Figure 2. Infection-induced inflammation as a potential trigger of Alzheimer’s disease pathology. Infection or inflammation activates microglial cells, triggering the release of pro-inflammatory cytokines. In sequence, the pro-inflammatory cytokines promote the formation of interferon-induced transmembrane protein 3 (IFITM3) in neurons and astrocytes, which binds to γ-secretase, increasing its activity and upregulating Aβ production. Released Aβ peptides have antimicrobial effects, preventing pathogen development by forming amyloid plaques. Brain Aβ deposition exacerbates the cerebral inflammatory response, accelerating AD pathological cascades. Aβ = amyloid-β; AD = Alzheimer’s disease.