In addition, PrP has been shown to be part of a receptor complex for soluble neurotoxic Alzheimer’s disease-associated amyloid-beta peptides [15, 16] and the presence or absence of PrP changes NSC self-renewal in response to amyloid-beta peptides [17], thereby suggesting that a putative neurogenic function of PrP may become corrupted during neurodegenerative disease. The gene discussed is PRNP; the disease is early-onset autosomal dominant Alzheimer disease.