Neurodegenerative disorders,including Alzheimer's disease(AD) and Parkinson's disease(PD),are common disorders of the central nervous system among aging populations.In the last 10 years insights concerning the etiology,diagnosis and pathogenesis of these diseases have come from research carried out by Chinese neuroscientists.Their findings include the description of Chinese patients with autosomal recessive early-onset PD,the function of the tau protein,molecular mechanisms underlying protein aggregation,and the identification of biomarkers for AD diagnosis and molecules/compounds with potential neuroprotective activities.
ZHOU JiaWei Institute of Neuroscience,Shanghai Institutes for Biological Sciences,Chinese Academy of Sciences,Shanghai,200031
On Nov 24,2009,the Proceedings of the National Academy of Sciences published online a research article from ION entitled'PKCδRegulates Cortical Radial Migration by Stabilizing the Cdk5 Activator P35'.This work was carried out by graduate students Chun-tao Zhao,Kun Li,Wang Zheng,Jun-tao Li, Xun-jun Liang,An-qi Geng and Ning Li from the laboratory of Dr.Xiao-bing Yuan.
目的探讨N-甲基-D-天门冬氨酸受体(N-methyl-D-aspartate receptor,NMDAR or NR)亚基NR2A在脑缺血再灌注引起的海马CA1区神经元树突棘丢失和认知功能障碍中的作用。方法制作三动脉阻断(3-VO)GFP转基因小鼠全脑缺血模型,小鼠随机分为假手术组、脑缺血再灌注(I/R)组和NVP-AAM077(NVP)干预组;应用跳台试验测试小鼠学习记忆能力,激光共聚焦和Neurolucida软件分析检测海马CA1区神经元形态及树突棘的变化。结果学习记忆能力测试发现,I/R组明显差于sham组(P<0.05),NVP干预组差于sham组和I/R组(P<0.05);I/R组CA1区神经元树突棘的数量明显少于假手术组(P<0.01),NVP干预能进一步增加缺血/再灌注所致的CA1区神经元树突棘的丢失(P<0.05)。结论 NMDA受体亚基NR2A在小鼠脑缺血再灌注所致树突棘丢失和脑认知功能损害中具有重要作用。
