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. 2019 Jun 26;11:143. doi: 10.3389/fnagi.2019.00143

Figure 1.

Figure 1

Microbes or LPS that access the CNS comprise “danger” signals, triggering an innate immune response: the release of β-amyloid by astrocytes to opsonize “the intruder,” preparing it for phagocytosis (Zhan et al., 2018). The LPS–β-amyloid complex is subsequently engulfed by microglia, eliminating the “danger.” Microglial TREM-2, a β-amyloid receptor, initiates phagocytosis by binding the entire complex (Zhao et al., 2018). This mechanism may explain the reason TREM-2 genetic variants (with loss of function) present with impaired phagocytosis and β-amyloid accumulation (Guerreiro et al., 2012; Zhan et al., 2018).