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[tau蛋白相关痴呆症治疗的现状与未来]

[Present and future of the tau dementia therapy].

作者信息

Takashima Akihiko

机构信息

Department of Neurobiology, National Center for Geriatrics and Gerontology.

出版信息

Rinsho Shinkeigaku. 2013;53(11):1040-2. doi: 10.5692/clinicalneurol.53.1040.

Abstract

Neurofibrillarly tangles (NFTs) are seen most patients, who shows dementia, while β amyloid deposition observed specifically in AD patients. NFTs observe first from coeruleus and entorhinal cortex, and then spread to neocortex, which well explain clinical progression of AD, such as memory problem to dementia. Tau fibrils are the major component of NFT. Before forming tau fibrils, tau binds together, form soluble tau oligomer, and then granular tau oligomer. The soluble tau oligomer associates with synapse loss, and granular tau formation induces neuronal loss. Therefore, tau aggregation inhibitor is expected to halt the clinical progression of AD.

摘要

在大多数患有痴呆症的患者中可发现神经原纤维缠结(NFTs),而β淀粉样蛋白沉积则在阿尔茨海默病(AD)患者中特异性观察到。NFTs首先在蓝斑和内嗅皮质中被观察到,然后扩散到新皮质,这很好地解释了AD的临床进展,如从记忆问题发展到痴呆。tau原纤维是NFT的主要成分。在形成tau原纤维之前,tau蛋白聚集在一起,形成可溶性tau寡聚体,然后是颗粒状tau寡聚体。可溶性tau寡聚体与突触丧失有关,而颗粒状tau的形成会导致神经元丧失。因此,tau聚集抑制剂有望阻止AD的临床进展。

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