Parkinson's gene mutation explored
NEW YORK, Nov 04, 1998 (Reuters Health) -- Researchers have discovered
how a gene mutation associated with an early-onset
familial form of Parkinson's disease kills nerve cells in the brain.
Apparently, the abnormal protein causes other proteins to
aggregate, and these deposits kill nerve cells, according to the report
in the November issue of Nature Medicine.
The finding may lead to new treatments for Parkinson's disease, and may
also lead to new treatments for Alzheimer's disease,
one of the researchers told Reuters Health.
The mutation in question is in the gene that produces alpha-synuclein, a
compound found in Lewy bodies -- fibrous deposits
found in the dopamine-producing nerve cells of the brains of patients
with Parkinson's disease.
Parkinson's disease -- a progressive illness characterized by tremor,
difficulty walking and movement abnormalities -- is caused
by the degeneration of these nerve cells.
In laboratory studies, Dr. Peter T. Lansbury of Harvard Medical School,
Boston, Massachusetts, and colleagues found that
when a mutant type of alpha-synuclein, A53T, was concentrated and
encouraged to aggregate, it formed fibrils characteristic of
Lewy bodies more quickly than did the normal alpha-synuclein or another
mutant form, A30P.
The investigators detected another characteristic of Lewy bodies,
spherical assemblies, in A30P as well as A53T. They
speculate that such spherical assemblies ``are intermediates in fibril
formation.''
``What we should be able to do is make a drug and target it toward
inhibiting fibril formation,'' said Lansbury in an interview
with Reuters Health. ``If you could delay the age of onset of
Parkinson's disease by approximately 20 years, that would be a de
facto cure.''
Early-onset Parkinson's disease is similar to early-onset Alzheimer's
disease in that genetic mutations seem to accelerate the
development of the disease.
``Significantly, the prevalence of Alzheimer's disease in the
Parkinson's disease population, and vice versa, is far greater than
would be expected by chance,'' Lansbury explained. This observation, he
said, is ``consistent with the notion that both diseases
arise from similar processes and could be treated by similar
strategies.''
SOURCE: Nature Medicine 1998;4:1318-1320.
--
Judith Richards, London, Ontario, Canada
<[log in to unmask]>
^^^
\ /
\ | / Today’s Research
\\ | // ...Tomorrow’s Cure
\ | /
\|/
```````
