目的 通过肌酸抑制STAT1信号通路活化，探究肌酸治疗是否调控阿尔茨海默病(AD)中细胞因子信号转导抑制因子1（SOCS1）相关的神经元铁死亡。   方法 使用人脑额叶组织石蜡切片进行免疫组织化学染色，并对阳性结果计数，确定目的蛋白变化趋势。通过免疫荧光和Western blotting实验进行验证。11只FAD4T小鼠分为肌酸组6只和对照组5只。通过小脑延髓池穿刺术进行肌酸注射, 抑制STAT1磷酸化，处死小鼠取材后通过免疫组织化学和免疫荧光来检验目的蛋白的表达情况。  结果  与年龄对照组相比，AD患者脑皮层中STAT1信号通路的激活细胞因子干扰素γ（IFN-γ）和STAT1激活的负性调控因子SOCS1均显著上调，STAT1磷酸化增强，铁死亡标记物铁蛋白轻链（FTL）和胱氨酸/谷氨酸转运体 (xCT) (SLC7A11)明显增多；对FAD4T小鼠进行肌酸治疗后，脑内IFN-γ和SOCS1减少，铁死亡标志物FTL及xCT都明显降低。 结论 肌酸通过降低神经元STAT1-SOCS1信号活化，改善AD小鼠模型中神经元铁死亡。

Objective To explore whether creatine therapy regulates neuronal ferroptosis by inhibiting the activation of STAT1 signaling pathway associated with suppressor of cytokine signaling 1 (SOCS1) in Alzheimer’s disease.   Methods  Immunohistochemical staining and counting of positive results using paraffin sections of human brain frontal lobes were employed to determine the trend of changes in the target proteins. Further validation was performed by immunofluorescence and Western blotting. STAT1 phosphorylation was inhibited by creatine injection using eleven FAD4Tmice and by cerebellar medullary pool puncture, and the expression of target proteins was examined by immunohistochemistry and immunofluorescence after postmortem sampling.   Results  Compared with the age controls, interferon-γ (IFN-γ), an activating cytokine of the STAT1 signaling pathway, and SOCS1, a negative regulator of STAT1 activation, were both significantly up-regulated, STAT1 phosphorylation was enhanced, and the ferroptosis markers ferritin light chain (FTL) and cystine/glutamate transporter(xCT) increased markedly in the cortex of AD human brains; Creatine treatment of FAD4Tmice resulted in a reduction of both IFN-γ and SOCS1, and a significant decrease in the ferroptosis markers FTL and xCT (SLC7A11).  Conclusion  Creatine ameliorates neuronal ferroptosis in AD model mice by reducing neuronal STAT1SOCS1 signalling activation.