Alzheimer Related News Items
News as of 11/06/00
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410-992-7197)
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Copies of these reports are posted there
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Top Items
Antibiotic May Help AD - An antibiotic, clioquinoline
which was approved as a human drug decades ago, was tested on mice genetically
designed to mimic the effects of AD and it reduced and even eliminated
protein deposits that are a major feature of the disease, said Dr. Ashley Bush
of Massachusetts General Hospital and Harvard Medical School. The drug was
effective in the mice experiments not because it kills germs but because it
binds two metals, Bush said. The mice used in the initial experiments were
genetically programmed to overproduce beta-amyloid, which creates the sticky
plaques that are a major feature of AD. Copper and zinc
"decorate" those plaques -- and mice given clioquinoline, which
marries those metals, showed a 51 percent reduction in the plaques compared to
untreated mice from the same strain, Bush said. In one-third of the younger
animals, it eliminated the plaques, even though the animals continued to
over-produce beta-amyloid, he said. He believes this indicates that "the
brain can heal, can clear out the mess, if you get the plaque out of the
way." The mice also got healthier and did better on a test of general
behavior than untreated mice. Bush said he had not tested their ability to
learn. The drug is now being tested on 50 AD patients and researchers
expect to bring in more patients before the study is done a year from now. AP
11/6/00
Structure Of AD Enzyme Discovered - A team of scientists at the Oklahoma Medical Research Foundation in Oklahoma City has determined the structure of an enzyme that causes AD. The enzyme is named Memapsin 2 and it is one of two protein-cutting enzymes, called proteases, whose action is believed to lead to AD. Memapsin 2 works with another enzyme (called gamma-secretase) to cut a longer protein called Amyloid Precursor Protein (APP). The by-product from the cut is known as beta-amyloid, or "A-beta." A-beta then accumulates in the brain and forms plaques and tangles which lead to AD. The information on this structure could help them develop an inhibitor to block the enzyme. "We'd like to think we trimmed maybe two or three years off the design process" for AD drugs, Dr. Jordan Tang said. Still, the researchers said, it will be at least five years before anything is available for use. PR 10/5/00 Science (2000) 290 (5489):150-153
Drugs
Blocking Brain's Immune Response May Prove to Be Effective Treatment
- Researchers at the University of South Florida Roskamp Institute have found a
new molecule, CD45, that may be targeted to prevent the adverse immune
response that leads to AD. CD45 is a receptor on the surface of microglia,
cells that support neurons and participate in the brain's immune response. The
researchers showed that triggering CD45 is beneficial because it blocks a very
early step in the development of AD - microglial activation of the
brain's immune system. If unopposed, this immune reaction would result in
inflammation and progressive damage to neurons. The results provide evidence
that the brain's immune response is critically involved in the AD
process, perhaps much earlier than inflammation. "Once brain inflammation
occurs, it is probably too late for prevention," said Terrence Town, a
co-author of the articles on this subject. This may help explain why
nonsteroidal anti-inflammatory drugs (NSAIDs), only partially alleviate symptoms
in patients with AD. A more effective treatment may combine
anti-inflammatory drugs with drugs specifically designed to inhibit microglial
activation of nerve cell inflammation in the brain, the authors suggest.
"The next step is to apply these findings to new treatment strategies for AD,"
said Michael Mullan, MD, PhD, director of the USF Roskamp Institute. "We
are working with the pharmaceutical industry to screen for drugs that will
target the brain's immune cells." NewsRx.com 11/03/00 Journal of
Biological Chemistry 2000 Sept 7 [epub ahead of print] [NOTE free full text
article in pdf at http://www.jbc.org/cgi/reprint/M002006200v1
] and Journal of Neuroscience 2000, 20(20): 7587-7594
Depression Drug May Help Treat Brain Diseases - Lithium, currently used to treat symptoms of bipolar disorder, or manic-depressive illness, may someday be used to treat degenerative brain conditions such as AD or Parkinson's diseases, researchers at Wayne State University School of Medicine in Detroit, Michigan suggest. They analyzed the effect of lithium on 10 individuals with bipolar mood disorder. Bipolar disorder is a chronic condition characterized by emotional 'cycles' of manic highs and depressive lows. After 4 weeks of lithium treatment, 8 of the 10 study participants experienced an average 3% increase in their total brain gray-matter volume. The gray matter is the outer layer of the brain involved in thinking and processing information. "This is the first time a drug has been proven to increase gray matter in the human brain," said Dr. Gregory J. Moore, one of the researchers. "This has possible future implications for the treatment of neurodegenerative disorders, such as Parkinson's and AD,'" Moore told Reuters Health. "Specifically, if one can prevent neurons from dying or even increase the number or size of neurons in the brain after there has been some neuronal degeneration, one could potentially slow down, halt, or even reverse some of the effects of these devastating diseases." The researcher cautioned that even though these study results may be exciting, they "should be considered preliminary until larger numbers of (individuals) can be studied and until the findings can be replicated by other laboratories." By Charnicia E. Huggins Reuters Health10/6/00 The Lancet 2000;356:1241-1242.
