Abstract
Along with the impairment of mitochondrial respiration both mitochondrial fission/fusion and mitophagy have been shown to be altered in Parkinson's disease (PD). In both genetic and toxin-induced models of PD an imbalance in mitochondrial morphology is evident, as its correction through modulation of the fission/fusion proteins has been shown to be protective. From the study of the PD-associated genes, namely PINK1 and Parkin, compromised mitochondrial clearance through mitophagy has been associated with the disease etiopathogenesis. Here we propose that an interplay between defective mitochondrial morphology and clearance arises as a crucial player in sentencing neuronal fate in PD.
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