A Neuroinflammatory View of Alzheimer’s Disease

Numerous perspectives have been offered concerning the evolution of Alzheimer’s, here we focus upon current and emerging theories of how the inflammatory immune system might be involved in the disease. In this regard, β-amyloid senile plaques may not only provoke excessive harmful inflammatory reactions, but might also serve as a clinical target for immunotherapeutic interventions. However, the role for β-amyloid is far from clear and other pathological processes are important. We also focus upon possible environmental triggers for disease. This includes chemical or microbial factors and how these can interact with well-known vulnerability genes (e.g., APOE e4), as well as lesser known immune genes (e.g., TREM2, CD33) to cause disease. New technologies may ultimately fuel treatment approaches that allow specific manipulation or reprograming of glia and immune cells, thereby taking advantage of the beneficial effects of immunity (e.g., phagocytosis of plaques), while minimizing its deleterious aspects (e.g., oxidative stress).