The most widely accepted hypothesis suggests that sCJD results from a random misfolding event in PrPC or a somatic mutation in the PRNP gene [44], analogous to spontaneous mutations observed in other neurodegenerative diseases, such as Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis (ALS). The gene discussed is PRNP; the disease is early-onset autosomal dominant Alzheimer disease.