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EMBARGOED FOR RELEASE: 12 JANUARY 2001  AT 17:00 ET US
Contact: Emily Huang
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516-367-6834
Cold Spring Harbor Laboratory

Stalking a Parkinson’s protein
In struggling to find the cause of Parkinson’s disease, scientists have
recently homed in on a mysterious protein called alpha-synuclein.
Researchers suspect abnormal activity of alpha-synuclein is involved
not only in inherited, but also in non-inherited forms of the devastating
disease.  In the January issue of Genome Research, Robert Nussbaum
and colleagues from the National Institutes of Health use information on
human and mouse genomes to uncover a novel genetic element that
controls alpha-synuclein activity.
Mutations in the alpha-synuclein gene cause some cases of inherited
Parkinson’s.  In addition, deposits of alpha-synuclein protein are found
in Lewy bodies, the protein aggregates found in the brains of
Parkinson’s patients.  For these reasons, scientists suspect that even
common, non-inherited forms of Parkinson's may involve abnormal gene
activity or damage to the protein itself.  To pinpoint factors that
influence alpha-synuclein function, Nussbaum and colleagues looked
for DNA sequences in the human genome that can control alpha-
synuclein gene activity.  They compared the region of the human
genome containing alpha-synuclein to its equivalent region in mouse,
reasoning that sequences common to both species represent important
genetic elements.  The comparison identified several potential control
elements for alpha-synuclein.  Nussbaum and colleagues found that
removing one such element (NACP-REP1) greatly diminishes gene
activity, indicating the identified elements may indeed be important for
the normal (and abnormal) functioning of this Parkinson's-related protein.

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Contact (author):
Robert Nussbaum
National Human Genome Research Institute
National Institutes of Health
Bethesda, MD 20892
USA
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http://www.eurekalert.org/releases/cshl-spp010301.html

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