Prenatal infection as a risk factor for schizophrenia
Prenatal infection as a risk factor for schizophrenia
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DOI：
10.1093/schbul/sbj052
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发表时间：
2006-04-01
影响因子：
6.6
通讯作者：
Brown, AS
中科院分区：
文献类型：
--
作者：
Brown, AS
越来越多的证据表明，产前暴露于感染有助于精神分裂症的病因。出生队列研究利用前瞻性获得的感染和免疫生物标志物血清学检测数据，推进了这一研究路线。这些研究为这一假设提供了进一步的支持，并允许调查与精神分裂症风险有关的新的传染性病原体。与精神分裂症相关的产前感染包括风疹、流感和弓形虫病。母体细胞因子，包括白细胞介素-8，也显着增加怀孕引起精神分裂症的情况下。虽然这些发现的复制是必需的，这一机构的工作可能最终有重要意义的预防精神分裂症，阐述这种疾病的致病机制，并调查基因与环境的相互作用。
Accumulating evidence suggests that prenatal exposure to infection contributes to the etiology of schizophrenia. This line of investigation has been advanced by birth cohort studies that utilize prospectively acquired data from serologic assays for infectious and immune biomarkers. These investigations have provided further support for this hypothesis and permitted the investigation of new infectious pathogens in relation to schizophrenia risk. Prenatal infections that have been associated with schizophrenia include rubella, influenza, and toxoplasmosis. Maternal cytokines, including interleukin-8, are also significantly increased in pregnancies giving rise to schizophrenia cases. Although replication of these findings is required, this body of work may ultimately have important implications for the prevention of schizophrenia, the elaboration of pathogenic mechanisms in this disorder, and investigations of gene-environment interactions.