Supporting experimental evidence is provided by: (a) reduced Aβp production in cultured cells when cholesteryl-ester levels were reduced by inhibiting Acyl-CoA cholesterol acyltransferase (ACAT) [101]; (b) reduced amyloid and tau deposition, by enhancing autophagy with ACAT1 inhibition, in cell culture and whole animal mouse models of AD [102,103,104]; and (c) cholesterol depletion decreased Aβp production in rat hippocampal neurons [105]. This evidence concerns the gene MAPT and Alzheimer disease.