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Researchers have found that a protein active during
fetal brain development, called REST, switches back on later in life to protect
aging neurons from various stresses, including the toxic effects of abnormal
proteins. But in those with Alzheimer's and mild cognitive impairment, the
protein -- RE1-Silencing Transcription factor -- is absent from key brain
regions.
"Our work raises the possibility that the
abnormal protein aggregates associated with Alzheimer's and other
neurodegenerative diseases may not be sufficient to cause dementia; you may
also need a failure of the brain's stress response system," said Bruce
Yankner, Harvard Medical School professor of genetics and leader of
the study, in a release.
"If true, this opens up a new area in terms of
treatment possibilities for the more than 5 million Americans currently living
with Alzheimer's disease," said Yankner, who in the 1990s was the first to
demonstrate the toxic effects of amyloid beta, the hallmark abnormal protein in
Alzheimer's.
The research, published in the journal Nature, underscores a different way of
looking at neurodegenerative diseases. Instead of focusing on the negative
changes that cause disease, researchers examined trouble spots in the brain's
ability to protect itself over time.
Yankner said the study suggests a person may be able
to resist the toxic effects of Alzheimer's if REST levels remain high.
"If we could activate this stress-resistance
gene network with drugs, it might be possible to intervene in the disease quite
early," he added in a release. "Since Alzheimer's strikes late in
life, delaying the onset of disease by just a few years could have a very
substantial impact."
In separate, but related research, a new study out
of Temple University's School of Medicine this week suggests chronic sleep
disturbances could speed up the onset of dementia and Alzheimer's
disease in older adults.
Yet another recent study found that a simple blood test could detect with 90 percent
accuracy whether or not a healthy person will develop Alzheimer's.
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