Alzheimer Related News Items
News as of 10/06/02
For more info on these abstracts write/call Ed Cabic (edcabic@comcast.net or 410-992-7197)
NOTE - e-mail address change to new address as of 2/02
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
Anti-Inflammatories May Protect Against AD - New research suggests that aspirin and
other common anti-inflammatory drugs may reduce the risk of AD. In a 5-year study of
several thousand elderly Utah residents, people who had taken aspirin or other nonsteroidal
anti-inflammatory drugs (NSAIDs) for at least 2 years before the study began had less than half
the risk of the disease. But the risk of AD was not lower in people currently taking aspirin or
other NSAIDs unless they had started taking the medications several years before.
"Long-term NSAID use may reduce the risk of AD, provided such use occurs well before the
onset of dementia," according to Dr. John C.S. Breitner of the Veterans Affairs Puget Sound
Health Care System in Seattle, Washington and colleagues. Breitner's team followed residents of
a Utah county who were age 65 and older. From 1995 to 1996, they assessed the participants for
signs of dementia and asked them about their use of NSAIDs and other common medications.
Three years later, 104 of the 3,227 participants who were still alive had developed AD. Of these,
people with a history of long-term (over 2 years) regular use of NSAIDs were found to be 55%
less likely than non-users or more current users to develop AD. The study showed that people
who reported taking NSAIDs other than aspirin (such as ibuprofen or naproxen) the longest were
least likely to be diagnosed with AD. However, use of non-aspirin NSAIDs while enrolled in the
study did not seem to reduce the risk unless participants had been taking them for more than 2
years before the start of the study. Similarly, the study showed that people who reported taking
aspirin for more than 2 years were less likely to develop AD. That NSAID use appeared to
reduce the risk of AD only in people who had taken the medications several years before the
study started supports the concept of a "lag period," the researchers point out. Combined with
other studies, the findings suggest that long-term use of NSAIDs may prevent or postpone AD
"only if they are taken during a critical window in the latent stages of the disease, before damage
to the integrity of the brain is sufficient to provoke demonstrable cognitive symptoms," Breitner
and colleagues conclude. Despite the encouraging findings, the researchers caution that the only
way to know for sure that aspirin and other NSAIDs protect against AD is to compare them
head-to-head with a placebo (a pill with no active ingredients). Reuters Health 9/23/02
Neurology 2002;59:880-886
Brain Signal Balance May Identify AD Risk - An imaging technique that detects imbalances in
brain signals holds promise as a screen for early-stage AD, new research from the Medical
College of Wisconsin in Milwaukee suggests. Assuming that the screen passes the next round of
testing, which will take several years, it may be useful in identifying the elderly most in need of
drugs to delay the symptoms of AD, according to the study's lead author, Dr. Shi-Jiang Li.
Neurological deposits called plaques - - made of substances called amyloid-beta proteins - - and
twisted strands of fibers called tangles are hallmarks of AD. The AD process is thought to begin
years or decades before symptoms appear. In comments to Reuters Health, Li said that the
hippocampus, a part of the brain that is important for making memories, is one of the first places
where plaques and tangles form, so the identification of abnormalities in the hippocampus "could
provide the earliest sign of the initiation of irreversible disease progression." Li and his
colleagues developed a tool called the COSLOF - - coefficients of spontaneous low
frequency- index that measures the balance of signals from different parts of the brain. The
idea, according to Li, is that AD gradually throws off the balance of brain signals as it progresses.
Since the hippocampus is one of the first places in the brain to be affected by AD, Li and his
colleagues suspected that the COSLOF index, which measures the balance of brain signals,
would be lower within the hippocampus in people with AD. The researchers tested the index
in a study that included 10 people with AD and 5 with mild cognitive or mental impairment, a
condition that is less severe than dementia but still causes problems with memory and other
mental abilities. The study also included a "control" group of 10 healthy elderly individuals. Li's
team calculated each participant's COSLOF index based on a noninvasive brain scan of the
hippocampus called functional magnetic resonance imaging (fMRI). The results of the study,
which Li said were preliminary, "supported our hypothesis that the COSLOF index in AD
patients is significantly lower than (in) age-matched, elderly control subjects" With a higher
score representing a better balance of brain signals, the average score of people with mild mental
impairment fell between the other two groups. The next step, according to Li, is "to firmly
establish" a marker for AD that appears before symptoms start. To see whether measuring the
COSLOF index can predict a person's risk of AD, Li said that he and his colleagues are
proposing a 5-year study of people with mild cognitive impairment. "If the COSLOF index is
validated to be a preclinical marker for AD," Li explained, people with mild cognitive
impairment who have low scores could get early treatment before AD symptoms begin.
