Koenig James I, Kirkpatrick Brian, Lee Paul
Maryland Psychiatric Research Center, Department of Psychiatry, University of Maryland School of Medicine, Baltimore, MD 21228, USA.
Neuropsychopharmacology. 2002 Aug;27(2):309-18. doi: 10.1016/S0893-133X(01)00396-7.
While genetic factors play a role in the etiology of schizophrenia, environmental factors contribute to the etiology of the disorder as well. If a woman is exposed during the second trimester of gestation to stressors such as the death of a loved one, influenza infection, or natural and man-made disasters, her baby has an increased risk of developing schizophrenia later in life. A common mechanism may mediate the effects of these diverse risk factors: a stress response during a restricted period of gestation may affect fetal brain development and, given the appropriate genetic predisposition, result in schizophrenia in adult life. Findings in animals exposed to prenatal stress strengthen the hypothesis that exposure to high glucocorticoid levels and/or other components of the stress response increases the risk of schizophrenia. These clinical and preclinical studies could be used to develop hypotheses that could then be tested in patients with schizophrenia.
虽然遗传因素在精神分裂症的病因中起作用，但环境因素也对该疾病的病因有影响。如果一名女性在妊娠中期暴露于诸如亲人死亡、流感感染或自然及人为灾难等应激源下，她的孩子日后患精神分裂症的风险会增加。一种常见机制可能介导这些不同风险因素的影响：妊娠特定时期的应激反应可能影响胎儿大脑发育，并且在有适当遗传易感性的情况下，导致成年后患精神分裂症。暴露于产前应激的动物研究结果强化了这样的假说，即暴露于高糖皮质激素水平和/或应激反应的其他成分会增加患精神分裂症的风险。这些临床和临床前研究可用于提出假说，然后在精神分裂症患者中进行检验。
