Prenatal infection and schizophrenia: a review of epidemiologic and translational studies.
Prenatal infection and schizophrenia: a review of epidemiologic and translational studies.
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DOI：
10.1176/appi.ajp.2009.09030361
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发表时间：
2010-03
期刊：
影响因子：
--
通讯作者：
Derkits EJ
中科院分区：
文献类型：
--
作者：
Brown AS;Derkits EJ
来自流行病学、临床和临床前研究的新兴文献提供了证据，表明妊娠期感染导致精神分裂症的病因。近年来，这些研究已经从根据人群流行病确定感染的生态设计，转向利用个体妊娠中可靠的生物标志物进行的调查。这些研究记录了似乎与精神分裂症风险升高相关的特定候选感染。受这项工作启发，母体免疫激活的动物模型揭示了有趣的发现，表明行为、神经化学和神经生理学异常与精神分裂症的观察结果一致。在人类和动物的平行研究中，研究人员正在努力揭示子宫内感染导致精神分裂症风险的细胞和分子机制。在这篇综述中，作者讨论并批判性地评估了关于子宫内感染和精神分裂症的流行病学文献，总结了母体免疫激活的新兴动物模型，并讨论了子宫内感染改变神经发育、可能增加精神分裂症易感性的假定独特和常见机制。子宫内感染与遗传变异之间相互作用的例子说明了这项工作有望促进精神分裂症遗传研究中易感位点的识别。然后，作者详细阐述了这项工作可能产生的影响，包括使用预防措施来降低精神分裂症的发病率。最后，他们讨论了旨在解决该研究领域当前挑战的新方法。
An emerging literature from epidemiologic, clinical, and preclinical investigations has provided evidence that gestational exposure to infection contributes to the etiology of schizophrenia. In recent years, these studies have moved from ecologic designs, which ascertain infection based on epidemics in populations, to investigations that have capitalized on reliable biomarkers in individual pregnancies. These studies have documented specific candidate infections that appear to be associated with an elevated risk of schizophrenia. Animal models of maternal immune activation inspired by this work have revealed intriguing findings indicating behavioral, neurochemical, and neurophysiologic abnormalities consistent with observations in schizophrenia. In parallel studies in humans and animals, investigators are working to uncover the cellular and molecular mechanisms by which in utero exposure to infection contributes to schizophrenia risk. In this review, the authors discuss and critically evaluate the epidemiologic literature on in utero exposure to infection and schizophrenia, summarize emerging animal models of maternal immune activation, and discuss putative unique and common mechanisms by which in utero exposure to infection alters neurodevelopment, potentially increasing susceptibility to schizophrenia. The promise of this work for facilitating the identification of susceptibility loci in genetic studies of schizophrenia is illustrated by examples of interaction between in utero exposure to infection and genetic variants. The authors then elaborate on possible implications of this work, including the use of preventive measures for reducing the incidence of schizophrenia. Finally, they discuss new approaches aimed at addressing current challenges in this area of research.
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DOI：
10.1523/jneurosci.1815-08.2008
发表时间：
2008-07-02
期刊：
The Journal of neuroscience : the official journal of the Society for Neuroscience
影响因子：
--
作者：
Chen YJ;Johnson MA;Lieberman MD;Goodchild RE;Schobel S;Lewandowski N;Rosoklija G;Liu RC;Gingrich JA;Small S;Moore H;Dwork AJ;Talmage DA;Role LW
通讯作者：
Role LW
影响因子：
17.7
作者：
Clarke, Mary C.;Tanskanen, Antti;Cannon, Mary
通讯作者：
Cannon, Mary
影响因子：
15.1
作者：
Buka, SL;Tsuang, MT;Yolken, RH
通讯作者：
Yolken, RH
影响因子：
3.3
作者：
Babovic, D.;O'Tuathaigh, C. M.;Waddington, J. L.
通讯作者：
Waddington, J. L.
影响因子：
10.6
作者：
Bo Mortensen, Preben;Norgaard-Pedersen, Bent;Yolken, Robert H.
通讯作者：
Yolken, Robert H.