Gene Research Suggests How Parkinson's
Might Arise
By Amy Norton
NEW YORK, June 30, 2001 (Reuters Health) - Research into the genetic
roots of inherited forms of Parkinson's disease (news - web sites) may
have opened the door to understanding how all forms of the degenerative
disorder arise. An international team of scientists has found that two
proteins linked to inherited Parkinson's interact in healthy
brains--suggesting that a misstep in this interaction may be involved in
all cases of Parkinson's.
If future research bears out this concept, it may be possible to design
a drug that specifically targets the protein-gone-wrong, study co-author
Dr. Michael G. Schlossmacher of Harvard Medical School (news - web
sites) in Boston, Massachusetts, said in an interview.
He and his colleagues report their findings in the June 28th issue of
Sciencexpress, the online edition of the journal Science.
Not long ago, researchers believed Parkinson's disease had no genetic
component. But in recent years, scientists have identified gene
mutations linked to inherited Parkinson's--rare forms of the disease
that typically strike relatively young people. Parkinson's usually
affects people older than 50, causing tremors, muscle rigidity, and
balance and coordination problems that worsen over time.
All cases of Parkinson's are marked by a loss of certain brain cells
that help control movement. All patients also have an accumulation of a
protein called alpha-synuclein in their brains, according to
Schlossmacher. In fact, scientists recently discovered that a mutation
in the gene for alpha-synuclein is responsible for one of the inherited
forms of the disease.
Mutations in another gene, called parkin, have been implicated in
causing a second inherited type of Parkinson's.
To see what role the parkin and alpha-synuclein proteins might play in
common forms of Parkinson's, Schlossmacher and his colleagues
examined both healthy brain tissue and tissue from patients with
Parkinson's due to a parkin mutation. They found that parkin and
alpha-synuclein interact in healthy brains, with parkin helping to clear
alpha-synuclein from cells. In brains affected by the inherited form of
Parkinson's, however, parkin could not do its job, causing
alpha-synuclein to accumulate.
Because parkin and alpha-synuclein have a healthy working relationship
in normal brains, Schlossmacher and his colleagues hypothesize that an
abnormality in this interaction may be at the root of Parkinson's. Even
though most patients do not have an overt mutation in these genes,
Schlossmacher explained, they may have a ``subtle abnormal tuning'' in
the interaction between the two proteins that allows alpha-synuclein to
accumulate in the brain.
If alpha-synuclein build-up is the trigger for the loss of nerve cells
in Parkinson's, it may be possible to design drugs that bring down
levels of alpha-synuclein, Schlossmacher said. However, he stressed,
this scenario remains about 10 years away.
This study, he said, is a ``first and significant step'' in
understanding how Parkinson's disease begins.
SOURCE: Sciencexpress 2001;10.1126.
Copyright © 2001 Reuters Limited.
Copyright © 2001 Yahoo! Inc.
--
Judith Richards, London, Ontario, Canada
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