PRKN and Parkinson disease: The results of the above studies thus support the hypothesis that altered protein expression and/or neurotoxic events may lead to the intracellular mis-processing and aggregation of GPR37 receptor molecules, a condition which is strongly enhanced in the absence of efficient, parkin-mediated ubiquitination/proteasomal degradation, and constitutes a specific causative factor in the PD-associated, selective degeneration of substantia nigra neurons [11,12,18,19,20].