Laboratory of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Biomedicum, Karolinska Institutet, 17177 Stockholm, Sweden.
Laboratory of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Biomedicum, Karolinska Institutet, 17177 Stockholm, Sweden.
Trends Immunol. 2024 Oct;45(10):750-759. doi: 10.1016/j.it.2024.08.003. Epub 2024 Sep 24.
Neural cells in our central nervous system (CNS) have long been thought to be mere targets of neuroinflammatory events in neurodegenerative diseases such as multiple sclerosis (MS) or Alzheimer's disease. While glial populations such as microglia and astrocytes emerged as active responders and modifiers of pathological environments, oligodendroglia and neurons have been associated with altered homeostasis and eventual cell death. The advent of single-cell and spatial omics technologies has demonstrated transitions of CNS-resident glia, including oligodendroglia, into disease-associated (DA) states. Anchored in recent findings of their roles in MS, we propose that DA glia constitute key nexus of disease progression, with DA oligodendroglia contributing to the modulation of neuroinflammation in certain neurodegenerative diseases, constituting novel putative pharmacological targets for such pathologies.
我们中枢神经系统（CNS）中的神经细胞长期以来一直被认为是神经退行性疾病（如多发性硬化症（MS）或阿尔茨海默病）中神经炎症事件的单纯靶点。虽然神经胶质细胞群体（如小胶质细胞和星形胶质细胞）作为病理性环境的积极反应者和调节剂出现，但少突胶质细胞和神经元与改变的内稳态和最终细胞死亡有关。单细胞和空间组学技术的出现证明了中枢神经系统驻留的神经胶质细胞（包括少突胶质细胞）向疾病相关（DA）状态的转变。基于它们在 MS 中的作用的最新发现，我们提出 DA 神经胶质细胞构成疾病进展的关键枢纽，DA 少突胶质细胞有助于某些神经退行性疾病中神经炎症的调节，为这些疾病构成新的潜在药理学靶点。
