Increased neuronal apoptosis has been widely demonstrated in classic neurodegenerative disorders, often via grafted or β-amyloid-induced-neurodegeneration in AD models [44,64] through 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine-(MPTP)-induced-neurodegeneration in PD models [65], through 3-nitropropionic acid (NP3)- or malonate-induced neurodegeneration in HD models [46,66] and through superoxide dismutase-1 (SOD1)-mutations in ALS models [47,67]. The gene discussed is SOD1; the disease is Alzheimer disease.