Neurodevelopmental model of schizophrenia: update 2012.
Neurodevelopmental model of schizophrenia: update 2012.
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DOI：
10.1038/mp.2012.23
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发表时间：
2012-12
影响因子：
11
通讯作者：
Gogtay, N.
中科院分区：
文献类型：
--
作者：
Rapoport, J. L.;Giedd, J. N.;Gogtay, N.
精神分裂症的神经发育模型，假定疾病是在疾病发作前数年开始的异常神经发育过程的终态，被广泛接受，并且长期以来一直是儿童期发作的神经精神障碍的主导。这篇选择性综述更新了我们2005年对最近影响精神分裂症神经发育模型或最有可能改变或扩展精神分裂症神经发育模型的研究的综述。纵向整体人群研究支持精神病的维度，而不是分类的概念。新的研究表明，胎盘病理学可能是未来产前高风险研究的关键措施。令人惊讶的是，常见和罕见的遗传变异在诊断上都是非特异性的，与精神分裂症相关的拷贝数变异（CNV）通常也与自闭症、癫痫和智力缺陷有关。大型死后基因表达研究和前瞻性发育多模态脑成像研究为未来的临床和高风险发育脑研究提供了关键数据。是否可以有更大的分子特异性的表型表征是目前激烈的研究和辩论的主题，是神经元表型使用人类多能诱导干细胞的可能性。生物学上的非特异性，如早期大脑发育的时间或性质，为广泛的预防性治疗提供了新的靶点。
The neurodevelopmental model of schizophrenia, which posits that the illness is the end state of abnormal neurodevelopmental processes that started years before the illness onset, is widely accepted, and has long been dominant for childhood-onset neuropsychiatric disorders. This selective review updates our 2005 review of recent studies that have impacted, or have the greatest potential to modify or extend, the neurodevelopmental model of schizophrenia. Longitudinal whole-population studies support a dimensional, rather than categorical, concept of psychosis. New studies suggest that placental pathology could be a key measure in future prenatal high-risk studies. Both common and rare genetic variants have proved surprisingly diagnostically nonspecific, and copy number variants (CNVs) associated with schizophrenia are often also associated with autism, epilepsy and intellectual deficiency. Large post-mortem gene expression studies and prospective developmental multi-modal brain imaging studies are providing critical data for future clinical and high-risk developmental brain studies. Whether there can be greater molecular specificity for phenotypic characterization is a subject of current intense study and debate, as is the possibility of neuronal phenotyping using human pluripotent-inducible stem cells. Biological nonspecificity, such as in timing or nature of early brain development, carries the possibility of new targets for broad preventive treatments.
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影响因子：
1.7
作者：
Carpenter DM;Tang CY;Friedman JI;Hof PR;Stewart DG;Buchsbaum MS;Harvey PD;Gorman JG;Davis KL
通讯作者：
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影响因子：
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作者：
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作者：
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作者：
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通讯作者：
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影响因子：
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作者：
Arseneault, L;Cannon, M;Moffitt, TE
通讯作者：
Moffitt, TE