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阿尔茨海默病中依赖刺激的脊髓内微管与突触功能障碍:综述

Stimulation-dependent intraspinal microtubules and synaptic failure in Alzheimer's disease: a review.

作者信息

Mitsuyama Fuyuki, Futatsugi Yoshio, Okuya Masato, Kawase Tsukasa, Karagiozov Kostadin, Kato Yoko, Kanno Tetsuo, Sano Hirotoshi, Nagao Shizuko, Koide Tadashi

机构信息

Department of Neurosurgery, Fujita Health University, 1-98, Kutsukake, Toyoake, Aichi 470-1101, Japan.

出版信息

Int J Alzheimers Dis. 2012;2012:519682. doi: 10.1155/2012/519682. Epub 2012 Mar 8.

Abstract

There are many microtubules in axons and dendritic shafts, but it has been thought that there were fewer microtubules in spines. Recently, there have been four reports that observed the intraspinal microtubules. Because microtubules originate from the centrosome, these four reports strongly suggest a stimulation-dependent connection between the nucleus and the stimulated postsynaptic membrane by microtubules. In contrast, several pieces of evidence suggest that spine elongation may be caused by the polymerization of intraspinal microtubules. This structural mechanism for spine elongation suggests, conversely, that the synapse loss or spine loss observed in Alzheimer's disease may be caused by the depolymerization of intraspinal microtubules. Based on this evidence, it is suggested that the impairment of intraspinal microtubules may cause spinal structural change and block the translocation of plasticity-related molecules between the stimulated postsynaptic membranes and the nucleus, resulting in the cognitive deficits of Alzheimer's disease.

摘要

轴突和树突干中有许多微管,但人们一直认为棘突中的微管较少。最近,有四份报告观察到了棘突内的微管。由于微管起源于中心体,这四份报告有力地表明,微管在细胞核与受刺激的突触后膜之间建立了一种依赖于刺激的连接。相比之下,有几条证据表明,棘突伸长可能是由棘突内微管的聚合引起的。相反,这种棘突伸长的结构机制表明,在阿尔茨海默病中观察到的突触丢失或棘突丢失可能是由棘突内微管的解聚引起的。基于这一证据,有人提出,棘突内微管的损伤可能导致棘突结构改变,并阻断可塑性相关分子在受刺激的突触后膜与细胞核之间的转运,从而导致阿尔茨海默病的认知缺陷。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/34b9/3310171/ff77f7936171/IJAD2012-519682.001.jpg

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