The environment and susceptibility to schizophrenia.
The environment and susceptibility to schizophrenia.
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DOI：
10.1016/j.pneurobio.2010.09.003
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发表时间：
2011-01
影响因子：
6.7
通讯作者：
Brown AS
中科院分区：
文献类型：
--
作者：
Brown AS
本文对精神分裂症中环境因素的假定作用进行综述和综合。从最近的研究积累的证据表明，环境暴露可能发挥更重要的作用，这种疾病的发病机制比以前认为的。这种不断扩大的知识基础主要是流行病学研究方法（包括出生队列调查）和临床前研究方法（受不断发展的环境暴露动物模型文献的启发）改进的结果。本文共分为四个部分。首先，回顾精神分裂症的描述性流行病学。这包括对发病率、患病率和城乡、邻里、流动人口和出生季节等指标的差异以及时间趋势的一般研究。在第二部分中，我们讨论了环境危险因素在胎儿和围产期的作用，这些因素包括感染[如风疹，流感，弓形虫（T。弓形虫），单纯疱疹病毒2型（HSV-2）]，营养缺乏（例如，饥饿、叶酸、铁、维生素D）、父亲年龄、胎儿/新生儿缺氧和其他产科损伤和并发症、母体压力和其他暴露[例如铅、恒河猴（Rh）不相容性、母体压力]。其他假定的神经发育决定因素，包括大麻，社会经济地位，创伤，以及儿童和青少年时期的感染也包括在内。在第三部分中，这些研究结果进行了综合，并讨论了它们对预防和揭示生物学机制的影响，包括氧化应激，细胞凋亡和炎症。包括母体免疫激活在内的动物模型已经产生了证据，表明这些暴露导致的大脑和行为表型与在精神分裂症患者中观察到的结果类似。在最后一节中，未来的研究，包括新的，更大的，更严格的流行病学调查，研究转化和临床神经科学，基因-环境相互作用，表观遗传学，发展轨迹和脆弱性的窗口，详细说明。这些研究旨在确认观察到的风险因素，确定新的环境暴露，阐明发育机制，并进一步阐明在没有这些综合方法的情况下可能无法确定的基因和暴露。精神分裂症的环境因素的研究可能有重要的意义，这种疾病的原因和预防的识别，并提供了潜在的补充和完善，现有的努力解释神经发育模型。
In the present article the putative role of environmental factors in schizophrenia is reviewed and synthesized. Accumulating evidence from recent studies suggests that environmental exposures may play a more significant role in the etiopathogenesis of this disorder than previously thought. This expanding knowledge base is largely a consequence of refinements in the methodology of epidemiologic studies, including birth cohort investigations, and in preclinical research that has been inspired by the evolving literature on animal models of environmental exposures. This paper is divided into four sections. In the first, the descriptive epidemiology of schizophrenia is reviewed. This includes general studies on incidence, prevalence, and differences in these measures by urban–rural, neighborhood, migrant, and season of birth status, as well as time trends. In the second section, we discuss the contribution of environmental risk factors acting during fetal and perinatal life; these include infections [e.g. rubella, influenza, Toxoplasma gondii (T. gondii), herpes simplex virus type 2 (HSV-2)], nutritional deficiencies (e.g., famine, folic acid, iron, vitamin D), paternal age, fetal/neonatal hypoxic and other obstetric insults and complications, maternal stress and other exposures [e.g. lead, rhesus (Rh) incompatibility, maternal stress]. Other putative neurodevelopmental determinants, including cannabis, socioeconomic status, trauma, and infections during childhood and adolescence are also covered. In the third section, these findings are synthesized and their implications for prevention and uncovering biological mechanisms, including oxidative stress, apoptosis, and inflammation, are discussed. Animal models, including maternal immune activation, have yielded evidence suggesting that these exposures cause brain and behavioral phenotypes that are analogous to findings observed in patients with schizophrenia. In the final section, future studies including new, larger, and more rigorous epidemiologic investigations, and research on translational and clinical neuroscience, gene–environment interactions, epigenetics, developmental trajectories and windows of vulnerability, are elaborated upon. These studies are aimed at confirming observed risk factors, identifying new environmental exposures, elucidating developmental mechanisms, and shedding further light on genes and exposures that may not be identified in the absence of these integrated approaches. The study of environmental factors in schizophrenia may have important implications for the identification of causes and prevention of this disorder, and offers the potential to complement, and refine, existing efforts on explanatory neurodevelopmental models.
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影响因子：
--
作者：
Amminger, G. Paul;Schafer, Miriam R.;Berger, Gregor E.
通讯作者：
Berger, Gregor E.
DOI：
10.1016/0736-5748(86)90019-5
发表时间：
1986-01-01
影响因子：
1.8
作者：
BENSHACHAR, D;ASHKENAZI, R;YOUDIM, MBH
通讯作者：
YOUDIM, MBH
影响因子：
6.6
作者：
BENES, FM
通讯作者：
BENES, FM
影响因子：
10.6
作者：
Arion, Dominique;Unger, Travis;Mirnics, Karoly
通讯作者：
Mirnics, Karoly
影响因子：
10.5
作者：
Allardyce, J;Gilmour, H;McCreadie, RG
通讯作者：
McCreadie, RG