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Increased levels of the
enzyme neprilysin may help clear up a protein in the brain called beta amyloid
that forms the plaques that are a hallmark of Alzheimer's disease, according to
a study reported in the March 15 issue of the Journal of Neuroscience.
The study
suggests closer evaluation of the potential for neprilysin therapy,
according to the researchers.
Previous
research has shown that neprilysin is reduced in areas vulnerable to plaque formation
and that mice without the neprilysin gene have increased levels of beta amyloid
in the brain. Test tube studies have also shown that neprilysin could help stop
the production of beta amyloid.
The
study is the first to report that increased levels of neprilysin decrease the
deposition of amyloid in animals. Researchers injected
gene vectors carrying human neprilysin into the amyloid-containing brains of mice.
The gene transfer was concentrated in two areas of the brain where plaque formation
occurs in humans.
At
the end of the treatment, the researchers reported, introduction of the neprilysin
appeared to increase degradation or reduce the growth of already existing plaques.
Some plaque formations were reduced to less than half of those found in comparable,
non-treated areas.
"If
we find a way to shift the balance between amyloid production, clearance and degradation,
I believe we can find a way to interfere with the processes involved in Alzheimer's
disease," said lead researcher Fred H. Gage, of the Salk Institute. "Further
study will help define the role of neprilysin in regulating amyloid and possibly
treating or preventing Alzheimer's disease."
Brad
Wise, of the National Institute of Aging, said most studies have focused on blocking
the production of proteins that form Alzheimer's disease plaques. He said this
study is different in suggesting that plaques might be cleared if they do build
up in the brain. "These are very new ways of addressing the problem,"
he said. Other
sources: Salk Center for Biological Studies |