Humanin拮抗AD相关毒性作用的研究进展  

Recent Progress in Neuroprotection of Humanin Against Alzheimer' s Disease-relevant Neurotoxicity

作　　者：崔爱玲[1] 赵丽[1] 李灵敏[1] 乔健天[1] 张策[1] 

机构地区：[1]山西医科大学生理学教研室,太原030001

出　　处：《生理科学进展》2006年第4期302-306,共5页Progress in Physiological Sciences

基　　金：国家自然科学基金(30572085);山西省自然科学基金(20031099)资助课题

摘　　要：阿尔采末病(A lzheimer's d isease,AD)严重威胁着老年人的健康与生存质量,由于其发病原因复杂、机制不明,目前尚缺乏有效的防治措施。Humanin是近年来发现的能特异性抑制AD相关毒性的分泌性短肽,通过自身二聚化在细胞外发挥神经保护作用。Humanin通过直接或间接作用抑制β-淀粉样蛋白(Aβ),以及家族性AD(FAD)基因如早老基因突变诱发的神经毒,而对AD不相关的毒性作用如凋亡诱导剂etoposide及Fas诱导的细胞死亡却不表现拮抗作用。因此,Humanin可通过特异性拮抗AD相关的神经毒而发挥重要的神经保护作用。Alzheimer＇s disease （AD） is the leading cause of dementia for aging people, and far from control due to its obscure mechanism. Humanin, a 24-aa peptide encoded by a newly identified gene cloned from an apparently normal region of AD brain, can specifically attenuate AD-related neurotoxicity. It protects neurons from insults of various AD genes, anti-APP antibodies and Abeta by forming a ho- modimer outside and interfering directly or indirectly with the activity of Abeta. Humanin seems, howev- er, not to inhibit other toxic insults to neurons, such as Fas or etoposide, an agent against carcinomatous cells in clinical therapy. So Humanin rescues neurons from various AD-related toxicity specifically with efficiency.

关 键 词：HUMANIN 神经保护 阿尔采末病 Β-淀粉样蛋白 神经毒 

分 类 号：R388.25[医药卫生—医学寄生虫学]