Although there is no cure for AD, Li noted that drug therapy could delay symptoms or stop the
progression of the disease. By Merritt McKinney Reuters Health 10/1/02 Radiology
2002;225:253-259
Drugs
Antipsychotic Drug Has Few Side Effects in AD Patients - A drug quetiapine (brand name
Seroquel) used to help control psychotic behavior in people with schizophrenia holds promise
for controlling similar symptoms in the early stages of AD, a new study by Ohio State
researchers suggests. The advantage of this drug is its apparent lack of serious side effects,
such as confusion, muscle stiffness and imbalance in the joints, said Douglas Scharre, a study
co-author and an associate professor of clinical neurology at Ohio State University. None of the
10 subjects in the study reported any of these symptoms during a 12-week trial. "Quetiapine
should be considered the first line of treatment for psychosis in AD patients because of its lack
of serious side effects," Scharre said, adding that while no antipsychotic medication is currently
approved by the Food and Drug Administration to treat AD-related psychosis, physicians can
prescribe it as an "off-label" use. The average dose of quetiapine at the end of the study was 50
mg twice daily. Dosing ranged from 50 mg to 150 mg per patient per day, a fraction of what is
normally required to control psychotic behavior in schizophrenic patients. "Schizophrenics don't
show much of a response until the dose is 150 mg or higher, and may require up to 600 to 800
mg of quetiapine to ease psychotic symptoms," Scharre said. At the end of the current study,
quetiapine at the 50 to 150 mg level did not significantly worsen cognitive function in the AD
subjects. In fact, the average ADAS-cog scores improved slightly after six weeks. "The decrease
in aggression and psychotic behavior at this point may also have contributed to the improvement
in cognitive scores," Scharre said. PR 9/17/02 Alzheimer Disease and Associated Disorders
2002;16:128-130
Withdrawal of Memantine FDA Application is Not a Problem - Forest Laboratories Inc.
recently withdrew its FDA application to market Memantine, its treatment for moderate-to-severe AD. This should be considered as good news because new data from a recent late-stage
study reveal that Memantine has more potential than found in initial trials. The results show
when the drug is combined with an AD treatment called Donepezil, (brand name Aricept),
it offers major benefits to moderate to severe patients when compared with the use of
Donepezil alone. Specifically, the combination improves cognition, or the ability to understand
information and events. "The decision to pull the application was strategic," said analyst Cynthia
Glass of ThinkEquity Partners. "They're refiling with this new exciting data and giving the FDA
the full apple instead of a bite halfway through. This improves the odds of getting the study
results into the initial label." By Marilyn Much Investor's Business Daily 10/3/02
Genes & Genetic Issues
AD Mechanism Comes to Light - Researchers at The Jackson Laboratory in Bar Harbor, Maine.
have found a gene known to incite death among cells also can prevent their demise. Studies of
specially engineered mice suggest the gene, called apoptosis inducing factor or AIF, protects
certain nerve cells in the brain and eye. The AIF gene can keep a damaging biochemical process
called oxidative stress at bay and avert cellular deterioration. Oxidative stress, resulting from an
unchecked proliferation of erratic molecules called free radicals, has been implicated in a
lengthening list of human ailments. "The authors describe a study in which (AIF)...staves off cell
death in neurons of the retina and certain regions of the brain (cerebellum) when these cells are
exposed to conditions of oxidative stress," Ed Levine, assistant professor of ophthalmology and
visual sciences at the Eccles Institute of Human Genetics at the University of Utah in Salt Lake
City, told United Press International. "This is somewhat surprising since AIF has previously
been shown to be involved with promoting cell death," Levine said. "(The study's) connection to
oxidative stress is interesting because oxidative stress is a common cause of cellular damage and
death that is associated with aging. Thus, targeting treatments to promote AIF activity in
specific neurodegenerations may have promise." It could be a target for treatment of
age-related mental decline associated with AD and other disorders. It turns out the mice have a
mutation in their AIF gene. The mutation severely curtails production of the corresponding AIF
protein, a scavenger of free radicals in the brain and retinal neurons, the investigators discovered.
