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精神分裂症患者尾状核头部前端神经元卫星少突胶质细胞缺乏。

Deficit of satellite oligodendrocytes of neurons in the rostral part of the head of the caudate nucleus in schizophrenia.

作者信息

Kolomeets N S, Uranova N A

机构信息

Laboratory of Clinical Neuropathology, Mental Health Research Center, Kashirskoe shosse 34, Moscow, 115522, Russia.

出版信息

Eur Arch Psychiatry Clin Neurosci. 2025 Apr;275(3):813-822. doi: 10.1007/s00406-024-01869-x. Epub 2024 Jul 29.

Abstract

Increasing evidence implicates compromised myelin integrity and oligodendrocyte abnormalities in the dysfunction of neuronal networks in schizophrenia. We previously reported a deficiency of myelinating oligodendrocytes (OL), oligodendrocyte progenitors (OP) and satellite oligodendrocytes of neurons (Sat-OL) in the prefrontal cortex and the inferior parietal cortex - cortical hubs of the frontoparietal cognitive network and default mode network (DMN) altered in schizophrenia. Deficiency of OL and OP was also detected in the head of the caudate nucleus (HCN), which accumulates cortical projections from the associative cortex and is the central node of these networks. However, the number of Sat-Ol per neuron in schizophrenia has not been studied in the HCN. In the current study we estimated the number of Sat-Ol per neuron in the rostral part of the HCN in schizophrenia (n = 18) compared to healthy controls (n = 18) in the same section collection that was previously used to study the number Ol and OP. We found a significant decrease of the number of Sat-Ol per neuron (- 50%, p < 0.001) in schizophrenia as compared to normal controls. Considering that the rostral part of the HCN is an individual network-specific projection zone of the DMN, the deficit of Sat-Ol found in schizophrenia may be related to the dysfunctional DMN-HCN connections, which has been repeatedly described in schizophrenia. The dramatic decrease of the number of Sat-Ol per neuron may be partially related to a pronounced excess of dopamine concentration in the rostral part of the HCN in schizophrenia.

摘要

越来越多的证据表明,精神分裂症患者神经网络功能障碍与髓鞘完整性受损和少突胶质细胞异常有关。我们之前报道过,前额叶皮质以及顶下小叶皮质(额顶认知网络和默认模式网络(DMN)的皮质枢纽,在精神分裂症中发生改变)中,有髓鞘形成的少突胶质细胞(OL)、少突胶质前体细胞(OP)和神经元卫星少突胶质细胞(Sat-OL)存在缺陷。在尾状核头部(HCN)也检测到OL和OP的缺陷,尾状核头部汇聚了联合皮质的皮质投射,是这些网络的中心节点。然而,精神分裂症患者中,HCN每个神经元的Sat-Ol数量尚未得到研究。在本研究中,我们估计了精神分裂症患者(n = 18)与健康对照者(n = 18)在HCN头端部分每个神经元的Sat-Ol数量,二者来自之前用于研究OL和OP数量的同一组切片样本。我们发现,与正常对照相比,精神分裂症患者每个神经元的Sat-Ol数量显著减少(-50%,p < 0.001)。鉴于HCN头端部分是DMN一个特定于个体网络的投射区域,精神分裂症中发现的Sat-Ol缺陷可能与功能失调的DMN-HCN连接有关,这在精神分裂症中已被多次描述。每个神经元Sat-Ol数量的显著减少可能部分与精神分裂症患者HCN头端部分多巴胺浓度明显过高有关。

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