Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129, USA.
Department of Neurology, The University of Tokyo Graduate School of Medicine, Tokyo 113-8654, Japan.
Int J Mol Sci. 2018 Jun 12;19(6):1743. doi: 10.3390/ijms19061743.
Even in adult brains, restorative mechanisms are still retained to maintain the microenvironment. Under the pathological conditions of central nervous system (CNS) diseases, several immature cells in the brain would be activated as a compensative response. As the concept of the neurovascular unit emphasizes, cell-cell interactions play important roles in this restorative process. White matter damage and oligodendrocyte loss are representative characteristics for many neurodegenerative diseases. In response to oligodendrocyte damage, residual oligodendrocyte precursor cells (OPCs) initiate their proliferation and differentiation for the purpose of remyelination. Although mechanisms of oligodendrogenesis and remyelination in CNS diseases are still mostly unknown and understudied, accumulated evidence now suggests that support from neighboring cells is necessary for OPC proliferation and differentiation. In this review, we first overview basic mechanisms of interaction between oligodendrocyte lineage cells and neighboring cells, and then introduce how oligodendrogenesis occurs under the conditions of neurodegenerative diseases, focusing on vascular cognitive impairment syndrome, Alzheimer’s disease, and multiple sclerosis.
即使在成人的大脑中，修复机制仍然保留以维持微环境。在中枢神经系统（CNS）疾病的病理条件下，大脑中的几种未成熟细胞会被激活作为代偿反应。正如神经血管单元的概念所强调的，细胞间的相互作用在这个修复过程中起着重要的作用。白质损伤和少突胶质细胞的丧失是许多神经退行性疾病的代表性特征。为了应对少突胶质细胞的损伤，残留的少突胶质前体细胞（OPC）会启动增殖和分化，以进行髓鞘修复。尽管 CNS 疾病中的少突胶质细胞发生和髓鞘修复的机制在很大程度上仍然未知且研究不足，但越来越多的证据表明，邻近细胞的支持对于 OPC 的增殖和分化是必要的。在这篇综述中，我们首先概述了少突胶质细胞谱系细胞与邻近细胞之间相互作用的基本机制，然后介绍了在神经退行性疾病条件下少突胶质细胞发生的情况，重点介绍血管性认知障碍综合征、阿尔茨海默病和多发性硬化症。
