Objective To investigate the differentiation of oligodendrocyte precursor cells after neural injury utilizing Sox10 cell lineage tracing in the cortical tissue. Methods  C57BL/6 mice and Sox10-CreERT2/red fluorescent protein(RFP) model mice were used in the current study. The Sox10-CreERT2/RFP model mice generated by crossing Sox10-CreERT2 and Ai9 were 8-week-old F1 mice (n =16), which were randomly divided into control group (n =4) and 7 days (n =4), 14 days (n =4), and 30 days feed groups (n =4). Tamoxifen(TAM) was used to induce the expression of RFP. The control group received tamoxifen dissolved in sunflower seed oil by gavage (40 mg/kg once daily for three consecutive days) and the brain tissues were obtained after 4 days. The feed group mice were fed with tamoxifen-containing feed to induce RFP expression, and the brain tissues were obtained after 7, 14, and 30 days, respectively. Immunofluorescent staining was performed to detect the expressions of neuronal nuclei (NeuN), microtubuleassociated protein 2 (MAP2), phosphorylated histone 2AX (γ-H2AX), cluster of differentiation 13 (CD13), γaminobutyric acid (GABA), glial fibrillary acidic protein (GFAP), cluster of differentiation 11b (CD11b), vesicular glutamate transporter 2 (VGLUT2), and adenomatous polyposis coli (APC, CC-1) in the brains of each group mice. The number of positive cells was counted, and the proportion was calculated. Eight-week-old male C57BL/6 mice were randomly divided into wild type(WT) group (n =4) and WT+TAM group (n =4). They were fed with regular feed and tamoxifencontaining feed for 30 days, respectively, and then brain tissues were obtained. Immunofluorescent double-labeling was used to detect the expressions of γ-H2AX positive neurons in the cortex of mice in both groups.   Results  In the control group, feed 7 days,14 days, and 30 days groups, the proportions of RFP⁺ pericytes among all RFP⁺ cells in the cortical tissue were (0.8±0.1)%, (2.7±0.1)%, (3.2±0.1)%, (4.0 ±0.1)%, respectively, and the proportion of mature oligodendrocytes (CC-1⁺ RFP⁺) in the feed 7 days group was (51.2±0.7)%. The proportions of RFPpositive neurons in the cortex after 14 and 30 days of tamoxifen feed were (0.7±0.1)% and (1.5±0.1)%, respectively, while no conversion to RFP-positive neurons was observed in the gavage group and 7 days feed group. RFP cells in the cortex of the 7 days or 30 days feed group did not express GFAP or CD11b. Extensive γ-H2AX⁺ NeuN⁺ staining was observed in the WT group and WT+TAM group. Conclusion  Long-term administration of tamoxifen can promote the differentiation of Sox10 cells into pericytes and neurons. Further investigation into the role of OPC in the neurovascular unit repair mechanism may contribute to a better understanding of the pathogenesis underlying AD.