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Yea, but thanks for thinking of me.  I'm linked to an information exchange
network for PD.  Listed below.
It's somewhat depressing; you read personal stories about people with PD and
their caregiver's struggles.
Guy


-----Original Message-----
From: Parkinson's Information Exchange Network
[mailto:[log in to unmask]]On Behalf Of rayilynlee
Sent: Wednesday, January 02, 2008 5:17 PM
To: [log in to unmask]
Subject: possible PD cause

A glitch in the way cells clear damaged proteins could be the trigger for
the symptoms of Parkinson's disease, researchers said in a finding that
could lead to new treatments for the incurable condition.
The U.S. 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 potentially 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. "What we
have found is dopamine modifies alpha-synuclein that really resembles the
mutation," Cuervo said. "That is why they have the same symptoms."
Problems in this process have also been linked with other neurodegenerative
conditions such as Alzheimer's and Huntington's disease, though the specific
mechanisms that cause problems in those conditions are different, she said.
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. "This is not something that is going to lead to a treatment
tomorrow," she said. "The hope is within five years we can get companies to
find a drug able to activate this system."

Rayilyn Brown
Board Member AZNPF
Arizona Chapter National Parkinson's Foundation
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