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阿尔茨海默病海马体中的氧化应激:一项地形学研究。

Oxidative stress in Alzheimer's disease hippocampus: a topographical study.

机构信息

Institute of Neurological and Gerontological Sciences, Faculty of Medicine, International University of Catalonia, Josep Trueta, s/n. 08195 Sant Cugat del Vallès, Barcelona, Spain.

出版信息

J Neurol Sci. 2010 Dec 15;299(1-2):163-7. doi: 10.1016/j.jns.2010.08.029. Epub 2010 Sep 22.

Abstract

Advanced glycation end-products (AGEs) and their receptor (RAGE) are molecules related to oxidative stress demonstrated in aging and in several pathological disorders including Alzheimer's disease (AD). Aging has been considered the main risk factor for AD. Amyloid deposits (Aβ-D) and neurofibrillary tangles (NFT) are pathological changes related to AD involving hippocampal regions. Different degrees of AD pathology have been described according to distribution of NFTs in different topographical regions of hippocampus and cerebral cortex. The hippocampus shows a selective vulnerability under several noxes especially those including hypoxia. Hypoxia in the nervous tissue induces oxidative stress. In an attempt to find out more about anatomical distribution of the oxidative stress through hippocampal regions in AD, a collection of brains were studied. Samples from deceased patients who had suffered from AD and from age-matched controls were immunohistochemically studied with AGE and RAGE antibodies according to a topographical division of the hippocampus and brain cortical regions. Results suggest that an oxidative stress pathway starts in the CA3 sector progresses to CA1 and then continues to other hippocampal and cortical areas building a pathoclitic pathway for Alzheimer's disease progression.

摘要

晚期糖基化终产物(AGEs)及其受体(RAGE)是与氧化应激有关的分子,在衰老和包括阿尔茨海默病(AD)在内的几种病理紊乱中都有表现。衰老被认为是 AD 的主要危险因素。淀粉样蛋白沉积(Aβ-D)和神经原纤维缠结(NFT)是与 AD 相关的病理变化,涉及海马区。根据 NFT 在海马和大脑皮层不同拓扑区域的分布,描述了不同程度的 AD 病理学。海马在几种毒物,特别是包括缺氧在内的毒物下表现出选择性易损性。神经组织中的缺氧会引起氧化应激。为了更深入地了解 AD 中海马区域的氧化应激的解剖分布,研究了一组大脑。根据海马和大脑皮层区域的拓扑分区,对患有 AD 和年龄匹配对照的已故患者的样本进行了 AGE 和 RAGE 抗体的免疫组织化学研究。结果表明,氧化应激途径从 CA3 区开始,进展到 CA1,然后继续到其他海马和皮质区域,为阿尔茨海默病的进展建立了一条病理途径。

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