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Use it or Lose it?
Brain Cell Activity Increases Levels of Key
Ingredient in Alzheimer's Plaques
"Cognitive idleness is not good from the perspective
of Alzheimer's risk"
By Michael Purdy
Dec. 23, 2005 - Increased communication between
brain cells increases levels of amyloid beta, the key ingredient in
Alzheimer's brain plaques, scientists at Washington University School of
Medicine in St. Louis have found.
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The findings showed that turning up brain cell
firing rates drove up levels of amyloid beta in the spaces between brain
cells. Corresponding drops in amyloid beta levels occurred when brain
cells' ability to send messages was dampened or blocked completely.
The results, produced in mouse models of
Alzheimer's, appear in the journal Neuron on Dec. 22. They complement a
Washington University study published earlier this year that used
functional brain imaging to show that the brain areas that develop
Alzheimer's plaques are also the regions that are the most active in
healthy young people who are daydreaming or not carrying out a specific
cognitive task (http://news-info.wustl.edu/news/page/normal/5621.html).
The two papers have researchers considering the
possibility of someday slowing or preventing the development of
Alzheimer's disease by using pharmaceuticals to selectively reduce some
communication between brain cells.
However, researchers still have to determine if
increased levels of amyloid beta can be partially linked to particular
classes of the nerve cell messengers and receptors that cells use to
communicate with each other.
"Ideally, we will be hoping to find a drug or
mechanism that could very specifically target the processes that lead to
increased amyloid beta levels," says lead author John Cirrito, Ph.D., a
postdoctoral research associate in neurology and psychology. "If we can
identify these and find ways to modulate them, we'd have new ways of
intervening in Alzheimer's disease."
Senior author David Holtzman, M.D., the Andrew B.
and Gretchen P. Jones Professor and head of the Department of Neurology,
says that the results do not contradict earlier studies that suggested
crossword puzzles, exercise and other mental stimulation can reduce the
chances of developing Alzheimer's disease.
According to Holtzman, their new results and the
WUSTL study published earlier this year instead offer further evidence
that "cognitive idleness is not good from the perspective of Alzheimer's
risk." The lead author of the earlier study, published in The Journal of
Neuroscience, was Randy Buckner, Ph.D., a former Washington University
faculty member now at Harvard University.
Together, these two studies may provide an
explanation why specific regions are vulnerable to this disease.
Holtzman and Cirrito speculate that activities such
as crosswords and exercise may increase activity in brain areas less
likely to be damaged by Alzheimer's and cause a corresponding reduction
in activity levels in the regions consistently damaged by Alzheimer's
disease.
"Almost all neurological diseases involve selective
vulnerability—only certain classes of nerve cells or nerve cells found
in particular regions are affected," Holtzman says. "Why that
vulnerability is so selective often can be very difficult to determine,
and Alzheimer's disease is no exception."
Washington University researchers became interested
in connections between nerve cell activity levels and amyloid beta
production when they read a paper two years ago from researchers at Cold
Spring Harbor Laboratory and the University of Chicago that linked
increased activity in nerve cell cultures to increased levels of amyloid
beta.
Cirrito had previously modified a technique known
as microdialysis to enable repeated sampling and measurement of amyloid
beta levels in the brains of mice genetically modified to model human
Alzheimer's disease.
With Holtzman, Steven Mennerick, Ph.D., associate
professor of psychiatry, and others, Cirrito used direct electrical
stimulation and a variety of injected compounds to turn nerve cell
communication up and down in the brains of living mice. They assessed
the resulting effect on amyloid beta levels once every 30 minutes.
Through a series of these experiments, researchers
linked increased amyloid beta levels to the release of synaptic
vesicles, small packets containing chemical messengers known as
neurotransmitters.
The primary way nerve cells send messages to each
other is to release the vesicles waiting at the synapse, a structure
where the arms of two nerve cells almost touch. The neurotransmitters
cross the synapse and bind to receptors on the surface of the receiving
nerve cell.
Normal brain physiology produces amyloid beta and
naturally clears it from the brain, so Cirrito conducted a series of
follow-up experiments to try to get a sense for whether increased
synaptic vesicle release was affecting amyloid beta production or
clearance.
"It's probably not clearance, and the effect on
production is probably pretty small," he says. "Instead, it appears that
synaptic activity is regulating the amount of amyloid beta that gets
released from inside brain cells, where amyloid beta is produced. We're
going to follow up with studies of whether particular neurotransmitters
can be linked to changes in amyloid beta levels."
Information Sources:
Cirrito JR, Yamada KA, Finn MB, Sloviter RS, Bales
KR, May PC, Schoepp DD, Paul SM, Mennerick S, Holtzman DM. Synaptic
activity regulates brain ISF Aß in vivo. Neuron, Dec. 22, 2005.
Funding from the National Institutes of Health, the
Alzheimer's Association, Eli Lilly and the MetLife Foundation supported
this research.
Washington University School of Medicine's
full-time and volunteer faculty physicians also are the medical staff of
Barnes-Jewish and St. Louis Children's hospitals. The School of Medicine
is one of the leading medical research, teaching and patient care
institutions in the nation, currently ranked third in the nation by U.S.
News & World Report. Through its affiliations with Barnes-Jewish and St.
Louis Children's hospitals, the School of Medicine is linked to BJC
HealthCare.
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