ArticleEuropean archives of psychiatry and clinical neuroscience2025
Deficit of satellite oligodendrocytes of neurons in the rostral part of the head of the caudate nucleus in schizophrenia.
Article in European archives of psychiatry and clinical neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Concomitant pathologies and their impact on schizophrenia: a narrative overview of current evidence.Journal of neural transmission (Vienna, Austria : 1996) · 2026Review
- Ultrastructural disturbances of pericapillary microglia, perioligodendrocyte microglia, oligodendrocytes and their interactions in postmortem caudate nucleus in schizophrenia.European archives of psychiatry and clinical neuroscience · 2026Article
- Ultrastructural disturbances in microglia-neuron interactions in the head of the caudate nucleus in schizophrenia.European archives of psychiatry and clinical neuroscience · 2025Article
- Aerobic exercise therapy in severe mental disorders: from methods to underlying mechanisms.European archives of psychiatry and clinical neuroscience · 2025Article
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2 authors.
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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.
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