Cholesterol-Lowering Drugs May Reduce AD Risk - The cholesterol-lowering drugs lovastatin and pravastatin appear to reduce the risk of AD in older patients by up to 73%, suggest the results of a study by Loyola University Medical Center in Maywood, Illinois. The relationship between statin therapy and the diagnosis of probable AD was examined using data on more than 60,000 patients older than age 60. While the prevalence of probable AD in the overall sample was lower than expected, the prevalence in patients using lovastatin and pravastatin was even lower. Specifically, the use of these two statins reduced the risk of probable AD by nearly 70% compared with the patients in the population as a whole, and by 57% to 73% compared with patients using other medications for high blood pressure or cardiovascular disease. The association between statin therapy and the risk of AD "warrants further study," the authors conclude. "Future studies will allow us to determine the relation between the length of time taking medication, the dose of medication, cholesterol levels, and the degree of risk reduction for AD. Reuters Health 10/19/00 Archives of Neurology 2000;57:1439-1443.
Nefiracetam in the Treatment of AD - Some of the thinking difficulties of AD patients may be due to a deficiency in a brain chemical called acetylcholine, which helps transmit messages between nerve cells. Nefiracetam is a new drug that stimulates acetylcholine. The National Institute of Neurological Disorders and Stroke (NINDS) is sponsoring a study and currently recruiting patients for the study. The study will test whether Nefiracetam can safely improve memory, thinking and activities of daily living in patients with mild to moderate intellectual impairment due to AD. Animal studies showed that Nefiracetam improved learning impairment and memory in rats with dementia. In a small study of humans, about one-fourth of patients who were given a low dose of the drug had improved intellectual function, and about one-half who received a higher dose improved. See http://clinicaltrials.gov - in the Search Clinical Trials window type alzheimer and see this trial along with 17 others. Web page updated 10/18/00
Genes & Genetic Issues
New Genes Implicated in Neurodegenerative Diseases - Although
many genes are known to be responsible for diseases such as AD,
Parkinson's and Huntington disease, there is little understanding of how they
cause neurons to degenerate and die. But, scientists are beginning to track down
the molecular accomplices to these devastating disorders. By studying the
disease process from the time neuronal degeneration begins, a research team led
by Dr. Juan Botas, a professor at Baylor College of Medicine, discovered certain
genes that can modify the development of these diseases. Using the common fruit
fly Drosophila, the researchers studied spinocerebellar ataxia type 1 or SCA1,
a hereditary neurological disease caused by an error in the gene that codes for
the protein known as ataxin-1. "Because of previous work, Botas said they
expected to find genes that are involved in protein folding and the destruction
of abnormal proteins. And indeed, we saw neurons in the fly that went through
all the pathogenic processes that characterize these neurons in human patients,
including the formation of the protein clumps or aggregates, a hallmark of these
diseases. These observations helped confirm those protein clearance mechanisms
were taking place. "But, we also found new genes involved in other pathways
not previously known to be involved in neurodegenerative diseases," he
said. Among the new mechanisms implicated in SCA1 are genes involved in RNA
processing, transcriptional regulation, and the detoxification of cells. Now
researchers must identify the corresponding genes in humans and determine how
they contribute to the development of neurodegenerative diseases. "The SCA1
Drosophila model provides new insight into the multi-faceted nature of SCA1
pathogenesis, opening new areas of research. A better understanding of these
genes could lead to the development of drugs to slow or halt the degenerative
process," Botas said. PR 11/2/00 Nature 408, 101-106 (2000)
Adult Stem Cell Transplants May Be Feasible - Researchers at The Children's Hospital in Philadelphia, Pennsylvania, have succeeded in getting adult human bone marrow stem cells to grow into a variety of cell types including muscle, bone and cartilage when the stem cells were transplanted into fetal sheep. "Previously, we had been able to cause these stem cells to become more highly differentiated cells, like muscle cells, in the laboratory. Now, we wanted to find out what would happen if we put them into a living system," lead investigator Dr. Alan W. Flake told Reuters Health in an interview. "The transplanted human stem cells distributed to a variety of places in the sheep and were shown to persist in the sheep for up to a year without being rejected," Flake said. Stem cells have the potential to become many different types of cells and it is hoped that they can be used to replace cells damaged in many types of illnesses, including diabetes, Parkinson's disease or AD. A surprise finding of the study was the ability of the cells to persist in fetuses that had developed immune systems that might be expected to reject the transplants. "This suggests that these cells may have special immunologic properties that may allow transplantation between individuals or even between species without rejection or the need for toxic immunosuppressive drugs," Flake explained in a statement. Reuters Health 11/2/00 Nature Medicine 2000;6:1282-1286.
