目的:探讨生理性记忆认知功能减退与病理性记忆认知功能减退与内颞叶相关结构--杏仁体海马复合体关系,为正常生理性记忆认知功能减退与早期Alzheimer氏病(Alzheimer's disease,AD)所引起的病理性记忆认知功能减退鉴别诊断制定标准....目的:探讨生理性记忆认知功能减退与病理性记忆认知功能减退与内颞叶相关结构--杏仁体海马复合体关系,为正常生理性记忆认知功能减退与早期Alzheimer氏病(Alzheimer's disease,AD)所引起的病理性记忆认知功能减退鉴别诊断制定标准.方法:40例正常人与36例临床疑AD患者均进行MRI常规检查及倾斜冠状位T1WI检查.在倾斜冠状位T,WI图像上测量杏仁核海马体积并标准化处理,应用Statistic Package for Social Science(SSPS)软件进行统计学处理.结果:正常组与AD组不同年龄阶段杏仁核海马复合体体积数据呈正态分布,且方差性齐.40～50岁与51～60岁之间无显著性组间差异;61～70岁与71～79岁之间存在显著组间差异(P＜0.05).每个年龄阶段不同侧别之间无显著差异,不同组别标准后复合体体积随年龄呈负相关.经方差分析,无论左右侧,AD组杏仁核海马复合体体积明显小于对照组,P＜0.01.结论:内颞叶相关结构-杏仁核海马复合体积MRI测量对鉴别正常生理性记忆功能减退与早期AD引起的病理性记忆认知功能障碍有极大价值.展开更多
Objective： To investigate the preventive treatment effects of electroacupuncture（EA） on cognitive changes and brain damage in senescence-accelerated mouse prone 8（SAMP8） mice. Methods： The 5-month-old male SAMP8...Objective： To investigate the preventive treatment effects of electroacupuncture（EA） on cognitive changes and brain damage in senescence-accelerated mouse prone 8（SAMP8） mice. Methods： The 5-month-old male SAMP8 and age-matched homologous normal aging mice（SAMR1） were adopted in this study. EA stimulation at Baihui（GV 20） and Yintang（EX-HN 3） was performed every other day for 12 weeks, 4 weeks as a course. Morris water maze test and Nissl-stained with cresyl violet were used for cognitive impairments evaluation and brain morphometric analysis. Amyloid-β（Aβ） expression in hippocampus and parietal cortex was detected by immunohistochemistry, and apoptosis was observed by TUNEL staining. Results： After 3 courses of EA preventive treatment, the escape latencies of 8-month-old SAMP8 mice in EA group were significantly shortened than those of un-pretreated SAMP8 mice. Compared with SAMR1 mice, extensive neuronal changes were visualized in the CA1 area of hippocampus in SAMP8 mice, while these pathological changes and attenuate cell loss in hippocampal CA1 area of SAMP8 mice markedly reduced after EA preventive treatment. Furthermore, Aβ expression in hippocampus and parietal cortex of SAMP8 mice decreased significantly after EA treatment, and neuronal apoptosis decreased as well. Conclusion： EA preventive treatment at GV 20 and EX-HN 3 might improve cognitive deficits and neuropathological changes in SAMP8 mice, which might be, at least in part, due to the effects of reducing brain neuronal damage, decreasing neuronal apoptosis and inhibiting Aβ-containing aggregates.展开更多
基金supported by grants from the National Students’ Innovation and Entrepreneurship Training Program of China (No. 201810443009)Students’ Innovation and Entrepreneurship Training Program of Jining Medical University (No. cx2018005)+1 种基金A Project of Shandong Province Higher Educational Science and Technology Program (No. J18KA124)Supporting Fund for Teachers’ Research of Jining Medical University (No. JY2017KJ036, JY2017KJ034)
文摘目的:探讨生理性记忆认知功能减退与病理性记忆认知功能减退与内颞叶相关结构--杏仁体海马复合体关系,为正常生理性记忆认知功能减退与早期Alzheimer氏病(Alzheimer's disease,AD)所引起的病理性记忆认知功能减退鉴别诊断制定标准.方法:40例正常人与36例临床疑AD患者均进行MRI常规检查及倾斜冠状位T1WI检查.在倾斜冠状位T,WI图像上测量杏仁核海马体积并标准化处理,应用Statistic Package for Social Science(SSPS)软件进行统计学处理.结果:正常组与AD组不同年龄阶段杏仁核海马复合体体积数据呈正态分布,且方差性齐.40～50岁与51～60岁之间无显著性组间差异;61～70岁与71～79岁之间存在显著组间差异(P＜0.05).每个年龄阶段不同侧别之间无显著差异,不同组别标准后复合体体积随年龄呈负相关.经方差分析,无论左右侧,AD组杏仁核海马复合体体积明显小于对照组,P＜0.01.结论:内颞叶相关结构-杏仁核海马复合体积MRI测量对鉴别正常生理性记忆功能减退与早期AD引起的病理性记忆认知功能障碍有极大价值.
基金Supported by the National Natureal Science Foundation of China(No.30701121)
文摘Objective： To investigate the preventive treatment effects of electroacupuncture（EA） on cognitive changes and brain damage in senescence-accelerated mouse prone 8（SAMP8） mice. Methods： The 5-month-old male SAMP8 and age-matched homologous normal aging mice（SAMR1） were adopted in this study. EA stimulation at Baihui（GV 20） and Yintang（EX-HN 3） was performed every other day for 12 weeks, 4 weeks as a course. Morris water maze test and Nissl-stained with cresyl violet were used for cognitive impairments evaluation and brain morphometric analysis. Amyloid-β（Aβ） expression in hippocampus and parietal cortex was detected by immunohistochemistry, and apoptosis was observed by TUNEL staining. Results： After 3 courses of EA preventive treatment, the escape latencies of 8-month-old SAMP8 mice in EA group were significantly shortened than those of un-pretreated SAMP8 mice. Compared with SAMR1 mice, extensive neuronal changes were visualized in the CA1 area of hippocampus in SAMP8 mice, while these pathological changes and attenuate cell loss in hippocampal CA1 area of SAMP8 mice markedly reduced after EA preventive treatment. Furthermore, Aβ expression in hippocampus and parietal cortex of SAMP8 mice decreased significantly after EA treatment, and neuronal apoptosis decreased as well. Conclusion： EA preventive treatment at GV 20 and EX-HN 3 might improve cognitive deficits and neuropathological changes in SAMP8 mice, which might be, at least in part, due to the effects of reducing brain neuronal damage, decreasing neuronal apoptosis and inhibiting Aβ-containing aggregates.
