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主要精神疾病患者前壳核中少突胶质细胞和少突胶质细胞簇的数量密度。

Numerical density of oligodendrocytes and oligodendrocyte clusters in the anterior putamen in major psychiatric disorders.

机构信息

Laboratory of Clinical Neuropathology, Mental Health Research Center, Zagorodnoe shosse 2, Moscow, Russia, 117152.

出版信息

Eur Arch Psychiatry Clin Neurosci. 2020 Oct;270(7):841-850. doi: 10.1007/s00406-020-01108-z. Epub 2020 Feb 14.

Abstract

There is increasing evidence to support the notion that oligodendrocyte and myelin abnormalities may contribute to the functional dysconnectivity found in the major psychiatric disorders. The putamen, which is an important hub in the cortico-striato-thalamo-cortical loop, has been implicated in a broad spectrum of psychiatric illnesses and is a central target of their treatments. Previously we reported a reduction in the numerical density of oligodendrocytes and oligodendrocyte clusters in the prefrontal and parietal cortex in schizophrenia. Oligodendrocyte clusters contain oligodendrocyte progenitors and are involved in functionally dependent myelination. We measured the numerical density (Nv) of oligodendrocytes and oligodendrocyte clusters in the putamen in schizophrenia, bipolar disorder (BPD) and major depressive disorder (MDD) as compared to healthy controls (15 cases per group). Optical disector was used to estimate the Nv of oligodendrocytes and oligodendrocyte clusters. A significant reduction in both the Nv of oligodendrocytes (- 34%; p < 0.01) and the Nv of oligodendrocyte clusters (- 41%; p < 0.05) was found in the schizophrenia group as compared to the control group. Sexual dimorphism for both measurements was found only within the control group. The Nv of oligodendrocytes was significantly lower in male schizophrenia cases as compared to the male control cases. However, the Nv of oligodendrocyte clusters was significantly lower in all male clinical cases as compared to the male control group. The data suggest that lowered density of oligodendrocytes and oligodendrocyte clusters may contribute to the altered functional connectivity in the putamen in subjects with schizophrenia.

摘要

越来越多的证据支持这样一种观点,即少突胶质细胞和髓鞘异常可能导致主要精神疾病中发现的功能连接中断。壳核是皮质-纹状体-丘脑-皮质回路的重要枢纽,与广泛的精神疾病有关,也是其治疗的重要靶点。我们之前曾报道过精神分裂症患者前额叶和顶叶皮层的少突胶质细胞和少突胶质细胞簇的数量密度减少。少突胶质细胞簇包含少突胶质细胞前体细胞,参与功能依赖性髓鞘形成。我们测量了精神分裂症、双相情感障碍(BPD)和重度抑郁症(MDD)患者与健康对照组(每组 15 例)壳核中的少突胶质细胞和少突胶质细胞簇的数量密度(Nv)。光学分割法用于估计少突胶质细胞和少突胶质细胞簇的 Nv。与对照组相比,精神分裂症组的少突胶质细胞(-34%;p<0.01)和少突胶质细胞簇(-41%;p<0.05)的 Nv 均显著降低。仅在对照组中发现了这两种测量方法的性别二态性。与男性对照组相比,男性精神分裂症患者的少突胶质细胞 Nv 明显降低。然而,与男性对照组相比,所有男性临床病例的少突胶质细胞簇 Nv 明显降低。数据表明,少突胶质细胞和少突胶质细胞簇密度降低可能导致精神分裂症患者壳核功能连接改变。

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