【摘 要】
：
Objective Cerebral ischemia may contribute to the pathogenesis of Alzheimers disease (AD), however, the neuropathological relationship between these 2 disorders is largely unclear.We investigated axon
【机 构】
：
Department of Anatomy, Brain Paralysis Research Center, Medical College of Zhengzhou University, Zhe
【出 处】
：
中国神经科学学会第九届全国学术会议暨第五届会员代表大会
论文部分内容阅读
Objective Cerebral ischemia may contribute to the pathogenesis of Alzheimers disease (AD), however, the neuropathological relationship between these 2 disorders is largely unclear.We investigated axonal changes after transient cerebral ischemia/reperfusion and their relationship to the expression of Aβ42 and hyperphosphorylated Tau, which has been considered as a key neuropathological process of AD.Methods Adult Wistar rats were subjected to either sham operation or middle cerebral artery occlusion (MCAO).At the desired time after the onset of reperfusion (6 h, 24 h, 1 w, 2 w, 3 w and 4 w), animals were carried out for in vivo tracing and sacrificed for tracer detection, immunochemistry and morphological analysis of axons, and immunoblotting test for hyperphosphorylated Tau was also underwent.Results Axonal changes, consisting of swollen axons and varicosities, were found 6 h after ischemia/reperfusion in ischemic regions, such as the sensory and motor cortex and striatum, as well as the perilesional cortex and hippocampus, and were observed for up to 4 weeks.We did not observe Aβ plaques or overexpression of Aβ42 in the ischemic brain areas; nevertheless, site-specific hyperphosphorylated Tau could be detected in the ischemic cortex.Conclusion Transient cerebral ischemia/reperfusion induces long-term axonal changes (axonopathy), which may be an important mechanism contributing to the development of AD after stroke.
其他文献
Objective Diabetic cognitive dysfunction (DCD), usually accompanied with chronically elevated glucocorticoids and hippocampal astrocytic alterations, is one of the most serious complications in patien
Objective Allelic expression imbalance (AEI) assays are a sensitive method for detecting genetically regulated expression of mRNAs in human tissues.Based on these measurements, it is often possible to
Inhibition of glycosphingolipid (GSL) synthesis reduces amyloid-beta (Aβ) production in vitro.Previous studies indicate that glucosylceramide synthase (GCS) inhibitors modulate phosphorylation of extr
Formaldehyde (FA), a common environmental pollutant, has toxic effects on central nervous system.The detailed mechanism of FA neurotoxicity has not been fully elucidated.In this study, we found that C
In the adult mammals, axotomy of mature neurons in the central nervous system (CNS) triggers massive cell death and failure to spontaneous axon regeneration.The relationship between axotomy-induced ne
Objective Cofilin is the major actin-depolymerizing factor in the CNS for regulation of actin dynamics.Neurodegenerative stimuli can induce the formation of cofilin rod, a pathological structure compo
Malignant glioma is the most common and fatal tumor in central nervous system, with the poor prognosis even with the advanced treatments.Seeking new prognostic factors and molecular targets may contri
目的 采用十四种近交系小鼠，观察并比较其在三叉神经痛模型前后对疼痛刺激敏感性的变化。方法 采用眶下神经切断手术制备三叉神经痛模型，记录手术前和手术后第14天小鼠耳廓、后爪和尾对机械痛、热痛刺激的反应。机械痛和热痛分别以von Frey毛和激光热刺激诱发。动物的行为学反应按反应强度进行量化。设假手术对照组，仅暴露同侧眶下神经但不切断。结果 (1)生理状况下，对von Frey毛机械刺激，雄性和雌性M
背景 肌细胞增强因子2D (myocyte enhancer factor-2D,MEF2D)属于转录调节因子MADS-box家族,最初被认为是肌细胞特异性DNA结合蛋白,其蛋白多结合在许多肌特异性基因的调控区域控制转录过程,发挥控制肌细胞分化过程中的基因转录功能。最近的研究表明,MEF2D还参与了多种细胞的信号传导过程,在调节细胞分化、增殖、存活和凋亡等方面发挥着重要的作用。在一些脑退行性疾病细