Dysfunctional glial cells play a pre-eminent role in schizophrenia pathophysiology. Post-mortem studies have provided evidence for significantly decreased glial cell numbers in different brain regions of individuals with schizophrenia. Reduced glial cell numbers are most pronounced in oligodendroglia, but reduced astrocyte cell densities have also been reported. This review highlights that oligo- and astroglial deficits are a key histopathological feature in schizophrenia, distinct from typical changes seen in neurodegenerative disorders. Significant deficits of oligodendrocytes in schizophrenia may arise in two ways: (i) demise of mature functionally compromised oligodendrocytes; and (ii) lack of mature oligodendrocytes due to failed maturation of progenitor cells. We also analyse in detail the controversy regarding deficits of astrocytes. Regardless of their origin, glial cell deficits have several pathophysiological consequences. Among these, myelination deficits due to a reduced number of oligodendrocytes may be the most important factor, resulting in the disconnectivity between neurons and different brain regions observed in schizophrenia. When glial cells die, it appears to be through degeneration, a process which is basically reversible. Thus, therapeutic interventions that (i) help rescue glial cells (ii) or improve their maturation might be a viable option. Since antipsychotic treatment alone does not seem to prevent glial cell loss or maturation deficits, there is intense search for new therapeutic options. Current proposals range from the application of antidepressants and other chemical agents as well as physical exercise to engrafting healthy glial cells into brains of schizophrenia patients.

功能失调的神经胶质细胞在精神分裂症病理生理学中起着突出的作用。尸检研究提供了精神分裂症患者不同大脑区域的神经胶质细胞数量显着减少的证据。神经胶质细胞数量减少在少突胶质细胞中最为明显，但也报道了星形胶质细胞密度降低。本综述强调，少胶质细胞和星形胶质细胞缺陷是精神分裂症的一个关键组织病理学特征，与神经退行性疾病中的典型变化不同。精神分裂症中少突胶质细胞的显着缺陷可能以两种方式出现：（i） 功能受损的成熟少突胶质细胞死亡;（ii） 由于祖细胞成熟失败而缺乏成熟的少突胶质细胞。我们还详细分析了关于星形胶质细胞缺陷的争议。无论其来源如何，神经胶质细胞缺陷都有多种病理生理学后果。其中，由于少突胶质细胞数量减少而导致的髓鞘形成缺陷可能是最重要的因素，导致精神分裂症中观察到的神经元与不同大脑区域之间的脱节。当神经胶质细胞死亡时，它似乎是通过退化，这一过程基本上是可逆的。因此，（i） 帮助拯救神经胶质细胞 （ii） 或改善其成熟的治疗干预措施可能是一种可行的选择。由于单独的抗精神病药物治疗似乎不能防止神经胶质细胞丢失或成熟缺陷，因此人们正在紧张地寻找新的治疗选择。目前的建议范围从应用抗抑郁药和其他化学试剂以及体育锻炼到将健康的神经胶质细胞移植到精神分裂症患者的大脑中。