From the other perspective, when the CNS is confronted with neurodegenerative events such as during AD development, the abnormal expression of tau protein can enhance the combination of the complement fragment C1q and synapses and, as a result, over-activate microglial phagocytosis of synapses (Dejanovic et al., 2018; Bie et al., 2019). This evidence concerns the gene MAPT and Alzheimer disease.