Monji Akira, Kato Takahiro, Kanba Shigenobu
Department of Neuropsychiatry, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Psychiatry Clin Neurosci. 2009 Jun;63(3):257-65. doi: 10.1111/j.1440-1819.2009.01945.x.
The etiology of schizophrenia remains unclear, while there has been a growing amount of evidence for the neuroinflammation and immunogenetics, which are characterized by an increased serum concentration of several pro-inflammatory cytokines. Despite the fact that microglia comprise only <10% of the total brain cells, microglia respond rapidly to even minor pathological changes in the brain and may contribute directly to the neuronal degeneration by producing various pro-inflammatory cytokines and free radicals. In many aspects, the neuropathology of schizophrenia has recently been reported to be closely associatedwith microglial activation. Previous studies have shown the inhibitory effects of some typical/atypical antipsychotics on the release of inflammatory cytokines and free radicals from activated microglia, both of which have recently been known to cause a decrease in neurogenesis as well as white matter abnormalities in the brains of patients with schizophrenia. The microglia hypothesis of schizophrenia may shed new light on the therapeutic strategy for schizophrenia.
精神分裂症的病因仍不清楚,而神经炎症和免疫遗传学方面的证据越来越多,其特征是几种促炎细胞因子的血清浓度升高。尽管小胶质细胞仅占脑内细胞总数的不到10%,但小胶质细胞对脑内即使是轻微的病理变化也会迅速做出反应,并可能通过产生各种促炎细胞因子和自由基直接导致神经元变性。在许多方面,最近有报道称精神分裂症的神经病理学与小胶质细胞激活密切相关。先前的研究表明,一些典型/非典型抗精神病药物对激活的小胶质细胞释放炎性细胞因子和自由基具有抑制作用,最近人们发现这两者都会导致精神分裂症患者脑内神经发生减少以及白质异常。精神分裂症的小胶质细胞假说可能为精神分裂症的治疗策略提供新的思路。