With the protein numbers diminished, the radicals remain free to roam, leading to oxidative
stress and, eventually, nerve cell death. By Lidia Wasowicz UPI Senior Science Writer 9/25/02
Nature 419, 367-374 (2002)
Scientists Complain That Stem Cell Rules Hamper Research - Advances in medical research
are being hindered by federal rules governing the use of embryonic stem cells, scientists told a
Senate panel 9/25/02. Many researchers believe these cells could hold the key to solving such
diverse maladies as Parkinson's disease, AD, spinal cord injuries and diabetes. However,
President George W. Bush, citing ethical concerns, restricted federal funding for research on
embryonic stem cells to 78 already existing cell lines. Gaining access to those limited cell lines
has been inordinately difficult, several researchers complained, citing costs, problems
negotiating agreements with the cells' owners and restrictions imposed by governments of
foreign countries, where many of the cells are located. Responding to the complaints, Dr.
Elias Zerhouni, director of the National Institutes of Health, said that his agency is "diligently
working with as many sources as we can to make more cell lines available." By Randolph E.
Schmid, Associated Press Writer 9/25/02 Dr. Zerhouni's testimonry is at
http://olpa.od.nih.gov/hearings/107/session2/testimonies/stemcelltest.asp
Caregivers
Psychiatric Symptoms Often Accompany Dementia - Depression, irritability, apathy and other
psychiatric symptoms often affect elderly people who have dementia or mild mental impairment,
according to a new report. "Neuropsychiatric symptoms are common in dementia and mild
cognitive impairment," the study's lead author, Dr. Constantine G. Lyketsos of the Johns
Hopkins Hospital in Baltimore, Maryland, told Reuters Health. "This study further confirms the
view that the symptoms are almost universal over the course of the illness." But Lyketsos noted
that treatment, including but not limited to medications, can alleviate psychiatric symptoms, so
caregivers or family members "should bring them to the attention of the doctors in their
early stages so that they can be effectively managed before they become disabling." The
researchers evaluated psychiatric symptoms in 682 participants with dementia or mild cognitive
impairment. In a confirmation of previous research, the study found that 75% of demented
individuals had experienced at least one psychiatric symptom in the month before the evaluation.
More than half reported two or more symptoms and 44% had at least three psychiatric symptoms.
