“…2,3 The conventional view of AD, according to the "amyloid hypothesis", is that β-amyloid (Aβ), the product of proteolytic cleavage of the large transmembrane Aβ precursor protein (AβPP), occupies a central place in the pathology of disease. 4,5 AD is characterized by increased load of Aβ in the brain, especially the peptides 42 amino acids in length, leading to accumulation of Aβ, amyloid plaques, neurofibrillary tangles, synaptic failure, neuronal cell death, excitotoxicity, inflammation, mitochondrial dysfunction, and oxidative stress. 3 In contrast, there is growing evidence that mitochondrial damage and oxidative stress lead to activation of the Aβ cascade.…”