Oxidative reductions in parkin solubility in a mouse model of sporadic PD coincides with increased PARIS levels and reduced PGC-1α signaling.

Restoration of PGC-1α abrogates losses in mitochondrial function and degeneration of nigral dopaminergic neurons associated with this model.

These findings suggest PGC-1α as therapeutic target for the treatment of not only familial PD, but also sporadic forms of the disorder.