Authors: Lauren Pulling
Researchers at the Buck Institute (Novato, CA, USA) have demonstrated that the same mechanism that contributes to cell death in familial Parkinson’s disease (PD) is also involved in the sporadic form of the disease. These findings indicate that the mechanism could be targeted in future drug development research.
The new study, published in Neurobiology of Disease, focused on parkin, a protein involved in the destruction of damaged proteins and mitochondria via lysosomal autophagy. Previous research has linked the mutated parkin protein to a rare familial form of PD, leading to an accumulation of damaged proteins and mitochondria in dopamine-producing neurons.