable AD, and 25 adults with no parental probable AD found that adult children of parents with AD "find" non-existent symptoms of AD in themselves. Excessive worry about getting AD prompted them to repeatedly check for signs of AD, misinterpret signals and seek validation for this misinterpretation. This study is designed to help caregivers in dealing with stressed family members fearful about their own fate. PR 12/13/99 article in American Journal of Alzheimer's Disease Nov/Dec issue

Coping With AD During the Holidays - Families dealing with AD patients around the
holidays will need to have a number of coping strategies, says Naomi Nelson, a psychologist at Baylor College of Medicine in Houston. It's unrealistic to expect holiday gatherings to be like they once were if a family member suffers from memory loss and other problems caused by AD," Nelson said. "Families are more likely to enjoy their time together if they don't expect perfection," she said. The following coping strategies may help AD patients and their families enjoy the holi-days. During the holidays, an AD patient may find it easier to focus if they are in the corner of a room, as opposed to the center, because they will experience fewer distractions. Family members should try to make the AD patient feel comfortable, giving them clues to help them process information and avoid correcting each missed detail. In the case of disturbing behavior, family members should be told it's often the result of being confused, and the AD patient can be taken to another room temporarily to calm them down. AP 12/22/99

Testing
Depression May Be an Early Sign of AD - In the elderly, symptoms of depression such as low energy and concentration problems may be early signs of AD, according to Swedish researchers at the Stockholm Gerontology Research Center. The results of their study suggest that these symptoms are not due to patients realizing that their memories are failing, but rather that depressive symptoms are part of the early stages of AD. In a 3-year study that followed 222 people aged 74 and older, researchers found that those who developed AD were 50% more likely than other participants to have suffered depressive symptoms at the study's start. "The people who developed AD weren't even close to a clinical diagnosis of depression, but they did have more symptoms of depression, such as a lack of interest, loss of energy and difficulty concentrating,'' said lead researcher Dr. Lars Backman. Although other investigators have noted a link between depression and AD, the nature of this relationship has been unclear. Some studies have suggested depression may be a risk factor for AD; other researchers have concluded that AD patients suffer depression as an emotional response to the loss of memory and thinking abilities that mark the disease. This study, according to Backman's team, suggests that depression is neither a response to AD nor a risk factor, but rather an early sign of the disease. Backman and colleagues looked at two types of depression among the study participants -- "mood-related" symptoms such as unhappiness, guilt and thoughts of death; and "motivation-related" symptoms including lack of energy and interest, and concentration problems. They found that at the start of the study, participants who would later develop AD commonly had motivation-related symptoms. "That provides further evidence that the symptoms are not related to people's feelings about their cognitive difficulties, and actually reflect changes in the brain regions involved in attention and energy," Backman explained in a statement that because the depressive symptoms which emerged in his study are fairly common among the elderly, they may be "easily overlooked" as early signs of AD. Reuters Health 12/9/99 Neurology 1999;53:1996-2002

Alzheimer's Association Survey Finds Americans Often Fail to Identify Key Disease Warning Signs - A new Alzheimer's Association survey finds Americans often confuse warning signs of AD with memory loss associated with normal aging and fail to recognize other thinking difficulties as warning signs. In response, the Association is conducting timely national outreach efforts to provide families with the knowledge they need to recognize symptoms, seek an early diagnosis and take action. More info at http://www.alz.org 

The 10 Warning Signs of AD are: Memory loss that affects job skills, Difficulty         performing familiar tasks, Problems with language, Disorientation to time and place,  Poor or decreased judgment, Problems with abstract thinking, Misplacing things, Changes in mood or behavior, Changes in personality, and Loss of initiative.

Early recognition and diagnosis of AD offers people with the disease the greatest opportunity to benefit from medical and behavioral interventions. Medical treatments have been shown to help sustain cognitive function (thinking and reasoning) and preserve a person's quality of life. The sooner someone with AD begins treatment, the more likely it will be that they will benefit. Currently, two drugs are available for the treatment of AD, donepezil (Aricept®) and tacrine (Cognex®). Several new medications will be available in the near future. In addition to treatment for cognitive symptoms, families often seek help from physicians to alleviate behavioral symptoms that may accompany AD, especially as the disease progresses. Often, behavioral problems can be alleviated by modifying a person's surroundings, such as adjusting lighting, removing clutter and providing safety (e.g., adjusting hot water temperature to prevent burns). In some cases, severe behavioral problems may be best treated with medication. PR 12/8/99

