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Parkinson's disease stopped in aimal model... /
Other ArticlesParkinson's disease stopped in animal model Molecular 'tweezers' break up toxic aggregations of proteins
Millions of people suffer from Parkinson's disease, a disorder
of the nervous system that affects movement and
worsens over time. As the world's population ages,
it's estimated that the number of people with the
disease will rise sharply. Yet despite several
effective therapies that treat Parkinson's symptoms,
nothing slows its progression.
While it's not known what exactly causes the
disease, evidence points to one particular culprit:
a protein called α-synuclein. The protein, which has
been found to be common to all patients with
Parkinson's, is thought to be a pathway to the
disease when it binds together in "clumps," or
aggregates, and becomes toxic, killing the brain's
neurons.
Now, scientists at UCLA have found a way to prevent
these clumps from forming, prevent their toxicity
and even break up existing aggregates.
UCLA professor of neurology Jeff Bronstein and UCLA
associate professor of neurology Gal Bitan, along
with their colleagues, report the development of a
novel compound known as a "molecular tweezer," which
in a living animal model blocked α-synuclein
aggregates from forming, stopped the aggregates'
toxicity and, further, reversed aggregates in the
brain that had already formed. And the tweezers
accomplished this without interfering with normal
brain function.
The research appears in the current online edition
of the journal Neurotherapeutics.
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