Both SAD and FAD patients share common clinical and neuropathological features including loss of neurons, intracellular neurofibrillary tangles (aggregates of hyperphosphorylated tau protein), and extracellular senile plaques, composed of β-amyloid (Aβ) deposits, which are derived from the proteolytic processing of the amyloid precursor protein (APP) [3]. Here, APP is linked to familial Alzheimer disease.