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人源素及其受体。

Humanin and the receptors for humanin.

机构信息

Department of Pharmacology, Tokyo Medical University, Shinjuku-ku, Japan.

出版信息

Mol Neurobiol. 2010 Feb;41(1):22-8. doi: 10.1007/s12035-009-8090-z. Epub 2009 Dec 9.

Abstract

Alzheimer's disease (AD) is a prevalent dementia-causing neurodegenerative disease. Neuronal death is closely linked to the progression of AD-associated dementia. Accumulating evidence has established that a 24-amino-acid bioactive peptide, Humanin, protects neurons from AD-related neuronal death. A series of studies using various murine AD models including familial AD gene-expressing transgenic mice have shown that Humanin is effective against AD-related neuronal dysfunction in vivo. Most recently, it has been shown that Humanin inhibits neuronal cell death and dysfunction by binding to a novel IL-6-receptor-related receptor(s) on the cell surface involving CNTFRalpha, WSX-1, and gp130. These findings suggest that endogenous Humanin [or a Humanin-like substance(s)] may suppress the onset of AD-related dementia by inhibiting both AD-related neuronal cell death and dysfunction.

摘要

阿尔茨海默病(AD)是一种常见的导致痴呆的神经退行性疾病。神经元死亡与 AD 相关的痴呆进展密切相关。越来越多的证据表明,一种 24 个氨基酸的生物活性肽 Humanin 可以保护神经元免受 AD 相关的神经元死亡。一系列使用包括家族性 AD 基因表达转基因小鼠在内的各种鼠 AD 模型的研究表明,Humanin 对体内 AD 相关的神经元功能障碍有效。最近的研究表明,Humanin 通过与细胞表面上的新型 IL-6 受体相关受体(s)结合,抑制神经元细胞死亡和功能障碍,该受体涉及 CNTFRalpha、WSX-1 和 gp130。这些发现表明,内源性 Humanin[或 Humanin 样物质(s)]可能通过抑制 AD 相关的神经元细胞死亡和功能障碍来抑制 AD 相关的痴呆的发生。

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