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Amyloid Beta and Tau Proteins as Therapeutic Targets for Alzheimers Disease Treatment: Rethinking the Current Strategy

机译:淀粉样β和Tau蛋白作为阿尔茨海默氏病治疗的治疗靶点:对当前策略的重新思考

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摘要

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.
机译:阿尔茨海默氏病(AD)的定义是同时存在由两种蛋白质组成的异常聚集体:淀粉样蛋白β(Aβ)和tau,以及包括神经突变性,神经元丧失和认知功能在内的细胞变化。基于它们在遗传和病理学上与疾病的密切联系,毫不奇怪的是,人们一直致力于开发针对聚集结构的疗法。不幸的是,当前的疗法仅具有轻微的益处。考虑到这一点,我们将重点研究突触可塑性与Aβ和tau蛋白的关系,以及它们作为治疗药物开发的潜在靶标的作用。最后,我们将为开发AD治疗的多因素策略提供观点。

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