Pathological or preventative? Amyloid-β as an effector of innate immunity

Amyloid-β (Aβ)-mediated inflammation, neurotoxicity, and plaque formation in the brain have long been regarded as pathological hallmarks of Alzheimer’s disease. However, emerging evidence indicates that Aβ also serves a normal physiological role in the innate immune defense against infectious agents. A growing body of literature supports the hypothesis that Aβ is produced in response to infection and is an antimicrobial peptide-like molecule capable of inhibiting microbial growth through mechanisms such as membrane disruption and microbial entrapment. Additionally, evidence positions Aβ as an innate immune effector that can induce pro-inflammatory signals during infection. In this minireview, we discuss the clinical, in vivo , and in vitro evidence supporting the antimicrobial and innate immune effector roles of Aβ in host defense. Collectively, these findings support a broader functional role for Aβ beyond its established association with Alzheimer’s disease pathology.