Mouse Genetic Code Will Help Understand Human Genes - Deciphering the genetic code of mice will one day help scientists better understand the function of human genes and develop enhanced disease treatments, a group of public research agencies said 10/6/00. The National Institutes of Health (NIH) and three private companies launched a $58 million program to provide a free public database that would map the entire mouse genome, or genetic code. The Mouse Sequencing Consortium (MSC), the NIH said, will help scientists better interpret the role and interactions of human genes. "The deciphering of genomes represents the ability to read and understand ultimately the fundamental information of biology and this allows us to develop a really scientific approach to health and disease," said Richard Klausner of the National Cancer Institute, one of the NIH's six agencies. Klausner said that mice and humans share a number of diseases and that comparing information from both species' genomes will in the future help to detect, diagnose and treat a large range of diseases including cancer and AD. The MSC said it will map out the entire gene pool of mice within the next six months. By Mark Wilkinson Reuters 10/6/00
Caregivers
New Study Suggests That Treatment For AD Reduces Caregiver Burden
- A recent study by the Institute for the Study of Aging suggests that treatment
of AD patients with donepezil, a cholinesterase inhibitor, may
reduce the burden of caring for loved ones with AD. The study results are
based on a self-administered, nationwide survey of AD caregivers in a
community setting that was conducted by Consumer Health Sciences. A caregiver
burden scale measured time demands and distress linked to commonly performed
caregiving tasks. Results demonstrated that donepezil caregivers reported
significantly lower scores on difficulty of caregiving. This study indicates
that treatment of AD with cholinesterase inhibitors such as donepezil
lessens the caregiving burden for caregivers. As a result, quality of life for
the both the patient and caregiver may be improved. In addition, since caregiver
burden accounts for a substantial part of the indirect costs of the disease,
improved treatment of AD could have a significant financial impact. PR
10/4/00 International Psychogeriatrics, volume 12, September 2000 The
Institute for the Study of Aging's website at http://www.aging-institute.org
has additional information on research conducted and/or sponsored by the
Institute.
Music Can Encourage AD Patients to Eat - Elderly people with dementia often forget to eat, leaving them with inadequate energy and nutrients to stave off disease. But recent study findings by Martha Sutton at Eastern Michigan University in Ypsilanti, Michigan suggest that music can motivate patients to eat more. "If we can improve their nutrition status, then quality of life is better and the decline in mental functioning is not as rapid," she told Reuters Health. She said malnutrition and dehydration are major problems in nursing homes. Music is one of several non-invasive therapies that seem to help. She found that adults consumed roughly 20% more calories when background music was played. What's more, socialization increased and staff seemed to relate better to residents, Sutton noted. "The overall social atmosphere improved and by sitting there longer, patients ate more," she said. By Suzanne Rostler Reuters Health 10/18/00
Caregivers Value Quality of Life in AD Therapy - People who care for the 4 million Americans suffering from AD consider quality of life just as important as efforts to prolong the patient's life when choosing treatment options, according to researchers at the University of Pennsylvania Health System in Philadelphia. Over 50% of caregivers said that improving the patient's quality of life was a more important treatment benefit than either lengthening survival time or delaying a move to a nursing home. Other benefits similarly valued included preserving the patient's memory; ability to communicate and recognize the family; improving the patient's mood; and improving the ability to manage basic daily physical activities. The researchrs found the caregivers' ability to assess quality-of-life issues was influenced by his or her own level of depression and burden--so their judgment when choosing treatment may be affected by a desire to alleviate their own related stresses. Overall, most caretakers were willing to risk possible side effects in order to delay the disease progression by 1 year--with the goal of delaying a move to a nursing home playing a major role in the caregivers' assessment of quality of life. By Alan Mozes Reuters Health 10/10/00 Neurology 2000;55:1008-1014.
