Neuropathologically, AD is characterized by extracellular senile amyloid plaques and intracellular neurofibrillary tangles (NFTs), along with other molecular changes such as neuroinflammation, brain atrophy, synaptic pathologies, and cerebral amyloid angiopathy [2, 3].More than 90% of patients with AD are sporadic cases and show dementia in their mid-60 s and later, and less than 10% of AD cases have the early-onset form of diseases that can be caused by a single genetic mutation in the APP genes (Presenilin 1, Presenilin 2, and Amyloid precursor protein APP) [4]. Here, PSEN1 is linked to Alzheimer disease.