While genetic mutations, such as those affecting the amyloid precursor protein or presenilin in Alzheimer’s disease (AD) and parkin or UCHL1 in Parkinson’s disease, are known to trigger abnormal protein folding and aggregation, these mutations account for only ax subset of cases, indicating the involvement of additional factors in the accumulation of misfolded proteins such as amyloid-β (Wyss-Coray and Mucke, 2002). The gene discussed is PRKN; the disease is Alzheimer disease.