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精神分裂症的基因、基因表达与神经病理学:论它们的趋同性问题。

Schizophrenia genes, gene expression, and neuropathology: on the matter of their convergence.

作者信息

Harrison P J, Weinberger D R

机构信息

Department of Psychiatry, University of Oxford, Warneford Hospital, Oxford, UK.

出版信息

Mol Psychiatry. 2005 Jan;10(1):40-68; image 5. doi: 10.1038/sj.mp.4001558.

Abstract

This review critically summarizes the neuropathology and genetics of schizophrenia, the relationship between them, and speculates on their functional convergence. The morphological correlates of schizophrenia are subtle, and range from a slight reduction in brain size to localized alterations in the morphology and molecular composition of specific neuronal, synaptic, and glial populations in the hippocampus, dorsolateral prefrontal cortex, and dorsal thalamus. These findings have fostered the view of schizophrenia as a disorder of connectivity and of the synapse. Although attractive, such concepts are vague, and differentiating primary events from epiphenomena has been difficult. A way forward is provided by the recent identification of several putative susceptibility genes (including neuregulin, dysbindin, COMT, DISC1, RGS4, GRM3, and G72). We discuss the evidence for these and other genes, along with what is known of their expression profiles and biological roles in brain and how these may be altered in schizophrenia. The evidence for several of the genes is now strong. However, for none, with the likely exception of COMT, has a causative allele or the mechanism by which it predisposes to schizophrenia been identified. Nevertheless, we speculate that the genes may all converge functionally upon schizophrenia risk via an influence upon synaptic plasticity and the development and stabilization of cortical microcircuitry. NMDA receptor-mediated glutamate transmission may be especially implicated, though there are also direct and indirect links to dopamine and GABA signalling. Hence, there is a correspondence between the putative roles of the genes at the molecular and synaptic levels and the existing understanding of the disorder at the neural systems level. Characterization of a core molecular pathway and a 'genetic cytoarchitecture' would be a profound advance in understanding schizophrenia, and may have equally significant therapeutic implications.

摘要

本综述批判性地总结了精神分裂症的神经病理学和遗传学、它们之间的关系,并对其功能趋同进行了推测。精神分裂症的形态学关联较为微妙,范围从脑容量略有减少到海马体、背外侧前额叶皮质和背侧丘脑特定神经元、突触和神经胶质细胞群的形态和分子组成的局部改变。这些发现促使人们将精神分裂症视为一种连接性和突触紊乱疾病。尽管这些概念很有吸引力,但却很模糊,区分原发性事件和附带现象一直很困难。最近鉴定出的几个假定的易感基因(包括神经调节蛋白、失调素、儿茶酚-O-甲基转移酶、精神分裂症相关基因1、RGS4、代谢型谷氨酸受体3和G72)为解决这一问题提供了一条途径。我们讨论了这些基因和其他基因的证据,以及它们在大脑中的表达谱和生物学作用,以及它们在精神分裂症中可能如何改变。现在有几个基因的证据很充分。然而,除了儿茶酚-O-甲基转移酶可能是个例外,尚未确定任何一个基因的致病等位基因或其导致精神分裂症的机制。尽管如此,我们推测这些基因可能都通过影响突触可塑性以及皮质微回路的发育和稳定在功能上汇聚到精神分裂症风险上。NMDA受体介导的谷氨酸传递可能特别涉及其中,尽管也存在与多巴胺和GABA信号传导的直接和间接联系。因此,这些基因在分子和突触水平上的假定作用与目前对该疾病在神经系统水平上的理解之间存在对应关系。确定核心分子途径和“遗传细胞结构”将是理解精神分裂症的一项重大进展,并且可能具有同样重要的治疗意义。

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