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Alzheimer's
Linked To Proteins
Associated With Aging
LOS
ANGELES (Reuters) - The irreversible brain disorder Alzheimer's
Disease may be caused by inflammatory processes associated with
aging and not--as generally believed--by plaque-like deposits
in the brain, researchers said on Friday.
The scientists
from the University of Southern California in Los Angeles and
Northwestern University in Evanston, Ill., said their findings
could open new avenues of exploring ways to treat or even cure
the disease.
Their findings,
published this week in the journal ``Trends in Neurosciences,''
still lays the blame for Alzheimer's on a molecule called amyloid
beta, but traces the basic cause of the disease to the formation
of toxic proteins rather than the build-up of plaque and tangles
inside nerve cells in the brain.
Amyloid plaques
are hard waxy deposits consisting of protein and polysaccharides
that result from the degeneration of tissue.
Alzheimer's,
which affects about four million Americans, starts with memory
loss and progresses to profound dementia and death. There is no
cure, although there are a few drugs that provide temporary relief
for some symptoms of the disease.
``We were
able to identify in laboratory test tubes a new kind of toxic
activity that is implicated as a root cause of Alzheimer's,''
Dr. Caleb Finch, director of the Neurogerontology Division at
the USC Andrus Center's Gerontology Research Institute, told Reuters
in an interview.
The researchers
discovered a novel form of wadded-up amyloid called ``amyloid
b-derived diffusible ligands''--ADDLs or ''addles'' for short--that
form in the presence of certain inflammatory proteins in the brain.
They have chemical and toxicological properties quite different
from either single beta-amyloid molecules or clumps of the molecules
called fibrils.
For nearly
two decades, Alzheimer's research has focused on ways to prevent
the formation of fibrils, which coalesce into even larger deposits
in the brain known as plaques, which have been shown to kill nerve
cells in the brain.
``ADDLs come
before fibrils,'' Finch said. ADDLs AFFECT BRAIN CELLS THAT ATROPHY
Also unlike
fibrils, ADDLs are highly selective in their toxicity. The researchers
found that ADDLs affect only the same types of brain cells that
atrophy in Alzheimer's patients. Fibrils, however, kill a broad
range of nerve cells--even destroying cell types that remain healthy
right up until patients die.
ADDLs are
also soluble, which means they are free to diffuse everywhere
in the brain. Fibrils are confined to the specific locations where
they first form and these locations correspond poorly with the
brain areas that wither as Alzheimer's progresses, according to
the researchers.
``These soluble
forms may be the answer to the riddle as to why fibrils don't
correlate with areas of that brain that are damaged by Alzheimer's,''
Finch said.
The researchers
also suggest that ADDLs begin to interfere with the brain's basic
mechanism of long-term memory well before they reach levels high
enough to kill brain cells.
``ADDLs result
from certain types of inflammatory proteins. If we can interfere
with this process, we can affect the progress of the disease,''
Finch said.
Given this,
the concept of developing an antibody-based vaccine to treat or
even prevent Alzheimer's makes sense, the researcher said. ``A
couple of years ago, people thought the vaccination approach was
the craziest idea. But if the real target is the soluble molecule
and not the fibrils, it is a consistent approach,'' Finch said.
Reference
Source 89
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