阿尔茨海默病的白质损伤:少突胶质细胞的贡献

IF 1.8 4区 医学 Q3 CLINICAL NEUROLOGY
Jinyu Zhou, Peng Zhang, Bo Zhang, Yuhan Kong
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引用次数: 0

摘要

阿尔茨海默病(AD)是一种与年龄相关的神经退行性疾病,严重影响人们的生活质量,是一个全球性的健康问题。影响阿尔茨海默病发病和发展的因素很多,但该病的具体机制尚不清楚。大多数研究都集中在中枢神经系统(CNS)的神经元和灰质上,但并没有找到有效的治疗方法。最近,越来越多的研究开始关注白质(WM)。磁共振成像和病理学研究显示,在注意力缺失症的发展过程中,白质会出现不同程度的异常。髓鞘是中枢神经系统白质的主要组成部分,它包裹并绝缘轴突,以确保快速动作电位的传导和轴突的完整性。中枢神经系统一个或多个区域的轴突、少突胶质细胞(OLs)和髓鞘逐渐退化是WM损伤的特征。直到最近,少突胶质细胞对注意力缺失症进展的贡献在很大程度上一直被忽视。OLs是髓鞘生成不可或缺的部分,OLs的增殖和分化是AD的早期特征,为临床前诊断和治疗提供了一个很有前景的靶点。然而,尽管取得了一些进展,但OLs对AD起作用的关键机制仍不清楚。鉴于医疗负担沉重,更好地了解AD的病理生理机制至关重要。本综述全面总结了有关AD中WM异常的研究结果,并探讨了OL祖细胞与AD发病机制之间的关系。最后,还讨论了潜在的分子机制和未来的研究方向。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

White Matter Damage in Alzheimer's Disease: Contribution of Oligodendrocytes.

White Matter Damage in Alzheimer's Disease: Contribution of Oligodendrocytes.

White Matter Damage in Alzheimer's Disease: Contribution of Oligodendrocytes.

Alzheimer's disease (AD) is an age-related neurodegenerative disease, seriously influencing the quality of life and is a global health problem. Many factors affect the onset and development of AD, but specific mechanisms underlying the disease are unclear. Most studies investigating AD have focused on neurons and the gray matter in the central nervous system (CNS) but have not led to effective treatments. Recently, an increasing number of studies have focused on the white matter (WM). Magnetic resonance imaging and pathology studies have shown different degrees of WM abnormality during the progression of AD. Myelin sheaths, the main component of WM in the CNS, wrap and insulate axons to ensure conduction of the rapid action potential and axonal integrity. WM damage is characterized by progressive degeneration of axons, oligodendrocytes (OLs), and myelin in one or more areas of the CNS. The contributions of OLs to AD progression have, until recently, been largely overlooked. OLs are integral to myelin production, and the proliferation and differentiation of OLs, an early characteristic of AD, provide a promising target for preclinical diagnosis and treatment. However, despite some progress, the key mechanisms underlying the contributions of OLs to AD remain unclear. Given the heavy burden of medical treatment, a better understanding of the pathophysiological mechanisms underlying AD is vital. This review comprehensively summarize the results on WM abnormalities in AD and explores the relationship between OL progenitor cells and the pathogenesis of AD. Finally, the underlying molecular mechanisms and potential future research directions are discussed.

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来源期刊
Current Alzheimer research
Current Alzheimer research 医学-神经科学
CiteScore
4.00
自引率
4.80%
发文量
64
审稿时长
4-8 weeks
期刊介绍: Current Alzheimer Research publishes peer-reviewed frontier review, research, drug clinical trial studies and letter articles on all areas of Alzheimer’s disease. This multidisciplinary journal will help in understanding the neurobiology, genetics, pathogenesis, and treatment strategies of Alzheimer’s disease. The journal publishes objective reviews written by experts and leaders actively engaged in research using cellular, molecular, and animal models. The journal also covers original articles on recent research in fast emerging areas of molecular diagnostics, brain imaging, drug development and discovery, and clinical aspects of Alzheimer’s disease. Manuscripts are encouraged that relate to the synergistic mechanism of Alzheimer''s disease with other dementia and neurodegenerative disorders. Book reviews, meeting reports and letters-to-the-editor are also published. The journal is essential reading for researchers, educators and physicians with interest in age-related dementia and Alzheimer’s disease. Current Alzheimer Research provides a comprehensive ''bird''s-eye view'' of the current state of Alzheimer''s research for neuroscientists, clinicians, health science planners, granting, caregivers and families of this devastating disease.
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