阻断ires介导的翻译通路作为治疗阿尔茨海默病的新方法

Q.Y. Liu
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引用次数: 1

摘要

科学家推测β-淀粉样蛋白(Aβ)斑块和tau蛋白缠结参与阿尔茨海默病(AD)的发展,淀粉样蛋白前体蛋白(APP)产生Aβ触发疾病过程。然而,APP本身正常的突触功能尚不完全清楚。一些研究结果表明,APP在正常情况下的学习和记忆中具有潜在的关键作用。然而,在细胞病理条件下,Aβ的异常积累会破坏APP的正常运作。因此,有一种假设认为,AD可以通过在细胞病理生理应激过程中减弱APP合成来治疗。先前的研究推测,细胞不能通过自我保护来减少APP的合成,这可能是因为APP是通过IRES介导的翻译来合成的。因此,阻断这种翻译可能是一种新的无害的高特异性治疗方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

Blocking IRES-mediated translation pathway as a new method to treat Alzheimer’s disease

Blocking IRES-mediated translation pathway as a new method to treat Alzheimer’s disease

Scientists theorized that β-amyloid (Aβ) plaques and tau tangles are involved in the development of Alzheimer’s disease (AD), and amyloid precursor protein (APP) produces Aβ to trigger the disease process. However, the normal synaptic function of APP itself is not fully understood. Several findings cast APP as a potential key player in learning and memory under normal condition. Nevertheless, the regular operation of APP will be disrupted by abnormal accumulation of Aβ under cellular pathological conditions. Herein, there is a hypothesis that AD could be treated by attenuating APP synthesis during cellular pathophysiological stress. In virtue of a previous study, it was speculated that cells could not decrease APP synthesis via self-protection maybe because APP is synthesized via internal ribosome entry segment (IRES)-mediated translation. Consequently, the blockage of this translation might be a new inoffensive and high-level specificity treatment.

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