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Gene therapy utilises anti-Alzheimer’s molecule
Journal of Neuroscience
March 25, 2003
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| Neprilysin gene lowers levels of beta-amyloid |
In gene
therapy research using mice, delivery of the neprilysin gene was found to
lower levels of the protein beta-amyloid, which constitutes the plaques
seen in people who have died of Alzheimer’s disease.
The protein fell almost 50 per cent when neprilysin was transferred, using
a modified version of the HIV virus, to neurons of transgenic mice, said
the researchers in the Journal of Neuroscience.
The gene therapy enables the scientists to show for the first time that
neprilysin inhibits beta-amyloid accumulation in animals.
“This study supports a role for neprilysin in the regulation of beta-amyloid,”
says study author Dr Inder Verma from San Diego’s Salk Institute. “It
highlights the potential of using viral vectors for a gene therapy
approach to treat, or perhaps prevent, Alzheimer’s disease.”
Dr Verma says the findings are particularly significant in showing that
neprilysin is not a drug but a molecule that “naturally” controls
beta-amyloid.
While usually controlled by neprilysin, beta-amyloid is known to exist in
normal brains at far lower levels than seen in people with Alzheimer’s
disease. Although its precise role in brain function remains in question,
there is speculation that it plays an important role in transporting
sub-cellular structures and molecules from one end of a nerve cell to
another.
The researchers are currently conducting experiments to assess whether
neprilysin gene therapy results in cognitive improvements in mice and how
the therapy works at different stages of the disease.
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