Abstract
The Roles of PINK1 and Parkin in Parkinson's Disease
Highlights
Research into the causes of both sporadic and familial Parkinson’s disease have led to the idea that a key risk factor might be mitochondrial dysfunction
Recent work showed that the protein Parkin, which is mutated in some forms of familial Parkinson’s disease, is recruited from the cytoplasm to damaged mitochondria and that this leads to the breakdown of the mitochondria by processes acting within the cell
In a new study in this issue of PLoS Biology, Youle and colleagues address the question of how Parkin recognises damaged mitochondria, and they find a crucial role for PINK1
Summary
Research into the causes of both sporadic and familial Parkinson’s disease have led to the idea that a key risk factor might be mitochondrial dysfunction. The neurons of the substantia nigra, which are lost in Parkinson’s disease, seem to be especially vulnerable to the effects of mitochondrial damage. Recent work showed that the protein Parkin, which is mutated in some forms of familial Parkinson’s disease, is recruited from the cytoplasm to damaged mitochondria and that this leads to the breakdown of the mitochondria by processes acting within the cell (autophagy).
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