Prevention
Year-End Report Finds Continuing Progress in Role Of Vitamin E Against Disease, Memory Loss in Elderly - A year-end summary of Vitamin E research by Veris Research Information Service shows continued findings that Vitamin E is playing an important role in helping protect against a number of diseases and illnesses, including new studies on cataracts, weakened arteries in middle-aged men and women, and memory problems in the elderly. Veris reported on antioxidants being protective "against memory loss, which is a major feature of dementing disorders such as AD." In a study of memory performance in 4,808 adults who were 60 years of age or older, it was found that lower Vitamin E concentrations "were consistently associated with increasing prevalence of poor memory" Veris said of the study reported in the American Journal of Epidemiology. PR 12/27/99 Am. J Epidemiol 1999 Jul 1:150(1):37-44

Look Ahead at Future of Medicine - The Associated Press asked experts in several medical specialties to make their best guesses about what we can expect in the next 25 or 30 years. In the field of "Aging and Longevity: Lowering risk factors for AD and others" the expert was Dr. Caleb E. Finch, director of the biogerontology program, University of Southern California. He notes the human lifespan has been increasing steadily for at least 100 years. One thing is clear: A number of unhealthy behaviors, including heavy smoking, exposure to toxins in the environ- ment, foods that lead to chronic elevations in blood sugar, and lack of exercise, can lead to shortened lifespan. Whether changing these will truly change the underlying pattern of human aging is unknown. We will know a lot about genetic risk factors for diseases. Already, there are four or five strong candidates each for AD, heart disease, cancer and diabetes. Relatively early in life, it will be possible for most people to know if they have any major genetic risk factors. There will be  specific recommendations and guidelines for how to minimize those risks. He said he is highly optimistic that human lifespan will include increasing duration of health. AP 12/15/99

Other Items
$80M Alzheimer's Project Launched - West Virginia University and Johns Hopkins will operate what they call the world's only major research center devoted to AD and other brain and memory disorders. The $80 million Blanchette Rockefeller Neurosciences Institute, named after the late mother of Sen. Jay Rockefeller, D-W.Va., will be housed on the WVU campus and bring together the world's top researchers in memory and cognition, the schools announced 12/14/99. It will be led by Dr. Daniel Alkon, a 29-year veteran of the National Institute of Health and a medical director in the U.S. Public Health Service. Alkon and his colleagues have developed a new model of how AD, at its earliest stage, causes molecular changes in brain cells. Their discovery may lead to new ways to diagnose and treat the disease. Johns Hopkins will exchange researchers, faculty and students with WVU, and conduct research at its campus in Montgomery County, Md. By Vicki Smith AP 12/14/99

PCOM Researchers Discover a Common Bacteria Enhances Amyloid Protein Processing Important in AD - Researchers at Philadelphia College of Osteopathic Medicine (PCOM) have discovered that a common bacteria, Chlamydia pneumoniae, which causes pneumonia and bronchitis, can enhance the processing of beta amyloid -- a major protein in the senile plaques found in AD patient's brains. The preliminary study establishes the possibility that the bacterium stimulates an increase in beta amyloid in infected cells, thereby increasing the amyloid burden in the nearby vicinity. These results suggest that C. pneumoniae infection may trigger one form of the pathology characteristic of sporadic AD. "Having first identified an infectious organism in AD brains, we now are trying to understand how it may promote neuropathogenesis," said Dr. Brian Balin at PCOM. The researchers are studying the effects of antibiotics in reducing the mental deterioration of early stage AD. "We believe that antibiotics may reduce the effects of the disease, and unsolicited feedback from physicians who have initiated this treatment shows the approach is plausible and revolutionary." PR 12/9/99

Nanomedicine Nears the Clinic - A small vanguard of medical explorers is exploiting the tools of nanotechnology to manipulate biomolecules that regulate life and death, illness and health. The key to these efforts is that researchers are learning how to tailor devices and materials on the scale of billionths of a meter, thereby acquiring the ability to engineer structures and machines no bigger than biomolecules such as DNA. Tejal Desai, http://www.techreview.com/tr100/profile.php3?Desai who is a bioengineer at the University of Illinois and who was recently named to TR100's list of young innovators at the Technology Review magazine's web site http://www.techreview.com/tr100/index.htm , is investigating the approach of smuggling cells into the body to restore normal function for use in the brain. She wants to bring in normal cells that would secrete neurotransmitters. Those neurotransmitters might be able to replace the ones lost when cells are damaged in diseases such as AD. Desai is utilizing the same nanopore fabrication technology used by others to make microcapsules for implanting neurons in the brain. Once the capsules are implanted, the neurons can be electrically stimulated to release neurotransmitters. Eventually, says Desai, this technology "could be used for such applications as treating AD or Parkinson's - basically any disorder where the basic neurosecretory-cells are missing or damaged." By David Voss Technology Review Jan/Feb 2000 http://www.techreview.com/articles/jan00/voss.htm

