Suppr超能文献

β-淀粉样蛋白作为阿尔茨海默病的分子治疗靶点

beta-Amyloid as a molecular therapeutic target in Alzheimer's disease.

作者信息

Adlard Paul A, James Simon A, Bush Ashley I, Masters Colin L

机构信息

The Oxidation Disorders Laboratory, The Mental Health Research Institute of Victoria, Parkville, Victoria, Australia.

出版信息

Drugs Today (Barc). 2009 Apr;45(4):293-304. doi: 10.1358/dot.2009.45.4.1353853.

Abstract

Alzheimer's disease is the most common form of dementia, primarily affecting individuals during or after their sixth decade of life. Despite decades of research, there are still no effective disease-modifying drugs available to treat this neurodegenerative disorder. Current FDA-approved medications primarily offer symptomatic relief and are based upon known neurotransmitter deficits. There are, however, many drugs in preclinical and clinical development which target other aspects of AD pathogenesis. Principal among these are drugs which modulate beta-amyloid, a protein that is believed to be central to the cascade which leads to the development of Alzheimer's disease. This article will outline the metabolism of beta-amyloid and review a number of different strategies, including pitfalls and future directions of such methods that are directed towards the modulation of this protein. It will become clear that beta-amyloid represents a potent molecular target for pharmacological manipulation to perhaps prevent the onset and progression of Alzheimer's disease.

摘要

阿尔茨海默病是最常见的痴呆形式,主要影响60岁及以上的人群。尽管经过了数十年的研究,但仍然没有有效的疾病修饰药物可用于治疗这种神经退行性疾病。目前美国食品药品监督管理局(FDA)批准的药物主要提供症状缓解,并且是基于已知的神经递质缺陷。然而,有许多处于临床前和临床开发阶段的药物,它们针对阿尔茨海默病发病机制的其他方面。其中主要的是调节β-淀粉样蛋白的药物,β-淀粉样蛋白是一种蛋白质,被认为是导致阿尔茨海默病发展的级联反应的核心。本文将概述β-淀粉样蛋白的代谢,并回顾一些不同的策略,包括针对该蛋白调节的此类方法的陷阱和未来方向。很明显,β-淀粉样蛋白是药物操纵的一个有力分子靶点,或许可以预防阿尔茨海默病的发生和进展。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验