基于脑缺血模型的阿尔茨海默病病因分析

Ryszard Pluta
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摘要

阿尔茨海默病(AD)是世界上常见的痴呆症。尽管对包括淀粉样蛋白和 tau 蛋白在内的阿兹海默症病因的研究已有 100 多年的历史,但研究一直停滞不前,没有得出任何结论。此外,许多旨在寻找 AD 治疗方法的项目也未能取得突破性进展。因此,抗淀粉样蛋白和抗tau蛋白疗法在治疗AD方面的失败极大地影响了我们对该疾病病因的思考。这种情况促使一批研究人员开始关注缺血性脑病,因为缺血性脑病与注意力缺失症一样,主要表现为海马体的改变。在这种情况下,有人提出,脑缺血事件可能在促进淀粉样蛋白和 tau 蛋白在 AD 神经变性中发挥重要作用。在这篇综述中,我们总结了数年来关于脑缺血事件在 AD 发病中的作用的实验和临床研究。研究表明,缺血后脑神经变性过程中会出现典型的 AD 变化,即大脑和海马体进行性萎缩、淀粉样蛋白生成增加和 tau 蛋白改变。在缺血后的大脑中,弥漫性和衰老性淀粉样蛋白斑块以及神经纤维缠结的发展显示出 AD 的特征。上述数据清楚地表明,脑缺血后,蛋白质折叠发生改变,导致大量神经元死亡和神经元网络受损,从而引发具有 AD 表型的痴呆症。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
A Look at the Etiology of Alzheimer's Disease based on the Brain Ischemia Model.

Alzheimer's disease (AD) is the frequent form of dementia in the world. Despite over 100 years of research into the causes of AD, including amyloid and tau protein, the research has stalled and has not led to any conclusions. Moreover, numerous projects aimed at finding a cure for AD have also failed to achieve a breakthrough. Thus, the failure of anti-amyloid and anti-tau protein therapy to treat AD significantly influenced the way we began to think about the etiology of the disease. This situation prompted a group of researchers to focus on ischemic brain episodes, which, like AD, mostly present alterations in the hippocampus. In this context, it has been proposed that cerebral ischemic incidents may play a major role in promoting amyloid and tau protein in neurodegeneration in AD. In this review, we summarized the experimental and clinical research conducted over several years on the role of ischemic brain episodes in the development of AD. Studies have shown changes typical of AD in the course of brain neurodegeneration post-ischemia, i.e., progressive brain and hippocampal atrophy, increased amyloid production, and modification of tau protein. In the post-ischemic brain, the diffuse and senile amyloid plaques and the development of neurofibrillary tangles characteristic of AD were revealed. The above data evidently showed that after brain ischemia, there are modifications in protein folding, leading to massive neuronal death and damage to the neuronal network, which triggers dementia with the AD phenotype.

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