老年性痴呆症发病机制及其防治措施的研究进展

被引:10
作者
叶伟
唐孝威
机构
[1] 浙江大学理工学院交叉学科实验室
关键词
老年性痴呆症; 发病机制; β淀粉样蛋白级联学说; 药物治疗;
D O I
暂无
中图分类号
R749.1 [脑器质性精神障碍];
学科分类号
100205 ;
摘要
老年性痴呆症是严重影响老龄人口健康的中枢神经系统退行性疾病,目前有许多有关老年性痴呆症发病机制的学说,其中β淀粉样蛋白级联学说是目前最广为接受的学说之一。此学说认为淀粉样蛋白多肽异常分泌和沉积是老年性痴呆症的核心环节,减少淀粉样蛋白多肽的产生、抑制其沉积是预防和治疗老年性痴呆症的根本途径。本综述重点介绍和评述了β淀粉样蛋白级联学说以及老年性痴呆症预防和治疗措施的研究进展。
引用
收藏
页码:379 / 381
页数:3
相关论文
共 16 条
[1]  
New neuropathological criteria for Alzheimer disease. Hyman,BT. Archives of Neurology . 1998
[2]  
An increased percentage of longamyloidβprotein secreted by familial amyloidβprotein precursor(βAPP717)mutants. Suzuki N,Cheung TT,Cai XD,et al. Science . 1994
[3]  
Binding sites of{gamma}-secretaseinhibitors in rodent brain:distribution,postnatal development,and effectof deafferentation. Yan XX,Li T,Rominger MC,et al. The Journal of Neuroscience . 2004
[4]  
Growth arrest of individualsenile plaques in a model of alzheimer’s disease observed by in vivo mul-tiphoton microscopy. Christie RH,Bacskai BJ,Zipfel WR,et al. The Journal of Neuroscience . 2001
[5]  
Naturally secreted oligomersof amyloidβprotein potently inhibit hippocampal long-term potentiation invivo. Walsh DM,Klyubin I,Fadeeva JV,et al. Nature . 2002
[6]  
Clogging of axons by tau,inhibition of axonal traffic and starving of synapses. Mandelkow EM,Stamer K,Vogel R,et al. Neurobiology of Aging . 2003
[7]  
Secretases as targets for the treatment ofAlzheimer’s disease:the prospects. Dewachter I,Van Leuven F. The Lancet Neurology . 2002
[8]  
Targeting small Aβoligomers:The solu-tion to an Alzheimer’s disease conundrum. Klein WL,Krafft G,Finch CE. Trends in Neurosciences . 2001
[9]  
Therapeutically effective an-tibodies against amyloid-beta peptide target amyloid-beta residues 4-10and inhibit cytotoxicity and fibrillogenesis. McLaurin J,Cecal R,Kierstead ME,et al. Nature Medicine . 2002
[10]  
Decreased prevalence ofalzheimer disease associated with 3-hydroxy-3-methyglutaryl coenzyme areductase inhibitors. Wolozin B,Kellman W,Ruosseau P,et al. Archives of Neurology . 2000