Prominent pathophysiological characteristics of Alzheimer’s disease include plaque and neurofibrillary tangle (NFT) formation. Plaques are formed by abnormal deposits of amyloid β protein (Aβ) in specific brain regions (Benilova, Karran, & De Strooper, 2012; Hardy & Selkoe, 2002). Aβ is derived by cleavage of amyloid precursor protein (APP) by β- or γ-secretase (e.g., PSEN-1). The long form of Aβ (Aβ42) is critical for plaque formation and is elevated in relation to the short Aβ40 form in the brain of AD patients. Neurofibrillary tangles consist of hyperphosphorylated microtubule-associated protein Tau (pTau) (Ballatore, Lee, & Trojanowski, 2007). Numerous studies have linked the expression of plaques, tangles, and the progression of cognitive decline in Alzheimer’s disease with Aβ and Tau expression (Buckley et al., 2016).
