Massive release of presynaptic glutamate caused by cerebrovascular ischemia causes a consequent increase in NMDA post-synaptic receptors (Szydlowska and Tymianski, 2010; Li Y. et al., 2016) and finally loss-of-function mutations in the parkin gene (hereditary PD PARK2 gene) inducing a proliferation of glutamate post-synaptic receptors, thus causing a sensitization to excitotoxicity in the substantia nigra in PD (Helton et al., 2008). Here, PRKN is linked to Parkinson disease.