Psychedelic Room Helps Dementia Patients - If you were in a foreign country - the people you talk to and the language they speak - everything is an unending stream of incomprehensible, sometimes frightening, activity. For many people living with conditions such as AD, this is a daily reality. Now, psychologists are reaching back to the psychedelic and "mind expanding" 1960s and updating research on sensory deprivation with the hope of offering relief to people suffering from this type of dementia. The treatment, which originated in the Netherlands and is called Snoezelen (pronounced snooze-lin), was originally used to help children suffering from autism. Previous research has shown that Snoezelen behavior therapy "reduces socially disturbed behavior, produces relaxation responses, improves mood enhances interpersonal interaction, facilitates verbal expression, improves memory recall, and enhances attention and concentration in dementia patients," said lead researcher Dr. Jason Staal of Beth Israel Medical Center in New York City. "Everything is done to maximize the wonderful joy of the experience. Remember these are people living in monochromatic, sensory deprived environments," Staal told Reuters Health, referring to bleak hospital rooms and the like. "The aim is to provide dementia patients with an experience that they can understand." Patients are exposed to the room anywhere from three to five times per week depending on their degree of dementia. Two therapists accompany them, one who assists the patient in the room and another who other acts as an observer. At first the patient is closely monitored to see which stimuli have the most positive effect. The therapist is then able to focus and heighten the patient's experience in subsequent visits into the room. "The current state of affairs in the day-to-day treatment for people with dementia is pretty miserable," said Staal. "Its great that the medical community is focused on a cure (for AD) but all you have now is medicated people languishing all day in monochromatic rooms staring at the wall." By Keith Mulvihill Reuters Health 11/2/00
Study: Elderly Often Get Wrong Drugs for Depression - Older U.S. patients are often being dosed with the wrong antidepressants and anti-anxiety drugs, which can leave them sleepy and prone to health problems such as urinary tract infections said researchers at South Dakota State University 10/4/00. They found up to 25 percent of patients over the age of 65 are getting antidepressants not recommended for use in the elderly -- and this may be only the tip of the iceberg for drugs wrongly prescribed for older people. They studied a very specific group -- patients over 65 who were prescribed six different antidepressants or anti-anxiety drugs, known as psychotropic medications. "One out of four of visits that involved a psychotropic agent were for inappropriate uses of those agents," said Jane Mort a professor who lead the study. The most common culprit was an antidepressant known as amitriptyline. Such drugs can make patients sleepy and can also affect muscles in the bladder and intestines, leading to constipation and an inability to urinate. In severe cases, patients can develop urinary tract infections and kidney failure. "It can be harder for them to walk," Mort said. "These people are more susceptible to falls and fractures." Safer antidepressants include the new class of drugs known as selective serotonin reuptake inhibitors or SSRIs, which include fluoxetine (Lilly's Prozac) and paroxetine, made by SmithKline Beecham under the name Paxil. Another misused class of drugs was the anti-anxiety class, including diazepam or Valium. Reuters 10/4/00
Wireless Device Designed To Help - The premise behind Digital Angel is simple: Build a microchip that can be worn like a watch, and have it send distress signals in times of medical emergencies. The current prototype is about the size of a quarter. Hooked to an antenna, it should be able to request help through existing wireless communications networks and the global positioning system. The chip would continually monitor the wearer's vital signs. Say the pulse stops, or the blood pressure gets too high. The chip would obtain location readings and notify a service center, which would then dispatch a doctor or other service provider. The service center could also initiate contact and track patients with AD, or perhaps soldiers in a battlefield. The company wants to test the prototype and have products ready for sale by the end of next year. By Anick Jesdanun AP 10/29/00
Prevention
Estrogen Therapy May Help Prevent Memory Decline in Elderly Women
- Normal aging does not affect immediate memory in older people. It functions as
well as it did when they were 30 years of age and the same goes for remote
memory. However, the capacity to learn - to code new information, to consolidate
and retrieve it - decreases with aging according to Prof. Barbara Sherwin at
McGill University. Her studies have found that estrogen replacement therapy
prevents some of the decline in the ability to learn and to remember new
material in postmenopausal women. Although her research findings have shown that
estrogen protects against some decline in explicit memory in healthy aging
women, Dr. Sherwin cautions that does not mean that it will cure AD.
