ReviewTranslational psychiatry2022
Abnormal oligodendrocyte function in schizophrenia explains the long latent interval in some patients.
Review in Translational psychiatry, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 28 citations in OpenAlex.
- Early oligodendrocyte dysfunction signature in Alzheimer's disease: Insights from DNA methylomics and transcriptomics.Molecular psychiatry · 2026Article
- Analysis of gene co-expression connectivity dynamics implicates aberrant neuron-oligodendroglia interactions in schizophrenia.Nature communications · 2026Article
- Oligodendrocyte: Development, Plasticity, Biological Functions, Diseases, and Therapeutic Targets.MedComm · 2026Review
- A systematic review investigating the relationship between green and blue spaces and depression in older adults via DNA methylation.Environmental epigenetics · 2026Review
- Targeting glial cells: Unveiling the neuroprotective mechanisms of Ginseng in the brain microenvironment.Acta pharmaceutica Sinica. B · 2026Review
- Repurposing medications to prevent psychosis.Npj mental health research · 2025Review
- Cortical myelin mapping in antipsychotic medication-naïve, first-episode psychosis patients.Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2025Article
- Glial cell deficits are a key feature of schizophrenia: implications for neuronal circuit maintenance and histological differentiation from classical neurodegeneration.Molecular psychiatry · 2025Review
- Multiomic single-cell profiling identifies critical regulators of postnatal brain.Nature genetics · 2025Article
- Exploring the molecular targets of fingolimod and siponimod for treating the impaired cognition of schizophrenia using network pharmacology and molecular docking.Schizophrenia (Heidelberg, Germany) · 2024Article
- Functional myelin in cognition and neurodevelopmental disorders.Cellular and molecular life sciences : CMLS · 2024Review
- Possible roles of deep cortical neurons and oligodendrocytes in the neural basis of human sociality.Anatomical science international · 2024Review
- The Effect of the Human Brainstem Myelination on Gait Speed in Normative Aging.The journals of gerontology. Series A, Biological sciences and medical sciences · 2023Article
- Astrocytes: Lessons Learned from the Cuprizone Model.International journal of molecular sciences · 2023Review
- Oligodendrocytes matter: a review of animal studies on early adversity.Journal of neural transmission (Vienna, Austria : 1996) · 2023Review
- Immune System and Brain/Intestinal Barrier Functions in Psychiatric Diseases: Is Sphingosine-1-Phosphate at the Helm?International journal of molecular sciences · 2023Review
- Lower Myelin Content Is Associated With Lower Gait Speed in Cognitively Unimpaired Adults.The journals of gerontology. Series A, Biological sciences and medical sciences · 2023Article
- Synergistic, long-term effects of glutamate dehydrogenase 1 deficiency and mild stress on cognitive function and mPFC gene and miRNA expression.Translational psychiatry · 2023Article
- Is It Time for a Paradigm Shift in the Treatment of Schizophrenia? The Use of Inflammation-Reducing and Neuroprotective Drugs-A Review.Brain sciences · 2023Review
Corrections and comments
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Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A puzzling feature of schizophrenia, is the long latency between the beginning of neuropathological changes and the clinical presentation that may be two decades later. Abnormalities in oligodendrocyte function may explain this latency, because mature oligodendrocytes produce myelination, and if myelination were abnormal from the outset, it would cause the synaptic dysfunction and abnormal neural tracts that are underpinning features of schizophrenia. The hypothesis is that latency is caused by events that occur in some patients as early as in-utero or infancy, because clones of abnormal, myelinating oligodendrocytes may arise at that time; their number doubles every ~2 years, so their geometric increase between birth and age twenty, when clinical presentation occurs, is about 1000-fold plus the effect of compounding. For those patients in particular, the long latency is because of a small but ongoing increase in volume of the resulting, abnormally myelinated neural tracts until, after a long latent interval, a critical mass is reached that allows the full clinical features of schizophrenia. During latency, there may be behavioral aberrancies because of abnormally myelinated neural tracts but they are insufficiently numerous for the clinical syndrome. The occurrence of behavioral symptoms during the long latent period, substantiates the hypothesis that abnormal oligodendrocytes explain the latency in some patients. Treatment with fingolimod or siponimod benefits both oligodendrocytes and neural tracts. Clinical trial would validate their potential benefit in appropriate patients with schizophrenia and, concurrently, would validate the hypothesis.
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