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

机译：β-淀粉样蛋白作为阿尔茨海默氏病的分子治疗靶标。

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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.
机译：阿尔茨海默氏病是痴呆症最常见的形式，主要影响个人生命的第六个十年或之后。尽管进行了数十年的研究，但仍没有有效的缓解疾病的药物来治疗这种神经退行性疾病。当前FDA批准的药物主要提供症状缓解，并基于已知的神经递质缺陷。但是，在临床前和临床开发中有许多针对AD发病机理其他方面的药物。其中主要的药物是调节β-淀粉样蛋白的药物，β-淀粉样蛋白被认为是导致阿尔茨海默氏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，并回顾许多不同的策略，包括此类方法的陷阱和针对该蛋白调节的未来方向。显然，β-淀粉样蛋白代表了药理学操纵的有效分子靶标，可能阻止了阿尔茨海默氏病的发作和发展。

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