"There is little or no evidence so far that estrogen can reverse the memory
loss that occurs in AD, possibly because these women have already lost
too many brain cells by the time a diagnosis has been made. However, several
studies have shown that estrogen replacement therapy reduces the incidence of AD
in older women," said Dr. Sherwin. In 1995-1996, 10,000 women over the age
of 69 were randomly assigned to treatment with estrogen or placebo for 9 years
to determine whether estrogen reduces the incidence of AD. "In 2005,
we should know whether or not estrogen replacement therapy indeed delays the
onset of AD in aging women," concludes Dr Sherwin. PR 10/11/00
Dietary Supplement Creatine Protects Against Traumatic Brain Injury - Creatine, a food supplement frequently used by professional and amateur athletes, may prevent brain damage following traumatic brain injury, according to a new research study led by Stephen Scheff, Ph.D., professor, University of Kentucky Sanders-Brown Center on Aging and UK College of Medicine Department of Anatomy and Neurobiology. Creatine is produced naturally in the body in the liver, kidney and pancreas and is used as a way to store energy. Many athletes now use creatine as a dietary supplement to increase muscle mass, strength, and the recovery time of muscles between bursts of activity. Each year about 7 million people in North America experience traumatic brain injuries (TBI) caused by motor vehicle accidents, falls, assaults and sports-related activities. TBI causes both primary and secondary damage. The primary damage occurs at the time of injury as a result of the trauma. Secondary damage develops following the injury and can occur as long as days after the initial trauma. The cause of the secondary injury is not well understood, but appears to be associated with disruption of the regulation of calcium levels in brain cells following injury. Regulation of calcium levels is crucial to mitochondrial function and to proper adenosine triphosphate (ATP) synthesis and use. ATP is a molecule that is present in all living cells and operates as the energy source for the majority of the chemical reactions which take place in cells. Scheff's research team demonstrated that brain damage in mice was reduced 21 percent and 36 percent when creatine was administered three and five days before the TBI respectively. The data also show that in rats fed a diet supplemented with creatine for four weeks before TBI, brain damage was reduced 50 percent when compared to rats fed a regular diet. "Our data show that creatine supplementation protects against secondary damage associated with TBI by inhibiting the calcium-induced activation of a protein in the mitochondrial membrane, which preserves proper function of the mitochondria. The damage also is reduced because creatine acts to maintain appropriate amounts of ATP in brain cells," Scheff said. "This strongly suggests that athletes may be gaining a neuroprotective benefit inadvertently by chronically supplementing their diet with creatine," Scheff said. PR 11/2/00 Annals of Neurology 2000;48:723-729 (Nov.)
Other Items
Evidence Links Protein Damage to Parkinson's - New evidence links
oxidative damage in a protein found in nerve cells to the development of
degenerative diseases of the nervous system, such as Parkinson's and AD.
"The protein, called alpha-synuclein, is one of the building blocks
of the brain lesions characteristic in patients with neurodegenerative
diseases," says Dr. Virginia Lee, a professor at the University of
Pennsylvania School of Medicine. Oxidative damage, she explains, normally occurs
when the body's cells are overwhelmed by molecules that have changed because
they have combined with nitrogen (nitration) or oxygen (oxidation). Both types
of oxidants damage lipids, nucleic acids, proteins, and other cellular
components much like oxidation causes rust damage to metal in cars and
buildings. This damage has been implicated in causing neurodegenerative
disorders. "We found that alpha-synuclein itself is a target of oxidative
stress, specifically nitration, within these lesions," says Lee. "This
is the first time anybody has identified nitration on a specific protein."
