Microglia can mediate synapse loss by engulfment of synapses, likely via a complement-dependent mechanism they can also exacerbate tau pathology and secrete inflammatory factors that can injure neurons directly or via activation of neurotoxic astrocytes. On the other hand, there is also abundant evidence that activated microglia can be harmful to neurons. There is mounting evidence that microglia protect against the incidence of AD, as impaired microglial activities and altered microglial responses to β-amyloid are associated with increased AD risk. The majority of risk genes for AD are highly expressed (and many are selectively expressed) by microglia in the brain. Human genetics data point to a key role for microglia in the pathogenesis of AD. Proliferation and activation of microglia in the brain, concentrated around amyloid plaques, is a prominent feature of Alzheimer’s disease (AD).
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