Brown Alan S
Department of Psychiatry, Columbia University College of Physicians and Surgeons, New York State Psychiatric Institute New York, NY, USA.
Front Psychiatry. 2011 Nov 23;2:63. doi: 10.3389/fpsyt.2011.00063. eCollection 2011.
We provide a brief review of findings supporting a role for prenatal infection in the etiology of schizophrenia. Our group and others have conducted birth cohort studies to address whether in utero exposure to infectious agents, prospectively documented by biomarker assays of archived maternal sera, and by detailed obstetric records, confer an increased risk of schizophrenia in adult offspring. Prenatal exposure to influenza, elevated toxoplasma antibody, rubella, genital-reproductive infections, and other infections have been associated with an increased risk of schizophrenia among offspring. Animal models have supported these epidemiologic findings by revealing that maternal immune activation causes phenotypes analogous to those found in patients with schizophrenia. Given that exposure to microbial agents are preventable or treatable, they suggest that interventions to diminish the incidence of infection during pregnancy have the potential to prevent an appreciable proportion of schizophrenia cases. Given the clear genetic component to schizophrenia, future studies should include investigations of interactions between prenatal infection and susceptibility genes in the pathogenesis of schizophrenia.
我们简要回顾了支持产前感染在精神分裂症病因学中起作用的研究结果。我们团队以及其他团队开展了出生队列研究，以探讨子宫内暴露于通过对存档的母体血清进行生物标志物检测以及详细产科记录前瞻性记录的传染原，是否会增加成年后代患精神分裂症的风险。产前暴露于流感、弓形虫抗体升高、风疹、生殖系统感染及其他感染与后代患精神分裂症风险增加有关。动物模型通过揭示母体免疫激活会导致类似于精神分裂症患者的表型，支持了这些流行病学研究结果。鉴于接触微生物制剂是可预防或可治疗的，这表明在孕期采取干预措施以减少感染发生率有可能预防相当一部分精神分裂症病例。鉴于精神分裂症有明确的遗传成分，未来研究应包括调查产前感染与易感性基因在精神分裂症发病机制中的相互作用。
