PINK1 and Alzheimer disease: Reduced mitophagy is likely a “culprit”, but not a “bystander” of AD, as pharmacological (NAD+ precursors, urolithin A, actinonin, kaempferol, rhapontigenin [11,12]) and genetic (e.g., overexpression of PINK1 [16]) upregulation of mitophagy restore mitochondrial homeostasis, abrogated AD-related pathology, and reduced memory loss in animal models of AD.