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Alzheimer's Study Finds Natural 'Fishnet'
Captures Damaging Beta-Amyloid
Raises question of
does age just create more of this protein or does 'fishnet' leak
March 21, 2006 Beta-amyloid fragments that lump
in the brain to form plaque has long been associated with Alzheimer's
disease. New research indicates that an organ in the brain called the
choroid plexus apparently plays a critical role in preventing the
accumulation of this protein, challenging a long-held theory that the
protein accumulates because it is overproduced by aging brain cells, or
neurons.
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The researchers found that the choroid plexus acts
as a sort of "fishnet" that captures the protein, called beta-amyloid,
and prevents it from building up in the cerebrospinal fluid, which
surrounds and bathes the brain and spinal cord.
Moreover, tissue in the
organ is able to soak up large amounts of the protein and may contain
enzymes capable of digesting beta-amyloid, said Wei Zheng, an associate
professor in the School of Health Sciences at Purdue University.
The findings represent the first time that
researchers have identified the potential existence of a natural
mechanism in the brain for removing beta-amyloid.
"This newly uncovered pathway may help explain how
normal brains balance this protein and how an imbalance caused by aging,
genetic or environmental factors may lead to or worsen Alzheimer's
disease," Zheng said.
Researchers had already known that the
cerebrospinal fluid in the brains of Alzheimer's patients contains
abnormally high quantities of beta-amyloid fragments. Beta-amyloid
deposits accumulate over a period of years, resulting in abnormal
clumps, or plaque, typical of Alzheimer's disease. Scientists do not yet
know whether the disease is caused by the plaque formations or
beta-amyloids themselves.
The discovery suggests that a malfunctioning
choroid plexus could allow too much of the protein to build up in the
brain.
Findings are detailed in a research paper written
by postdoctoral research associate Janelle S. Crossgrove, postdoctoral
fellow G. Jane Li and Zheng, all in the Purdue School of Health
Sciences. The researchers will be honored on April 2 with a best paper
award from the Society for Experimental Biology and Medicine.
Scientists do not know how beta-amyloid is
deposited in the brains of Alzheimer's disease victims, but a long-held
theory is that the protein is overproduced by aging brain cells, or
neurons.
"We are coming from a totally different point of
view," Zheng said. "We think that a balance of beta-amyloid is
maintained partly by the choroid plexus, which removes beta-amyloid, and
that this balance breaks down, leading to a buildup."
The majority of Alzheimer's research has
historically concentrated on how the brain produces beta-amyloid
protein, but the new findings point to the possibly critical importance
of the "garbage-removal" process in the choroid plexus, Zheng said.
"We think the choroid plexus plays a role of
removing all the garbage, including the beta-amyloid," Zheng said.
The research focused on how the choroid plexus
works to clean beta-amyloid from the cerebrospinal fluid. Studies using
rat brains indicated that choroidal cells removed about five times more
beta-amyloid from cerebrospinal fluid compared to how much of the
protein the cells allowed to pass into the fluid.
"These results appear to tell us that a healthy
choroid plexus can remove beta-amyloid from the cerebrospinal fluid,
suggesting a novel pathway for the brain to maintain a normal balance,"
Zheng said. "Of course, much more work needs to be done to verify this
theory."
The researchers also found that the choroid plexus
possesses an enormous capacity to absorb beta-amyloids. The findings
support the theory that the choroid plexus may possess a special enzyme
that breaks beta-amyloids into smaller pieces, making it possible to
soak up large quantities of the protein.
"The tissue must have a unique mechanism that is
different from brain cells, something that enables it to chop up these
beta-amyloids," Zheng said.
Future research may focus on efforts to isolate
possible enzymes.
Zheng said the findings suggest that aging may
degrade the organ's performance, and it is also possible that lead
poisoning might increase the risk of Alzheimer's disease by damaging the
choroid plexus and reducing its ability to filter beta-amyloids.
Alzheimers disease affects more than 4 million
Americans, and the findings might help researchers develop new methods
to treat the disease. The research paper was published last November in
the journal Experimental Biology and Medicine.
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