Our understanding of AD pathobiology has been greatly improved over the past two decades; however, no disease-modifying treatment is available for individuals diagnosed with AD.15 Age is the primary risk factor for AD and an accumulation of misfolded/aggregated proteins such as senile plaques and neurofibrillary tangles (NFTs) cause pathological changes in brain.16 The amyloid β peptides (Aβ) are natural cleavage products of the Aβ precursor protein (APP) by β- and γ-secretases and aggregate to form oligomers and fibrils. This evidence concerns the gene PPIB and Alzheimer disease.