Reagan's Condition Has Deteriorated, Wife Says - Former first lady Nancy Reagan says that five years after her husband was diagnosed with AD, he no longer is capable of having a conversation that makes sense. Reagan also said that friends of former president Ronald Reagan no longer are invited to their California home because he does not recognize them. The former president no longer swims or takes walks, she said. When asked what she has learned about the disease over the past five years, she replied "That it is probably the worst disease you can ever have, because you lose contact and you're not able to share. In our case, to share all of those wonderful memories that we have." She said she can no longer have a conversation with the president that makes sense to her. As to how she has learned to deal with her husband's condition, she said. "You just do it; you just get up and take each day as it comes and put one foot in front of the other.You just love." AP 12/19/99

Pfizer Canada Launches an Educational Health Centre on the Internet for the Public and Health Care Professionals - Pfizer Canada Inc. launched 12/15/99 an educational health centre for patients and healthcare professionals on its new web site at http://www.pfizer.ca . The company has been working in close collaboration with health care practitioners for several years, developing educational programs to optimize the outcome of pharmacological treatments and promote a better-informed use of available medication. The Learning Centre has two distinct components, one aimed at patients and the general public, the other at physicians and pharmacists. The patient-oriented component provides clear, easy-to-understand information on significant ailments that affect a growing number of Canadians. The resource material describes symptoms, explains available treatment options and offers advice on prevention. In addition, the Centre also clarifies medical jargon by providing a glossary of technical terms related to each ailment. In short, the Learning Centre offers a host of useful information for the general public as well as individuals coping with these diseases, and allows them to make informed treatment choices with the help of their physician. AD affects approximately 200,000 Canadians, and alters not only their memory, but also their emotions, moods, behavior and physical ability, which can greatly complicate the task for family caregivers. The Learning Centre can help those caring for someone with AD by providing valuable advice and offer ways to ease their burden by explaining the advantages of starting symptomatic treatment at the early or intermediary stages of the disease. PR 12/15/99

Mississippi Baptist Health Systems Hospitals Give I.R.B. Approval To Commence Clinical Trials In The Treatment Of AD Utilizing Jacobson Resonance Patented Technology - Jacobson Resonance Enterprises, Inc. will conduct a multi-site clinical study covering "The Utilization Of Low Frequency Pico Tesla Range Magnetic Fields For Treatment Symptom Of Patients With AD" under the supervision of Dr. James L. Parker at Baptist Hospital in Jackson, Mississippi. Jacobson Resonance is encouraged by the case controlled data which shows potential for the Jacobson Resonator to stop the progression of AD. Pre-clinical studies have shown that the Jacobson Resonator can affect the regeneration of damaged neuronal cells. PR 12/13/99

Nymox Scientists Find Additional Evidence That Spherons Are Cause of AD - Nymox Pharmaceutical Corp. announced 12/8/99 that new investigations of Spherons have confirmed previous studies linking Spherons to the cause of AD. Spherons are unique microscopic-sized protein balls found in every person's brain. Spherons slowly enlarge throughout life until they become so large that they burst, growing 200-fold in volume and forming amyloid plaques. The presence of amyloid plaques in brain tissue provides the definitive diagnosis of AD. The new studies of spherons examined infrared spectroscopic characteristics of intact and bursting spherons, and compared them to spectroscopic characteristics of other brain elements and other proteins, including AD amyloid plaque proteins. The studies clearly showed an identity between spheron components and AD amyloid plaques, which further establishes the causal role of spherons in the genesis of AD. Full details of the new studies will appear in a peer-reviewed medical journal publication. Nymox has developed promising drug candidates that have the ability to inhibit the damage from bursting spherons when the drugs are given to animals that have received human spherons. Without the Nymox drugs, the animals develop typical AD plaques. The company has begun the process of preparing the candidate drugs for formal testing. Nymox cautions that the spheron based Nymox AD candidate drugs, while showing dramatic positive effects in animals, and while showing no toxicity so far, have not yet been tested in humans. PR 12/8/99

Advocacy Group Criticizes NIMH Research Priorities - The National Alliance for the Mentally Ill released a report 12/6/99 that criticizes how the National Institute of Mental Health (NIMH) allocates research money, charging that the federal agency spends less on serious mental diseases than it should. According to the Arlington, Virginia-based advocacy group, the NIMH "failed in its primary mission to support research on schizophrenia, manic-depressive illness, and other severe mental illnesses." The group also criticized the Institute for using 15% of its funding to support research on other diseases, such as AIDS and AD, which are the primary responsibility of other institutes within the National Institutes of Health. In response to the report, another advocacy group, the National Mental Health Association (NMHA), said that it "takes strong objection" to the criticisms. It wrote that the alliance's recommendations that NIMH should limit its research to severe mental illness is "dangerous and short-sighted." Reuters Health 12/06/99

AD6\adnews0100f.wpd