A partial deficiency of Drp1 by using a genetic approach that involved crossing heterozygote knockout Drp1(+/−) mice with transgenic APP mice (Tg2576 strain or by crossing Drp1+/− mice with transgenic Tau mice (P301L line)) and creating double mutants (APP × Drp1+/−) or (Tau × Drp1+/−) mice protected against Aβ-induced mitochondrial and synaptic toxicities in AD neurons [87,88]. The gene discussed is APP; the disease is Alzheimer disease.