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.

中文翻译：

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精神分裂症的线粒体功能障碍：侧重于死后研究

精神分裂症的许多大脑异常与线粒体功能有关，例如氧化应激、能量代谢和突触功效。本文的目的是简要回顾线粒体结构和功能，然后介绍精神分裂症死后大脑中线粒体的异常，重点是解剖学。在多个精神分裂症队列中发现了各种线粒体基因的表达缺陷。复合物 I 和 IV 的活性降低以及组成电子传递链复合物的各个亚基的异常水平都很突出。超微结构研究显示线粒体的层、输入和细胞特异性减少。在皮层，轴突末端的线粒体较少，灰质和白质中锥体神经元和少突胶质细胞的神经元胞体。尾状核和壳核中的线粒体数量与症状和症状严重程度有关。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数量较少。在伏隔核和黑质中，与对照组相比，精神分裂症患者的线粒体在密度、大小和结构完整性方面相似。线粒体产生 ATP 和钙缓冲对于维持突触强度至关重要，这些过程中的异常可能导致新陈代谢下降和突触活动缺陷。少突胶质细胞中线粒体的异常可能导致髓鞘病理学并成为大脑连接障碍的基础。在精神分裂症中，