Mitochondrial dysfunction in schizophrenia: With a focus on postmortem studies.
Mitochondrial dysfunction in schizophrenia: With a focus on postmortem studies.
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DOI：
10.1016/j.mito.2020.11.009
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发表时间：
2021-01
期刊：
影响因子：
4.4
通讯作者：
Roberts RC
中科院分区：
文献类型：
--
作者：
Roberts RC
在精神分裂症的许多脑异常中，有一些与线粒体功能有关，如氧化应激、能量代谢和突触功效。本文的目的是对线粒体结构和功能进行简要回顾，然后以解剖学为重点介绍精神分裂症死后大脑线粒体的异常。在多个精神分裂症队列中发现了各种线粒体基因表达的缺陷。复合物I和IV的活性降低是突出的，以及包括电子传递链复合物的单个亚基的异常水平。超微结构研究表明，线粒体的层，输入和细胞特异性减少。在皮质区，无论是灰质还是白色质，轴突终末、锥体神经元胞体和少突胶质细胞内的线粒体均较少。在尾状核和壳核中，线粒体数量与症状和症状严重程度相关。虽然星形胶质细胞中的线粒体数量减少，但少突胶质细胞中的线粒体较小。与对照组相比，精神分裂症患者的中脑核和黑质中的线粒体在密度、大小和结构完整性方面相似。线粒体产生ATP和钙缓冲在维持突触强度中是必不可少的，这些过程中的异常可能导致代谢降低和突触活性缺陷。少突胶质细胞中线粒体的缺失可能导致髓鞘病理学和脑中的连接障碍。在精神分裂症中，线粒体受到不同影响，这取决于脑区域、它们所处的细胞类型、亚细胞位置、治疗状态、治疗反应和主要症状。
Among the many brain abnormalities in schizophrenia are those related to mitochondrial functions such as oxidative stress, energy metabolism and synaptic efficacy. The aim of this paper is to provide a brief review of mitochondrial structure and function and then to present abnormalities in mitochondria in postmortem brain in schizophrenia with a focus on anatomy. Deficits in expression of various mitochondrial genes have been found in multiple schizophrenia cohorts. Decreased activity of complexes I and IV are prominent as well as abnormal levels of individual subunits that comprise the complexes of the electron transport chain. Ultrastructural studies have shown layer, input and cell specific decreases in mitochondria. In cortex, there are fewer mitochondria in axon terminals, neuronal somata of pyramidal neurons and oligodendrocytes in both grey and white matter. In the caudate and putamen mitochondrial number is linked with symptoms and symptom severity. While there is a decrease in the number of mitochondria in astrocytes, mitochondria are smaller in oligodendrocytes. In the nucleus accumbens and substantia nigra, mitochondria are similar in density, size and structural integrity in schizophrenia compared to controls. Mitochondrial production of ATP and calcium buffering are essential in maintaining synaptic strength and abnormalities in these processes could lead to decreased metabolism and defective synaptic activity. Abnormalities in mitochondria in oligodendrocytes might contribute to myelin pathology and underlie dysconnectivity in the brain. In schizophrenia, mitochondria are affected differentially depending on the brain region, cell type in which they reside, subcellular location, treatment status, treatment response and predominant symptoms.
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