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β淀粉样蛋白和tau蛋白作为阿尔茨海默病治疗的靶点:重新思考当前策略。

Amyloid Beta and tau proteins as therapeutic targets for Alzheimer's disease treatment: rethinking the current strategy.

作者信息

Mondragón-Rodríguez Siddhartha, Perry George, Zhu Xiongwei, Boehm Jannic

机构信息

Le Groupe de Recherche sur le Système Nerveux Central, Département de Physiologie, Université de Montréal, Montréal, QC, Canada.

出版信息

Int J Alzheimers Dis. 2012;2012:630182. doi: 10.1155/2012/630182. Epub 2012 Mar 8.

Abstract

Alzheimer's disease (AD) is defined by the concurrence of accumulation of abnormal aggregates composed of two proteins: Amyloid beta (Aβ) and tau, and of cellular changes including neurite degeneration and loss of neurons and cognitive functions. Based on their strong association with disease, genetically and pathologically, it is not surprising that there has been a focus towards developing therapies against the aggregated structures. Unfortunately, current therapies have but mild benefit. With this in mind we will focus on the relationship of synaptic plasticity with Aβ and tau protein and their role as potential targets for the development of therapeutic drugs. Finally, we will provide perspectives in developing a multifactorial strategy for AD treatment.

摘要

阿尔茨海默病(AD)的定义是由两种蛋白质组成的异常聚集体的积累同时发生:淀粉样β蛋白(Aβ)和tau蛋白,以及包括神经突退化、神经元丧失和认知功能丧失在内的细胞变化。基于它们在遗传和病理上与疾病的紧密关联,致力于开发针对聚集结构的治疗方法也就不足为奇了。不幸的是,目前的治疗方法只有轻微的益处。考虑到这一点,我们将专注于突触可塑性与Aβ和tau蛋白的关系,以及它们作为治疗药物开发潜在靶点的作用。最后,我们将提供关于制定AD治疗多因素策略的观点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/0508/3310047/0a8860ff71de/IJAD2012-630182.001.jpg

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