Neurodegenerative diseases -- including Parkinson's, AD, diffuse Lewy
body disease, and multiple system atrophy -- are collectively called
synucleinopathies. "Our studies provide conclusive evidence of oxidative
damage in alpha-synuclein, and that such stress may be a primary event
leading to the onset and progression of neurodegenerative synucleinopathies,
particularly Parkinson's" says Lee. "This may pave the way for
developing therapies to stop or slow the oxidative damage, and thus slow \pard
softlineor reverse the progression of these diseases." PR 11/2/00
Science (2000), 290 (5493) 985-989
Lead Accelerates Aging Process Years after Exposure - Lead exposure on
the job can cause progressive declines in memory and learning abilities nearly
two decades later, according to a study conducted at the Johns Hopkins School of
Hygiene and Public Health in Baltimore, MD.
The study compared 535 former chemical manufacturing employees exposed to lead
at work to 118 non-exposed people from the same neighborhoods. "The effects
of the average level of bone lead found in former lead workers was like five
more years of aging on the brain said Brian Schwartz, MD, of Hopkins. "The
higher the peak level of lead determined in former lead workers, the greater the
decline in brain functions," Schwartz said. "Since these declines were
seen long after exposure to lead had stopped, it suggests that the effect of
lead on the brain is progressive." The workers not only had greater
declines in test scores due to lead, but also in normal age-related declines in
brain functions, Schwartz said. Significant differences were discovered between
the former workers and other participants in tests involved in visual
construction, verbal memory and learning, visual memory, planning and
organizational ability, and manual dexterity. "We know there's a decline in
brain power as we get older -- generally we call this ‘normal aging,’ "
said Schwartz. "Most of the research has been about how chemicals, like
lead, affect kids. This is the first study to explore long-term problems caused
by exposure to chemicals as adults. Some of what we have been calling ‘normal
aging’ may in fact be due to past exposures to chemicals or other agents that
can affect the central nervous system. This is potentially a very important
health problem." PR 10/23/00 Neurology 2000;55:1144-1150 A free copy
and a 7 page pdf file is at http://www.neurology.org/
Choose Oct. 2000 issue.
Researchers Say Find Key Nerve Injury Protein - Researchers reported on 11/1/00 they had identified a protein, inosine, that is key to helping injured nerve cells regenerate, and said it might be used to develop new treatments for spinal cord injuries and stroke damage. Inosine acts as a kind of master switch to turn on a number of genes involved in the growth of nerve cells, the team at Boston's Children's Hospital and Harvard University reports. Dr. Larry Benowitz, who led the research, in an interview with Reuters Health said "Inosine switches on a whole constellation of genes." When these newly grown axons met one another, they formed synapses -- the key connections that nerve cells use to send messages to one another. Inosine apparently passes through the nerve cell's membrane and activates an enzyme that in turn controls the cell's molecular program for axon growth. "We think it is directly targeting and activating a protein kinase, an enzyme, inside the cell, that is the linchpin of the signaling pathway that activates growth," Benowitz said. But, he added, "While inosine stimulates nerve growth very nicely, it doesn't do it as well as another molecule we have found -- AF-1." AF-1 is short for axogenic factor and Benowitz's lab is working to get enough to experiment with. "I have been banging my head on the wall trying to get enough of this stuff to purify," he said. "I don't think inosine alone is enough to activate everything optimally. There must be other positive and negative controls on that pathway." Boston Life Sciences is working with other researchers to develop inosine for use in stroke victims, who lose brain cells to damage caused by blood clots. It is not clear whether inosine gets new brain cells to grow or protects them from dying, said Benowitz. When a brain cell dies, it often sends out chemical signals that cause surrounding, healthy brain cells to die. It is not known why but finding a way to shut off this mechanism could help prevent damage from stroke and brain injury, as well as the progression of Parkinson's and AD. Reuters 11/1/00
Serious Head Injuries Linked to AD - A new analysis of head injuries among World War II veterans links serious head injury in early adulthood with AD in later life. The study, by researchers at Duke University and the National Institute on Aging (NIA), also suggests that the more severe the head injury, the greater the risk of developing AD. Why head injury may be involved in AD and dementia is still unknown. The researchers looked to see if the increased risk of AD associated with head injury was only present in those men with an APOE e4 allele. The analysis did not find a statistically significant interaction. The analyses also looked at other factors that possibly could influence the development of dementia among the veterans, including education, positive family history of dementia, and a history of alcohol or tobacco use, but none was involved in the association between head injury and dementia found in this study. Brenda L. Plassman and her colleagues note more generally that the findings are consistent with current thinking on the etiology, or course, of AD. The increased risk of dementia, some 50 years after the head injuries had occurred, is one more indication that AD is a chronic disease that unfolds over many decades, she points out. "Understanding how head injury and other AD risk factors begin their destructive work early in life may ultimately lead to finding ways to interrupt the disease process early on," says Plassman. PR 10/23/00 Neurology 2000;55:1158-1166 A free copy and a 9 page pdf file is at http://www.neurology.org/ Choose Oct. 2000 issue.