The most common symptoms among participants with dementia were apathy, depression and
agitation/ aggression. The study also demonstrated that a substantial percentage of people with
mild cognitive impairment, 43%, experienced at least one psychiatric symptom. The most
common ones were depression, apathy and irritability. For the most part psychiatric symptoms
were similar regardless of dementia type. According to the researchers, the fact that psychiatric
symptoms often accompanied mild cognitive impairment as well supports the idea that mild
cognitive impairment is not a separate condition from dementia but a step along the way to
dementia. The good news, according to Lyketsos, is that psychiatric symptoms are often
treatable, particularly if detected early. "Treatment not only helps the symptoms but also may
delay illness progression," he said. By alleviating symptoms, treatment can also benefit a
patient's caregivers, he added. By Merritt McKinney Reuters Health 9/24/02 The Journal of the
American Medical Association 2002;288:1475-1483
Rensselaer Research Team Sheds Light on a Good Night's Sleep for Those With AD - The results of a recent pilot study has found that AD patients sleep better through the night if they are exposed to blue LED lighting a few hours before bedtime. The study was conducted by a research team led by Mariana Figueiro at the Lighting Research Center (LRC) at Rensselaer Polytechnic Institute. Light regulates the 24-hour sleep-wake cycle in healthy humans. Typically, the body's temperature is high during the day, allowing people to remain alert and active. The temperature is low at night, which facilitates sleep. But those with AD often wake up numerous times at night causing them to fall asleep more often during the day. The major result is nighttime wandering, a top factor in why patients are institutionalized. Figueiro's team conducted the light study for 30 days. The team chose blue LEDs (light-emitting diodes) because recent research has shown that short wavelength (blue) light is maximally effective at affecting the circadian system whereas middle wavelengths (yellow-green) are better for visual performance. The circadian system is composed of rhythms that repeat at approximately every 24 hours. Four AD patients were exposed to about 20 watts of blue LED lighting two hours before bedtime, 6- 8 p.m., for two 10-day periods. Red LEDs were used to control for placebo effects. Figueiro's team found that blue light exposure delayed the decline of the patients' body temperatures by two hours. In other words, they slept better between two and four hours after the light exposure. Furthermore, the two patients who wore the wrist activity monitors showed more activity during daylight than at night. To confirm these findings, the LRC plans to replicate this study in a larger population. PR 9/25/02 An article about the study was accepted for publication in Sleep Review magazine
Caring for Sick Spouse Prompts Older Women to Retire Much Earlier than Men, Who Put
Income First, Cornell Study Finds - Working wives in late midlife are five times more likely to
retire early to care for ill or disabled husbands than wives who are not caregivers, according to a
new study by Cornell University sociologists. However, the study found, when men are
caregivers, they are slower to retire than those who are not taking care of their wives. "How
much caregiving influences whether an adult in late midlife will retire soon or not, however,
largely depends on the strength of the relationship between the worker and the person needing
caregiving," explains Marin Clarkberg, an assistant professor of sociology at Cornell and one of
the co-authors of the new study. "Caring for a spouse has the strongest -- and in the case of men,
the only significant -- impact on shaping retirement timing." "In our rapidly aging society, as
much as 80 percent of care to elderly and disabled Americans is performed by families," says
co-author Emma Dentinger. "We sought to determine how gender and the type of informal
caregiving that late midlife workers provide influence the timing of retirement." The researchers
found that caring for a spouse had a far more significant effect on a woman's decision to retire
than caregiving for anyone else, including parents. Indeed, of the respondents, almost half the
women and slightly fewer men were most likely to be caring for or had cared for elderly parents.
In general, the closer the relationship between the caregiver and the person being cared for, the
greater the influence on retirement decisions. Unlike women, however, men who are caregivers
are slower to retire than men who are not, the study found. These male caregivers reported not
only higher household incomes than their female counterparts but also less satisfaction from their
work. "The husbands seem to delay their retirement, therefore, for financial reasons, rather than a
greater work commitment or a desire to escape their family life," Clarkberg says. PR 10/4/02
The study is published in the October issue on care and kinship of The Journal of Family Issues
(Vol. 23:7, pp. 857-879)
Testing
PET Imaging - PET imaging is stepping out of the shadows of medicine, taking its place
alongside more widely used diagnostic tools such as MRIs and CT scans. Wider acceptance of
PET scanners is a big reason for the growth. The market is valued at $250 million and is growing
40% a year, industry sources say. In the past, the procedure's high costs discouraged all but the
largest medical centers from using it. Scanners alone cost up to $2.5 million each. Radiotracers
injected into patients beforehand can be produced only in machines called cyclotrons, which cost
$2 million. Only in recent years have insurers agreed to reimburse patients for PET images
beyond heart scans. Medicare began the process in 1998 with its allowance for pulmonary
nodules and initial staging of lung cancer. As other third-party payers followed Medicare's lead,
the $1,800 patient fee - including the radioactive tracers - came within reach of more patients. In
turn, increased volume made it more cost-effective for hospitals and other providers to buy more
units. "We're still just seeing the impact right now from those early (reimbursement) policies,"
said Edward Coleman, director of nuclear medicine at Duke University Medical Center. Since
1998, new medical indications for PET scans with Medicare reimbursement approval include
colorectal cancer, melanoma, lymphoma and head and neck cancer. Starting Oct. 1, Medicare
will start reimbursing for breast cancer treatment. Doctors say AD could be next in line.
