Department of Psychiatry and Psychotherapy, Ludwig Maximilian University, Munich, Germany.
J Psychopharmacol. 2012 May;26(5 Suppl):33-41. doi: 10.1177/0269881111431622. Epub 2012 Apr 2.
This non-systematic review of the literature summarizes the evidence that inflammation plays a major role in the psychopathology of schizophrenia and in the mechanisms that contribute to physical ill health that is commonly associated with schizophrenia. The impact of prenatal infections on the developing brain, the possible genetic link between the human lymphocyte antigen gene, inflammation, heart disease and diabetes, together with the increase in pro-inflammatory cytokines in the blood and cerebrospinal fluid provide convincing evidence that inflammation is a major factor in the pathology of this disorder. The changes in immune-related markers and specific neurotransmitters associated with the positive symptoms of schizophrenia are described. In addition, the possible mechanism whereby structural changes occur in the brain is associated with the neurotoxic effects of pro-inflammatory cytokines, together with the neurotoxic metabolites from the tryptophan-kynurenine pathway that is activated by pro-inflammatory cytokines, is also discussed. The role of effective antipsychotic drug treatment in attenuating the inflammatory response is described. However, evidence is limited regarding the causal connection between atypical antipsychotic drugs and the changes in glucose and lipid metabolism that could trigger the onset of physical ill health, including diabetes and heart disease. Indeed, there is evidence that there is a metabolic predisposition to diabetes in patients with schizophrenia that is exacerbated by obesity and thereby contributes to cardiovascular disease and other co-morbid illnesses. It is concluded that the effects of inflammatory mediators on the brain causally contribute to the pathology of schizophrenia and the ill health that accompanies the disorder.
这篇文献的非系统性综述总结了炎症在精神分裂症的精神病理学以及导致与精神分裂症相关的身体不健康的机制中起着重要作用的证据。产前感染对大脑发育的影响、人类淋巴细胞抗原基因、炎症、心脏病和糖尿病之间可能存在的遗传联系，以及血液和脑脊液中促炎细胞因子的增加，都提供了令人信服的证据，证明炎症是这种疾病发病机制的一个主要因素。本文描述了与精神分裂症阳性症状相关的免疫相关标志物和特定神经递质的变化。此外，还讨论了与促炎细胞因子的神经毒性作用以及由促炎细胞因子激活的色氨酸-犬尿氨酸途径的神经毒性代谢物相关的大脑结构变化的可能机制。还描述了有效抗精神病药物治疗在减轻炎症反应中的作用。然而，关于非典型抗精神病药物与葡萄糖和脂质代谢变化之间的因果关系的证据有限，这些变化可能引发身体不健康，包括糖尿病和心脏病。事实上，有证据表明，精神分裂症患者存在糖尿病的代谢易感性，肥胖会使其恶化，从而导致心血管疾病和其他合并症。总之，炎症介质对大脑的影响是导致精神分裂症发病机制和伴随该疾病的身体不健康的原因。
