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Potential mechanisms of M1 and M2 phenotypes of microglial cells in AD. Mounting evidence suggests that M1 and M2 microglia are involved in the pathological processes of Alzheimer’s disease (AD). The AD-associated pro-inflammatory and anti-inflammatory factors such as tumor necrosis factor-α (TNF-α) and interleukin-4 (IL-4) play important roles in regulating synaptic plasticity and neuronal death. Amyloid-β (Aβ)/tau aggregates are involved in regulating microglia-related inflammation.
