October 7, 2011
Study First To Link Mitochondrial Dysfunction And Alpha-Synuclein Multiplication In Human Fibroblasts
Published in the Journal of Parkinson's Disease
A new study in the Journal of Parkinson's Disease shows for the first time the effects of Î±-Synuclein (Î±-syn) gene multiplication on mitochondrial function and susceptibility to oxidative stress in human tissue. Mitochondrial dysfunction has been frequently implicated in the neurodegenerative process that underlies Parkinson's disease, but the basis for this has not been fully understood.
Mitochondrial function and cellular damage were partially rescued after siRNA knockdown of Î±-synuclein in fibroblasts after paraquat treatment. "We observed a significant increase in membrane potential and cellular ATP synthesis as well as a decrease in LDH release, supporting the hypothesis that Î±-synuclein expression levels are directly related to mitochondrial dysfunction," said Dr. SchÃ¼le.
According to Dr. William Langston, the Scientific Director and CEO of The Parkinson's Institute, and a co-author on the paper, these results are particularly exciting because they directly link a-syn over-expression and mitochondrial dysfunction in tissue from a parkinsonian patient. "One of the keys to unraveling this incurable and progressive disease is to solve the relationship between a-syn and mitochondrial dysfunction. In these results, we may have the first such link in human tissue," Langston said.
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