Li Ji-Feng, Wang Zhou, Sun Qin-Jian, Du Yi-Feng
Department of Neurology, Shandong Provincial Hospital Affiliated to Shandong University No. 324 Jingwuweiqi Road, Jinan 250021, China.
Department of Pathology, Shandong Provincial Hospital Affiliated to Shandong University No. 324 Jingwuweiqi Road, Jinan 250021, China.
Int J Clin Exp Med. 2015 Oct 15;8(10):19682-8. eCollection 2015.
The aim of this study was to investigate the relationship between chronic cerebral hypoperfusion and the occurrence and development of Alzheimer's disease (AD). A cerebral hypoperfusion rat model was established by two vessels occlusion (2VO). The cognitive function of the rats with chronic cerebral hypoperfusion and the expression of p-Tau protein in the hippocampus were observed dynamically. Before the operation, no differences were observed in the cognitive functions of the control and 2VO group (P > 0.05). However, a significant difference was found at 2, 4, 8, and 12 weeks after the operation. The shock number required to reach the "learned" standard in the 2VO group increased remarkably compared with that of the control group (P < 0.01). With the passage of time, the shock number in the model group increased gradually. The p-Tau-positive cells in the CA1 region of the hippocampus also increased markedly in the model group in a time-dependent manner as compared with that in the control group (P < 0.01). Cerebral hypoperfusion can cause and aggravate the phosphorylation of Tau protein in the brain, leading to cognitive dysfunction. Therefore, this protein is an important initiating and promoting factor involved in the development of AD.
本研究旨在探讨慢性脑灌注不足与阿尔茨海默病(AD)发生发展之间的关系。采用双侧颈总动脉结扎(2VO)法建立慢性脑灌注不足大鼠模型。动态观察慢性脑灌注不足大鼠的认知功能及海马区p-Tau蛋白的表达。术前,对照组和2VO组的认知功能无差异(P>0.05)。然而,术后2、4、8和12周发现有显著差异。与对照组相比,2VO组达到“学会”标准所需的电击次数显著增加(P<0.01)。随着时间的推移,模型组的电击次数逐渐增加。与对照组相比,模型组海马CA1区p-Tau阳性细胞也随时间显著增加(P<0.01)。脑灌注不足可导致并加重脑内Tau蛋白的磷酸化,导致认知功能障碍。因此,该蛋白是AD发生发展的重要起始和促进因素。