Genetic, biochemical, and transgenic mice studies of mutations that cause familial forms of AD (FAD) have identified the Aß peptide as central to AD pathogenesis, with Apolipoprotein E (ApoE), Tau, and microtubules being required for Aß to oligomerize/polymerize and induce synaptic loss, neurodegeneration, and dementia [4]–[7]. Here, APOE is linked to familial Alzheimer disease.