Parkin is a protein encoded by the PARK2 gene in humans. Mutations in PARK2 are most commonly linked to both sporadic and familial forms of PD; they diminish the cell's ability to recycle its internal garbage.
PD is characterized by the accumulation of damaged proteins and mitochondria in the area of the brain where the neurotransmitter dopamine is produced.
Rapamycin, an immunosuppressant and FDA-approved drug that extends lifespan in several species, prevented PD symptoms from occurring in middle-aged mice who had a human mutation in the PARK2 gene.
Scientists found that rapamycin not only boosted the mutated protein's ability to label cellular garbage, but also affected the process of recycling the garbage itself via up-regulation of a protein known as TFEB which increased the degradation and purging of both damaged proteins and mitochondria via a process known as lysosomal autophagy.
Apart from rapamycin's effects, research team also discovered that parkin is involved in mitochondrial biogenesis - via up-regulation of PGC1alpha, a protein which drives increased mitochondrial synthesis.