Figure 2.

Microglial priming and AD. At early stage, primed microglia enhances the ability of phagocytosis and releases more NFs to protect neurons and keep the homeostasis of the CNS. Later, the primed microglia are boosted to release pro-inflammation mediators, such as cytokine and chemokine, leading to a high level neuroinflammation which accelerate the activation of microglial cells in turn. Under this disrupted situation, β-amyloid peptides accumulate and change into amyloid plaque; meanwhile, dissociated tau is phosphorylated and aggregated to form neurofibrillary tangles in neurons especially in those whose gene is associated with APOEε4 mutation. Thus, primed microglia, directly and indirectly, result in neuron damage and loss, the main cause of AD onset or progression. AD, Alzheimer’s disease; CNS, central nervous system; AS, abnormal substances (cell debris, misfolded protein); NFs, neurotrophic factors.