2 Americans Celebrate Winning Nobel Medicine Prize - Paul Greengard of New York's Rockefeller University, Eric Kandel of New York's Columbia University and Arvid Carlsson, formerly of the University of Gothenburg, shared the prestigious Nobel Prize for Medicine for studies on how messages move around the nervous system. Greengard and Carlsson’s work related to studying Parkinson’s disease. Kandel’s work related to short and long term memory. He found the mechanism for this "short term memory" is that particular ion channels are affected in such a manner that more calcium ions will enter the nerve terminal. This leads to an increased amount of transmitter release at the synapse, and thereby to an amplification of the reflex. A more powerful and long lasting stimulus will result in a form of long term memory that can remain for weeks. The stronger stimulus will give rise to increased levels of the messenger molecule cAMP and thereby protein kinase A. These signals will reach the cell nucleus and cause a change in a number of proteins in the synapse. Eric Kandel thus demonstrated that short term memory, as well as long term memory in the sea slug is located at the synapse. The Nobel Prize announcment for Eric Kandel concluded as follows. "The fundamental mechanisms that Eric Kandel has revealed are also applicable to humans. Our memory can be said to be "located in the synapses" and changes in synaptic function are central, when different types of memories are formed. Even if the road towards an understanding of complex memory functions still is long, the results of Eric Kandel has provided a critical building stone. It is now possible to continue and for instance study how complex memory images are stored in our nervous system, and how it is possible to recreate the memory of earlier events. Since we now understand important aspects of the cellular and molecular mechanisms which make us remember, the possibilities to develop new types of medication to improve memory function in patients with different types of dementia may be increased." Reuters 10/9/00 and Nobel Prize Announcement http://nobel.sdsc.edu/announcement/2000/medicine.html Science magazine has free copies of articles by Kandel and Greengard at http://www.sciencemag.org/feature/data/nobelprize/
Afar Launches New Aging Research Website Infoaging.org, - The American Federation for Aging Research (AFAR) today launched a new website, http://www.infoaging.org , which will provide easy access to authoritative and current scientific research on aging and age-related diseases and conditions. The site is funded by an educational grant from the Pfizer Inc., which does not have any role in the selection or development of content for the website and is not a member of Infoaging.org's advisory board. PR 11/1/00
Neurome Gets $9 Million - La Jolla-based Neurome Inc., a biotech company that works in neurosciences, said 10/20/00 it raised $9 million in financing and started a commercial collaboration with Elan Pharmaceuticals. The three-year Elan partnership will look at the neurophysiology of AD in mice to find new treatments for the disease, and could raise up to $4 million in service fees. Newly established Neurome, which will look at ways of treating brain diseases and enhancing brain function, was co-founded by Dr. Floyd Bloom, retired editor of Science and chairman of neuropharmacology at The Scripps Research Institute. PR 10/20/00
Eyre's 'Elegy' Heads to Paramount - "Elegy for Iris," a drama headlined by Judi Dench, is headed for Paramount after being offloaded by Sony's Columbia Pictures over budget issues. "Iris" is an adaptation of John Bayley's memoir about his marriage to novelist and philosopher Iris Murdoch, and was long a pet project of Sony Pictures chairman John Calley. But studio brass there wanted to make the biopic at $5 million -- not the $8 million to $9 million price tag being touted by director Richard Eyre, and placed it into turnaround. Eyre then brought it to producer Scott Rudin (''Shaft''), who may make the picture before anticipated strikes from the actors and writers guild this spring. The project will mark the first time Eyre has directed a feature for an American studio. "Iris" covers Bayley and Murdoch's meeting over 40 years ago while teaching together at Oxford, their marriage and her subsequent struggle with AD. By Claude Brodesser Variety 11/1/00 Go to http://www.amazon.com & type in Elegy for Iris to get 5 pages of book reviews on this book
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