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Einstein Researchers Discover Important Clue To The Cause Of Parkinson's Disease
A glitch in the mechanism by which cells recycle damaged components may trigger
Parkinson's disease, according to a study by scientists at the Albert Einstein College of Medicine of
Yeshiva University. The research, which appears in the January 2 advance online issue of The Journal
of Clinical Investigation, could lead to new strategies for treating Parkinson's and other
neurodegenerative diseases.
All cells depend on a surveillance system known as autophagy (which literally means "self
eating") to digest and recycle the damaged molecules that arise as cells age. In autophagy, defective
proteins and other molecules are transported to membrane-bound sacs called lysosomes. After attaching
to the lysosomal membrane, the molecules enter the lysosome, where they are digested by enzymes.
This cleanup process may be particularly important for nerve cells, which generate defective molecules
more rapidly than most other types of cells. When autophagy is impaired, toxic compounds can
accumulate and cause cell death.
"It is widely suspected that accumulation of a particular protein, known as alpha-synuclein,
within affected nerve cells of Parkinson's disease patients contributes to the death of these cells," says
Dr. Ana Maria Cuervo, senior author of the article and associate professor of anatomy & structural biology at Einstein.
Dr. Cuervo previously showed that mutant forms of alpha-synuclein - found in
the five to 10 percent of patients who have familial Parkinson's disease - are poorly
digested via autophagy and also block the breakdown of other substances. While these
alpha-synuclein mutations are rare, other modifications of alpha-synuclein -
phosphorylated and oxidized forms, for example - can be found in the brains of all
Parkinson's disease patients.
In this study, Dr. Cuervo and her colleagues looked at how several different
modified forms of alpha-synuclein affected autophagy in vitro and in tissue culture. One
particular modification of alpha-synuclein was found to interfere with autophagy: the
compound created by the interaction of alpha-synuclein with dopamine, the main
neurotransmitter produced by the nerve cells damaged in Parkinson's disease.
"Alpha-synuclein molecules modified by dopamine bound tightly to the
lysosomal membrane, but they got stuck there and weren't effectively transported into the
lysosome," says Dr. Cuervo. As a result, the alpha-synuclein molecules altered by
dopamine were poorly degraded, and the presence of these molecules on the lysosomal
membranes interfered with autophagic digestion of other compounds as well.
"We propose that inhibition of autophagy caused by dopamine's alteration of
alpha-synuclein could explain the selective death of dopamine-producing nerve cells in
Parkinson's disease," says Dr. Cuervo, who notes that interference with autophagy has
also been implicated in other neurodegenerative diseases including Alzheimer's.
"By devising strategies for boosting autophagy in nerve cells or suppressing the
chemical reactions that interfere with the autophagy - by lowering alpha synuclein
expression, for example--we may be able to treat patients afflicted with these conditions,"
she says.
Other Einstein scientists involved in the research were lead author Marta
Martinez-Vicente, Susmita Kaushik, Ashish Massey and Dr. Antonia Follenzi. This work
also included collaborators from Columbia University, the University of Pennsylvania,
and Harvard Medical School.
http://www.aecom.yu.edu
Einstein Cercetatori Descoperiþi importante idee despre cauza boala Parkinson - Einstein Researchers Discover Important Clue To The Cause Of Parkinson's Disease - articole medicale engleza - startsanatate