"There's a large, pent-up need that has yet to be filled," Coleman said. By Marilyn Alva
Investor's Business Daily 9/16/02
Celera Signs Deals with LabCorp - Celera Diagnostics, a joint venture between Applera Corp's
Applied Biosystems Group and the Celera Genomics Group, said on 10/2/02 it had signed an
agreement with Laboratory Corp. of America to collaborate on tests for AD, breast cancer and
prostate cancer. Under the terms of the deals, Alameda, California-based Celera Diagnostics will
be the preferred vendor to LabCorp for certain molecular diagnostic products. Reuters 10/4/02
Prevention
Knowing That Your Memory Fails Is an Omen - Joking about "senior moment" memory
problems is common, even among people who aren't yet middle-aged. But very frequent
complaints about memory failure may be an omen, new research from UCLA suggests. The
higher the awareness of memory loss, the higher the risk of future memory decline, says Dr.
Gary Small, the director of the UCLA Center on Aging, who presented his new research 9/28/02
in Chicago at the First Annual Dementia Congress. "To some extent, subjective awareness of
memory changes predicts future decline in brain function in the memory centers," Small says.
For example, in a recent research study, he evaluated 39 people between the ages of 50 and 82,
all of whom had mild memory complaints. Some were carriers of the APOE-4 gene, a
susceptibility gene for AD, and some were not. He gave all of them a standardized memory
assessment test and asked them to rate their memory performance. Each person underwent
positron emission tomography (PET) scans of the brain on entering the study and then again two
years later. Small found that the perceived degree of memory loss correlated with a decline in
metabolism in the hippocampus, a region of the brain critical for learning and recall, regardless
of whether the APOE-4 gene was present. On average, the metabolism in that area declined about
four percent during the two years. "Awareness predicts the biological changes," Small says.
"This is what we predicted would happen." "These data are not surprising," Small adds. "Brain
aging occurs very early in life, even in young people. Some of these subjective memory changes
we notice actually have some biological meaning." People who experience such memory loss
often fear they are getting AD, which can begin with mild memory problems and progress to
more serious ones. But recent research suggests that a large number of people who suffer from
milder forms of cognitive problems might be able to protect the brain from further decline
by paying attention to lifestyle and environmental factors that play a role in progression of
the disease. "There is a lot we can do about it," Small says of cognitive decline. "We can keep
our brain young and healthy, improve our memory performance and even stave off future
decline." Genetics accounts for about one third of cognitive problems, Small says, while we have
some control over the other two-thirds. "Be proactive in protecting your brain," Small tells
people. To do that, he recommends mental activity, "what I call mental aerobics." Exercising the
mind with anything fun and stimulating works, he adds. Staying in good physical shape is
important, he says, as is eating a "brain-healthy" diet. He recommends, among other measures,
reducing saturated fats and focusing on "omega 3" or good fats, found in such foods as canola
oil, salmon and trout and stress reduction. "If you can cover those four areas, you can keep your
brain healthy." In his new book, The Memory Bible, Small talks about healthy brain aging and
how to improve memory. By Kathleen Doheny HealthScoutNews Reporter 9/27/02
Vitamin B3 Helps Beat Back AD - A team of scientists at the South Dakota State University's College of Pharmacy has found that a common vitamin, B3, can offer some protection against the effects of AD on brain cells. The research was performed on live brain cells cultured by the scientists. The cells were the same type as those found in the front part of the brain, where a portion of the memory function resides. In the experiment, the researchers exposed the brain cells to a chemical that kills cells in a similar manner to AD. When they first exposed the cells to nicotinamide, a form of Vitamin B3, the cells didn't deteriorate as quickly once the toxin was introduced. "It probably is preventing brain cells from dying," says lead author Suman Mukherjee. "Other researchers also think that this agent has promise. But we are still a long way from establishing it as the most promising one." By Ross Grant HealthScoutNews Reporter 9/25/02 The research is due to be published later this year in Neurotoxicity Research
New Era of Consumer Genetics Raises Hope and Concerns - Scientists are beginning to apply
genetics to diet, a new field known as nutritional genomics, or nutrigenomics. In the near term,
the study is expected to reveal how particular diet ingredients affect health. The ultimate goal
will be to tailor one's diet to genetic makeup. Mass market products like corn flakes may one day
come in different varieties, geared to different subsets of people based on their genes. And
dietary guidelines issued by the government or medical societies will have to make more
distinctions based on genetic profiles. "We're moving into an era where the one-size-fits-all
public health strategy for disease prevention will not apply as it currently does," said Dr. Muin J.
