Their abnormal activation can lead to neuroinflammation, which in turn promotes the deposition of β-amyloid and the hyperphosphorylation of tau protein, aggravating the condition of Alzheimer’s disease (Heppner et al., 2015; Maphis et al., 2015; Hong et al., 2016; Keren-Shaul et al., 2017; Sarlus and Heneka, 2017; Li Y. et al., 2023). The gene discussed is MAPT; the disease is early-onset autosomal dominant Alzheimer disease.