A short circuit in how cells digest and recycle damaged proteins
could trigger the symptoms of Parkinson's, U.S. researchers said in
a finding that could lead to new tretments for the incurable
disease.
The team focused on a process called autophagy in which cells
digest and recycle damaged molecules, including proteins, that
develop as cells grow older. This system essentially renews cells
to keep them functioning properly.
This mechanism is also important for nerve cells in the brain
where defective proteins can kill cells and cause the debilitating
symptoms of Parkinson's, such as tremors, said Ana Maria Cuervo, a
cell biologist who led the study.
"We have found in Parkinson's there are problems in removing
abnormal proteins," said Cuervo of the Albert Einstein College of
Medicine of Yeshiva University.
The finding could lead to drugs to treat the symptoms but not
cure the disease, which affects more than a million patients in the
United States alone and is marked by the death of brain cells that
produce dopamine. Dopamine is a neurotransmitter, or
message-carrying chemical, associated with movement.
Cuervo had previously shown how mutant forms of a protein called
alpha-synuclein -- found in a tiny percentage of Parkinson's
patients -- blocked the breakdown of substances and prevented cells
from clearing damaged proteins.
In the study in The Journal of Clinical Investigation on
Wednesday, the team showed how in the majority of patients dopamine
modifies normal proteins to act like the mutated ones to trigger
tremors and other symptoms.
Cuervo said a drug to fix the breakdown in Parkinson's patients
was years away because it would take researchers time to understand
fully how the process worked.
(Xinhua News Agency January 3, 2008)