This cascade has the potential to trigger AD pathogenesis through dysregulation of Amyloid Precursor Protein (APP) processing and intracellular Aβ accumulation, activation of Activator Protein 1 (AP-1), a transcription factor that regulates inflammatory genes expression, and hyperphosphorylation of tau protein, and aggregation of neurofibrillary tangles (Viana, Nunes, & Rodrigues, 2012). Here, APP is linked to Alzheimer disease.