AD has clinical features of progressive memory decline and cognitive disturbance, and neuropathological hallmarks amyloid plaques and neurofibrillary tangles in the postmortem brain [5, 6]. Amyloid plaques are extracellular aggregates of β-amyloid (Aβ), whereas neurofibrillary tangles consist of cytoplasmic filaments of hyper-phosphorylated tau (p-tau) proteins. Aβ is produced from APP through the sequential proteolytic action of β- and γ-secretases. PSEN1 is considered to be critical for the γ-secretase complex, acting as the catalytic component of this proteolytic enzyme [7].
