Rosa L.A. de Vries

TL;DR: It is suggested that Parkin, together with PINK1, modulates mitochondrial trafficking, especially to the perinuclear region, a subcellular area associated with autophagy, which may alter mitochondrial turnover which, in turn, may cause the accumulation of defective mitochondria and, ultimately, neurodegeneration in Parkinson's disease.

TL;DR: It is proposed that inefficient engulfment of cytosolic components by autophagosomes is responsible for their slower turnover, functional decay and accumulation inside HD cells.

TL;DR: Three putative models whereby PINK1 and Parkin may affect mitophagy are presented; 1) by shifting the balance between fusion and fission of the mitochondrial network, 2) by modulating mitochondrial motility and 3) by directly recruiting the autophagic machinery to damaged mitochondria.

TL;DR: It is suggested that Parkin and PINK1 modulate mitochondrial trafficking to the perinuclear region, a subcellular area associated with autophagy, and this process may be altered, inducing accumulation of defective mitochondria and, ultimately, causing neurodegeneration in Parkinson disease.

TL;DR: The question of mitochondrial biology as a primary mechanism in PD pathogenesis is revisited, this time from an angle of perturbation in mitochondrial dynamics and not from the angle of a deficit in respiration.