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本文引用的文献

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Epidemiology-driven neurodevelopmental animal models of schizophrenia.精神分裂症的流行病学驱动的神经发育动物模型。
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2
Developmental origins of health and disease: brief history of the approach and current focus on epigenetic mechanisms.健康与疾病的发育起源:该研究方法的简史及当前对表观遗传机制的关注
Semin Reprod Med. 2009 Sep;27(5):358-68. doi: 10.1055/s-0029-1237424. Epub 2009 Aug 26.
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Schizophrenia and birthplace of paternal and maternal grandfather in the Jerusalem perinatal cohort prospective study.耶路撒冷围产期队列前瞻性研究中精神分裂症与祖父和外祖父出生地的关系
Schizophr Res. 2009 Jun;111(1-3):23-31. doi: 10.1016/j.schres.2009.03.022. Epub 2009 Apr 9.
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Temporal association of cannabis use with symptoms in individuals at clinical high risk for psychosis.大麻使用与临床高危精神病个体症状的时间关联。
Schizophr Res. 2008 Dec;106(2-3):286-93. doi: 10.1016/j.schres.2008.08.008. Epub 2008 Sep 21.
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Acute maternal stress in pregnancy and schizophrenia in offspring: a cohort prospective study.孕期母亲急性应激与子代精神分裂症:一项队列前瞻性研究。
BMC Psychiatry. 2008 Aug 21;8:71. doi: 10.1186/1471-244X-8-71.
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Strong association of de novo copy number mutations with sporadic schizophrenia.新发拷贝数突变与散发性精神分裂症的强关联。
Nat Genet. 2008 Jul;40(7):880-5. doi: 10.1038/ng.162. Epub 2008 May 30.
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Imprinted genes and neuroendocrine function.印记基因与神经内分泌功能。
Front Neuroendocrinol. 2008 Jun;29(3):413-27. doi: 10.1016/j.yfrne.2007.12.001. Epub 2007 Dec 10.
8
Advanced paternal age associated with an elevated risk for schizophrenia in offspring in a Japanese population.在日本人群中,父亲年龄较大与后代患精神分裂症的风险升高有关。
Schizophr Res. 2005 Jul 15;76(2-3):337-42. doi: 10.1016/j.schres.2005.03.004. Epub 2005 Apr 21.
9
GABAA receptor beta3 subunit gene-deficient heterozygous mice show parent-of-origin and gender-related differences in beta3 subunit levels, EEG, and behavior.γ-氨基丁酸A型受体β3亚基基因缺陷杂合小鼠在β3亚基水平、脑电图及行为方面呈现出亲本来源和性别相关的差异。
Brain Res Dev Brain Res. 2005 Jun 30;157(2):150-61. doi: 10.1016/j.devbrainres.2005.03.014.
10
Paternal age and schizophrenia: a population based cohort study.父亲年龄与精神分裂症:一项基于人群的队列研究。
BMJ. 2004 Nov 6;329(7474):1070. doi: 10.1136/bmj.38243.672396.55. Epub 2004 Oct 22.

关键期与疾病的发育起源:精神分裂症的表观遗传学观点。

Critical periods and the developmental origins of disease: an epigenetic perspective of schizophrenia.

机构信息

New York University School of Medicine, Social and Psychiatric Initiatives (InSPIRES), New York, New York 10016, USA.

出版信息

Ann N Y Acad Sci. 2010 Sep;1204 Suppl(0):E8-13. doi: 10.1111/j.1749-6632.2010.05644.x.

DOI:10.1111/j.1749-6632.2010.05644.x
PMID:20840164
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4180658/
Abstract

Epigenetics holds promise to explain some puzzles concerning the risk and course of psychiatric disorders. Epigenetic information is essential as a set of operating instructions for the genome, which is heritable with DNA. The epigenetic regulation of gene expression can plausibly be influenced by the environment of one's ancestors, prenatal exposures, and by early life events. Some epigenetic mechanisms may alter neurophysiology throughout life by programming gene expression, perhaps in anticipation of certain life experiences. These epigenetic signals are only meta-stable and may be perturbed by stochastic events, errors, or by environmental toxins. This introduction considers the possibility that epigenetic change that may occur as paternal age advances or during fetal adversity may be causally related to the susceptibility for schizophrenia.

摘要

表观遗传学有望解释一些与精神疾病风险和病程相关的难题。表观遗传信息是基因组的一组操作指令,它与 DNA 一样具有遗传性。基因表达的表观遗传调控可以通过祖先的环境、产前暴露和生命早期事件来合理地影响。一些表观遗传机制可能通过编程基因表达来改变整个生命周期的神经生理学,也许是为了应对某些生活经历。这些表观遗传信号只是亚稳态的,可能会受到随机事件、错误或环境毒素的干扰。本引言考虑了这样一种可能性,即随着父亲年龄的增长或胎儿逆境时可能发生的表观遗传变化,可能与精神分裂症的易感性有关。