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机译:胰岛素信号转导途径的变化是阿尔茨海默病大鼠模型中学习/记忆缺陷的基础
Department of Neurology, Provincial Hospital Affiliated to Shandong University, 324#, Jingwu Weiqi Road, Jinan, 250021, People’s Republic of China;
Department of Neurology, No. 1 Central Hospital of Bao Ding City, Baoding, Hebei, People’s Republic of China;
Department of Neurology, Provincial Hospital Affiliated to Shandong University, 324#, Jingwu Weiqi Road, Jinan, 250021, People’s Republic of China;
Department of Neurology, Provincial Hospital Affiliated to Shandong University, 324#, Jingwu Weiqi Road, Jinan, 250021, People’s Republic of China;
Department of Neurology, Provincial Hospital Affiliated to Shandong University, 324#, Jingwu Weiqi Road, Jinan, 250021, People’s Republic of China;
Department of Neurology, Provincial Hospital Affiliated to Shandong University, 324#, Jingwu Weiqi Road, Jinan, 250021, People’s Republic of China;
Department of Neurology, Provincial Hospital Affilia;
Alzheimer’s disease; Soluble Aβ oligomers; Insulin-signaling transduction pathway; Rats;
机译:胰岛素信号转导途径的变化是阿尔茨海默病大鼠模型中学习/记忆缺陷的基础
机译:在肥胖和阿尔茨海默病的小鼠模型中看到线粒体异常和突触损失内存缺陷
机译:红花黄色衰减淀粉样蛋白诱导的阿尔茨海默病大鼠学习和记忆缺陷通过抑制神经节细胞活化和炎症信号通路
机译:AB(25-35)和D-半乳糖诱导阿尔茨海默病模型大鼠的记忆障碍
机译:血小板活化因子受体的遗传消融不会损害野生型小鼠的学习和记忆,也不会改变阿尔茨海默氏病转基因模型中的淀粉样斑块数
机译:在肥胖和阿尔茨海默氏病小鼠模型中发现的记忆缺陷是线粒体异常和突触丧失的基础
机译:线粒体异常和突触损失是肥胖和阿尔茨海默病小鼠模型中记忆缺陷的基础