Khoury, director of the Office of Genomics and Disease Prevention at the Centers for Disease
Control and Prevention. Another concern is that some genes that may be tested for dietary
purposes are risk factors for serious diseases. Should consumers be told, and do they risk being
denied insurance or jobs if that information leaks out? Do they need medical advice?People with a version of a gene called APOE, for instance, tend to have their cholesterol go up or
down more rapidly in response to dietary changes, Dr. Krauss said. But this same gene variant,
known as APOE4, also means a higher risk of AD. "We don't even like to measure APOE
anymore because it would get people worried about AD," he said. In some cases, he and
others said, it is not necessary to test genes. Other tests, like those for cholesterol, can help guide
diet decisions. Dr. Jose M. Ordovas, director of nutrition and genomics at the Agriculture
Department's Human Nutrition Research Center at Tufts, said dietary guidelines would soon
have to be customized. "There are some people at very high risk of cardiovascular disease who, if
they follow the current recommendations, they make it even worse," he said. Moderate alcohol
consumption, he said, is considered to reduce risk of heart disease. But for people with the
AD-linked APOE4 gene, alcohol consumption raises the level of bad cholesterol. People with a
certain variant of a gene called APOA1 should eat more polyunsaturated fats than called for in
the guidelines. By Andrew Pollack NY Times 10/1/02
Other Items
Plaque-Forming BACE Enzyme Rises in AD Brains - An enzyme involved in making
AD-related brain deposits, BACE, is present in higher levels and is more active in parts of the
brain where the disease takes the heaviest toll, researchers have found. The findings raise the
possibility that a drug that blocks the enzyme could reduce the formation of the deposits in
the brain even when AD has already reached an advanced stage, the investigators suggest.
Neurological deposits called plaques--made of substances called amyloid-beta proteins--are
hallmarks of AD. In an interview with Reuters Health, the study's senior author, Dr. Michael C.
Irizarry of Massachusetts General Hospital in Boston, explained that amyloid-beta proteins are
formed when two types of enzymes - - beta-secretase and gamma-secretase - - chop off different
parts of a protein called amyloid precursor protein. Irizarry and his colleagues suspected that
levels of a protein called BACE - - the primary form of the protein-clipping beta-secretase - -
would be elevated in parts of the brain where plaques usually form. The researchers developed
screens to detect beta-secretase and to measure its activity - - how efficiently it clips proteins.
