The major pathogenic concept in the field of AD research is the amyloid cascade hypothesis, which states that the sequence of pathological events leading to AD is characterized by the accumulation of Aβ peptides resulting from the aberrant processing of amyloid precursor protein (APP) and dysfunctional Aβ clearance, followed by the deposition of NFTs and the onset of synaptic dysfunction and neuronal loss. Here, APP is linked to Alzheimer disease.