The relevance of defective mitophagy to the pathogenesis of AD is further supported by the amelioration of cognitive dysfunction and Aβ proteinopathy in APP/PS1 mice following the restoration of neuronal and microglial mitophagy via supplementation with nicotinamide adenine dinucleotide (NAD+) precursors, urolithin A, and actinonin [160]. The gene discussed is APP; the disease is Alzheimer disease.