The BACE form of beta-secretase was more abundant and more active in the brains of AD
patients, but only in the parts of the brain where plaques usually develop. In the temporal
neocortex and the frontal neocortex - - both regions where plaques accumulate - - BASE activity
was 63% and 13% higher, respectively, in the AD group than in the control group. Similarly,
levels of the protein in these parts of the brain were higher in AD brains than in the control
group. The study "points out that this particular enzyme, beta-secretase, is a good target for
treatment," Irizarry said. He noted that in the temporal section of the brain, levels of
beta-secretase were highest in patients who had had AD the longest, suggesting that
beta-secretase "might be a target even late in the disease." He cautioned, however, that even if a
drug were developed to block beta-secretase in advanced AD, it might be too late to replace
many of the nerve cells already destroyed by the disease. Reuters Health 9/13/02 Archives of
Neurology 2002;59:1367-1368, 1381-1389
AD May Originate in the Brain's White Matter - Changes in the brain's white matter may play a major role in the onset of AD, whose baffling origin has traditionally been blamed on the gray matter. The new findings by researchers at Sun Health Research Institute in Sun City, Ariz. could provide a fresh direction for AD research in this neglected part of the brain, offering the potential for early diagnosis and enhanced therapies. Dr. Alex Roher the director of the Institute said theirs is the first study to present a detailed biochemical analysis of white matter tissue of AD patients. The study revealed that the total amounts of protein, lipids and cholesterol were significantly reduced in the myelin of AD patients in comparison to the control group. This erosion of the myelin sheath is referred to as demyelination. "These profound white matter alterations undoubtedly contribute to the origin and development of AD, and might possibly be the initiating step," Roher says. There are multiple reasons for arriving at this conclusion, according to Roher, but two in particular stand out. First, previous studies have demonstrated that patients with pre-clinical AD show deterioration in the white matter before the gray matter. Second, the current study suggests that white matter degeneration might be caused by a disease of the oligodendrocytes, whose main job is to produce the myelin sheath. A defective myelin coating could leave the axons unprotected, resulting in serious disturbances in nerve conduction and damage to brain functions, Roher says. Because neurons in the gray matter are vital to cognitive activity, scientists have generally assumed that AD - - with its memory loss and other cognitive debilitations - - must begin in the gray matter. But Roher says the white matter is just as critical to cognitive function. White matter axons play a major role in controlling mental activities like emotion, and all mental functions are fully expressed only when the axons are transmitting properly. PR 9/18/02 Biochemistry 2002 Sep 17;41(37) 11080-90
Findings Aid Understanding of Neurodegenerative Diseases - Northwestern University scientists have made a key molecular discovery that has implications for a wide range of diseases characterized by the loss of nerve function, including Huntington's, Parkinson's, AD and Lou Gehrig's diseases, cystic fibrosis and Creutzfeldt-Jakob disease, the human form of mad cow disease. The findings could lead to an understanding of how to prevent these diseases and to the development of effective drugs. All human neurodegenerative diseases have two things in common. First, misfolded and damaged proteins clump together to form toxic species that aggregate, destroy cell function and cause disease. Second, studies have shown that special protective proteins, called molecular chaperones, can suppress these toxic effects. This question remained: How do the chaperones and aggregates interact with each other? A research team led by Richard I. Morimoto, Professor of Biology, now can answer that question. The researchers have become the first to view, in living cells and in real time, the interactions between the beneficial molecular chaperone Hsp70 and the damaging protein aggregate, shedding light on how the chaperone works to minimize aggregate growth. "We now understand how the chaperone influences the aggregate's toxic effect on the cell," said Morimoto. "We observed that the chaperone is binding to and then coming off the aggregate all the time. This dynamic relationship is unusual because the aggregate, the result of a genetic mutation, brings healthy and otherwise normal proteins to aggregate irreversibly with them. But this clearly is not the case with the molecular chaperone." Instead, the molecular chaperone is allowed, for reasons not fully understood, to do its work preventing healthy proteins essential to cell function from being bound to the aggregate, a biochemical "black hole." The chaperone is continually sampling the aggregate to see what is there and to release any healthy proteins from the aggregates clutches. This could suppress the aggregates growth, prolonging the life of the cell and delaying the onset of disease. PR 9/29/02 Nature Cell Biology Oct 2002;4 (10) 826-831
Ronald Reagan May Not Recognize Wife - Nancy Reagan says her husband, in the advanced stages of AD may not even recognize her anymore. In a CBS "60 Minutes II" interview broadcast 9/25/02, the former first lady said Ronald Reagan's disease has robbed the couple of their post-White House golden years. The 91-year-old former president spends his days secluded in his Bel-Air home in Mrs. Reagan's care. Asked if her husband even knows who she is, she said, "I don't know." Although Mrs. Reagan is visited regularly by daughter Patti Davis, the former first lady said she is lonely. "Yes, it's lonely, because really, you know, when you come right down to it, you're in it alone and there's nothing that anybody can do for you," Mrs. Reagan said. AP 9/25/02
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