阿尔茨海默病少突胶质细胞祖细胞:从生理学到病理学。

IF 10.8 1区 医学 Q1 NEUROSCIENCES Translational Neurodegeneration Pub Date : 2023-11-14 DOI:10.1186/s40035-023-00385-7
Peibin Zou, Chongyun Wu, Timon Cheng-Yi Liu, Rui Duan, Luodan Yang
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引用次数: 0

摘要

少突胶质细胞祖细胞(OPCs)在髓磷脂形成和吞噬中起关键作用,与邻近细胞沟通,并有助于血脑屏障(BBB)的完整性。然而,在阿尔茨海默病(AD)的病理情况下,大脑的微环境发生了有害的变化,显著影响OPCs及其功能。从OPC的功能开始,我们深入探讨了OPC向产生髓磷脂的少突胶质细胞的转化,与中枢神经系统(CNS)中其他细胞复杂的信号相互作用,以及吞噬的奇妙过程,这些过程影响OPC的功能和影响中枢神经系统的稳态。此外,我们讨论了OPCs在血脑屏障形成中的重要作用,并强调了OPCs在形成cns保护性屏障中的重要贡献。在AD的背景下,讨论了大脑局部微环境的恶化,主要集中在神经炎症,氧化应激和有毒蛋白的积累。这些有害的变化扰乱了大脑的微妙平衡,影响了OPCs的再生能力,损害了髓磷脂的完整性。病理条件下,OPCs在迁移和增殖方面发生显著改变,导致分化受损,产生成熟少突胶质细胞的能力降低。此外,髓鞘变性和形成在AD中变得越来越活跃,有助于进行性神经变性。最后,我们总结了目前针对OPCs治疗AD的治疗方法。激活OPC衰老,调节信号通路以增强OPC分化,以及探索其他潜在的治疗途径有望减轻AD对OPC和中枢神经系统功能的影响。综上所述,本综述强调了OPCs在中枢神经系统功能中不可或缺的作用及其在AD发病机制中的作用。OPCs与AD脑微环境之间复杂的相互作用凸显了神经退行性疾病的复杂性。病理条件下对OPCs的研究为针对OPCs和促进神经变性的创新治疗策略提供了基础。未来的研究将促进我们对神经退行性疾病的理解和管理,最终为阿尔茨海默病和相关疾病患者提供有效治疗和改善生活质量的希望。
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Oligodendrocyte progenitor cells in Alzheimer's disease: from physiology to pathology.

Oligodendrocyte progenitor cells (OPCs) play pivotal roles in myelin formation and phagocytosis, communicating with neighboring cells and contributing to the integrity of the blood-brain barrier (BBB). However, under the pathological circumstances of Alzheimer's disease (AD), the brain's microenvironment undergoes detrimental changes that significantly impact OPCs and their functions. Starting with OPC functions, we delve into the transformation of OPCs to myelin-producing oligodendrocytes, the intricate signaling interactions with other cells in the central nervous system (CNS), and the fascinating process of phagocytosis, which influences the function of OPCs and affects CNS homeostasis. Moreover, we discuss the essential role of OPCs in BBB formation and highlight the critical contribution of OPCs in forming CNS-protective barriers. In the context of AD, the deterioration of the local microenvironment in the brain is discussed, mainly focusing on neuroinflammation, oxidative stress, and the accumulation of toxic proteins. The detrimental changes disturb the delicate balance in the brain, impacting the regenerative capacity of OPCs and compromising myelin integrity. Under pathological conditions, OPCs experience significant alterations in migration and proliferation, leading to impaired differentiation and a reduced ability to produce mature oligodendrocytes. Moreover, myelin degeneration and formation become increasingly active in AD, contributing to progressive neurodegeneration. Finally, we summarize the current therapeutic approaches targeting OPCs in AD. Strategies to revitalize OPC senescence, modulate signaling pathways to enhance OPC differentiation, and explore other potential therapeutic avenues are promising in alleviating the impact of AD on OPCs and CNS function. In conclusion, this review highlights the indispensable role of OPCs in CNS function and their involvement in the pathogenesis of AD. The intricate interplay between OPCs and the AD brain microenvironment underscores the complexity of neurodegenerative diseases. Insights from studying OPCs under pathological conditions provide a foundation for innovative therapeutic strategies targeting OPCs and fostering neurodegeneration. Future research will advance our understanding and management of neurodegenerative diseases, ultimately offering hope for effective treatments and improved quality of life for those affected by AD and related disorders.

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来源期刊
Translational Neurodegeneration
Translational Neurodegeneration Neuroscience-Cognitive Neuroscience
CiteScore
19.50
自引率
0.80%
发文量
44
审稿时长
10 weeks
期刊介绍: Translational Neurodegeneration, an open-access, peer-reviewed journal, addresses all aspects of neurodegenerative diseases. It serves as a prominent platform for research, therapeutics, and education, fostering discussions and insights across basic, translational, and clinical research domains. Covering Parkinson's disease, Alzheimer's disease, and other neurodegenerative conditions, it welcomes contributions on epidemiology, pathogenesis, diagnosis, prevention, drug development, rehabilitation, and drug delivery. Scientists, clinicians, and physician-scientists are encouraged to share their work in this specialized journal tailored to their fields.
期刊最新文献
α-Synuclein seeding amplification assays for diagnosing synucleinopathies: an innovative tool in clinical implementation. Cellular senescence in Alzheimer's disease: from physiology to pathology. Critical role of ROCK1 in AD pathogenesis via controlling lysosomal biogenesis and acidification. TRPV1 alleviates APOE4-dependent microglial antigen presentation and T cell infiltration in Alzheimer's disease. A tumorigenicity evaluation platform for cell therapies based on brain organoids.
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