The Interplay Between Accumulation of Amyloid-Beta and Tau Proteins, PANoptosis, and Inflammation in Alzheimer's Disease.

IF 3.3 4区医学 Q2 NEUROSCIENCES

NeuroMolecular Medicine Pub Date : 2024-12-29 DOI:10.1007/s12017-024-08815-z

Xianbo Zhuang, Jie Lin, Yamin Song, Ru Ban, Xin Zhao, Zhangyong Xia, Zheng Wang, Guifeng Zhang

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引用次数: 0

Abstract

Alzheimer's disease (AD) is a common progressive neurodegenerative disorder, and the vast majority of cases occur in elderly patients. Recently, the accumulation of Aβ and tau proteins has drawn considerable attention in AD research. This review explores the multifaceted interactions between these proteins and their contribution to the pathological landscape of AD, encompassing synaptic dysfunction, neuroinflammation, and PANoptosis. PANoptosis is a collective term for programmed cell death (PCD) modalities that encompass elements of apoptosis, pyroptosis, and necroptosis. The accumulation of Aβ peptides and tau proteins, along with the immune response in brain cells, may trigger PANoptosis, thus advancing the progression of the disease. Recent advancements in molecular imaging and genetics have provided deeper insights into the interactions between Aβ peptides, tau proteins, and the immune response. The review also discusses the role of mitochondrial dysregulation in AD. The exploration of the interplay between neurodegeneration, immune responses, and cell death offers promising avenues for the development of innovative treatments.

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淀粉样蛋白- β和Tau蛋白积累、泛光性痴呆和阿尔茨海默病炎症之间的相互作用。

阿尔茨海默病（AD）是一种常见的进行性神经退行性疾病，绝大多数病例发生在老年患者中。近年来，Aβ和tau蛋白的积累在AD研究中引起了相当大的关注。这篇综述探讨了这些蛋白之间多方面的相互作用及其对阿尔茨海默病病理图景的贡献，包括突触功能障碍、神经炎症和PANoptosis。PANoptosis是程序性细胞死亡（PCD）模式的统称，包括细胞凋亡、焦亡和坏死。β肽和tau蛋白的积累，以及脑细胞中的免疫反应，可能引发PANoptosis，从而促进疾病的进展。分子成像和遗传学的最新进展为Aβ肽、tau蛋白和免疫反应之间的相互作用提供了更深入的见解。本文还讨论了线粒体失调在AD中的作用。神经退行性疾病、免疫反应和细胞死亡之间相互作用的探索为创新治疗的发展提供了有希望的途径。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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来源期刊

NeuroMolecular Medicine 医学-神经科学

CiteScore

7.10

自引率

0.00%

发文量

审稿时长

>12 weeks

期刊介绍： NeuroMolecular Medicine publishes cutting-edge original research articles and critical reviews on the molecular and biochemical basis of neurological disorders. Studies range from genetic analyses of human populations to animal and cell culture models of neurological disorders. Emerging findings concerning the identification of genetic aberrancies and their pathogenic mechanisms at the molecular and cellular levels will be included. Also covered are experimental analyses of molecular cascades involved in the development and adult plasticity of the nervous system, in neurological dysfunction, and in neuronal degeneration and repair. NeuroMolecular Medicine encompasses basic research in the fields of molecular genetics, signal transduction, plasticity, and cell death. The information published in NEMM will provide a window into the future of molecular medicine for the nervous system.