Therapeutic targets in the biology of Alzheimer's disease

被引:13
作者
Bush, AI
机构
[1] Massachusetts Gen Hosp East, Lab Oxidat Biol, Genet & Aging Unit, Charlestown, MA USA
[2] Mental Hlth Res Inst Victoria, Parkville, Vic, Australia
关键词
D O I
10.1097/00001504-200107000-00018
中图分类号
R749 [精神病学];
学科分类号
100205 ;
摘要
The cause of Alzheimer's disease is closely associated with the accumulation of beta -amyloid in the neocortex. The neurochemical factors responsible for precipitating this otherwise normal, soluble protein are contentious. Nevertheless, in the absence of any other curative treatment for Alzheimer's disease, the majority of the research effort has focussed on inhibiting the production of beta -amyloid (using secretase inhibitors) or destroying the protein (vaccination with synthetic peptide). Both approaches assume that the protein serves no purposive function, In contrast, a new alternative has recently emerged employing small metal complexing agents that inhibit the neurotoxic hydrogen peroxide produced by beta -amyloid, and which facilitate the dissolution of brain amyloid deposits in vivo in transgenic mice. Currently in clinical trials, this class of agent may interdict the Alzheimer disease process at its most generic biochemical level. Curr Opin Psychiatry 14:341-348. (C) 2001 Lippincott Williams & Wilkins.
引用
收藏
页码:341 / 348
页数:8
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