Central nervous system (CNS) therapeutics based on the theoretical framework of neuroinflammation have only barely succeeded. We argue that a problem may be the wrong use of the term ‘neuroinflammation’ as a distinct nosological entity when, based on recent evidence, it may not explain CNS disease pathology. Indeed, the terms ‘neuroinflammation’ and ‘glia’ could be obsolete. First, unbiased molecular profiling of CNS cell populations and individual cells reveals striking phenotypic heterogeneity in health and disease. Second, astrocytes, microglia, oligodendrocytes, and NG2 cells may contribute to higher-brain functions by performing actions beyond housekeeping. We propose that CNS diseases be viewed as failed circuits caused in part by disease-specific dysfunction of cells traditionally called ‘glia’, and hence, favor therapies promoting their functional recovery.

基于神经炎症理论框架的中枢神经系统（CNS）治疗方法几乎没有成功。我们认为，一个问题可能是基于最近的证据无法正确解释中枢神经系统疾病的病理学，而将“神经炎症”一词误认为是独特的疾病学实体。实际上，术语“神经炎症”和“神经胶质”可能已过时。首先，中枢神经系统细胞群和单个细胞的无偏分子分析揭示了健康和疾病中显着的表型异质性。其次，星形胶质细胞，小胶质细胞，少突胶质细胞和NG2细胞可能通过执行除管家之外的动作来促进大脑的功能。我们建议将中枢神经系统疾病视为电路衰竭，部分原因是传统上称为“神经胶质细胞”的特定疾病的细胞功能障碍所致，因此，