Alzheimer's disease (AD) is the leading cause of dementia characterized by neuronal loss, and pathological accumulation of neurotoxic β-amyloid (Aβ) and hyperphosphorylated tau proteins, together with damaging chronic inflammation as indicated by activated microglia, which are the resident immune cells in the central nervous system (CNS) where they are important players in health as well as disease. In health, microglia execute supporting functions for the nervous tissue by trophic support, synapse maintenance and phagocytic removal of molecular and cellular debris, as well as surveillance of the tissue for pathogenic threats. 1-3 In AD, microglia are activated by an overabundance of Aβ, a reaction that is further augmented due to the increase in misfolded and aggregated forms of this peptide,