Parkin is inactivated in the nigrostriatum of post-mortem sporadic PD patients (Ko et al, 2010; Lonskaya et al, 2012a), and decreased parkin solubility is associated with defects in autophagic clearance of β-amyloid and p-Tau in post-mortem Alzheimer's disease (AD) brains (Lonskaya et al, 2012c). This evidence concerns the gene PRKN and Alzheimer disease.