ArticleASN neuro
Brain-derived neurotrophic factor deficiency restricts proliferation of oligodendrocyte progenitors following cuprizone-induced demyelination.
Article in ASN neuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.
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Who cites it
40 citing papers in PubMed, 68 citations in OpenAlex.
- Cell death in glioblastoma and the central nervous system.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- BDNF-TrkB Signaling Pathway in Spinal Cord Injury: Insights and Implications.Molecular neurobiology · 2025Review
- Neurotrophomodulatory effect of TNF-α through NF-κB in rat cortical astrocytes.Cytotechnology · 2025Review
- The Compelling Role of Brain-Derived Neurotrophic Factor Signaling in Multiple Sclerosis: Role of BDNF Activators.CNS neuroscience & therapeutics · 2024Review
- Stimulating myelin restoration with BDNF: a promising therapeutic approach for Alzheimer's disease.Frontiers in cellular neuroscience · 2024Review
- The neuroprotective effects of Chalcones from Ashitaba on cuprizone-induced demyelination via modulation of brain-derived neurotrophic factor and tumor necrosis factor α.Brain and behavior · 2023Article
- The Role of BDNF in Multiple Sclerosis Neuroinflammation.International journal of molecular sciences · 2023Review
- Neuronal activity and remyelination: new insights into the molecular mechanisms and therapeutic advancements.Frontiers in cell and developmental biology · 2023Review
- Adaptive and maladaptive myelination in health and disease.Nature reviews. Neurology · 2022Review
- Wuzi Yanzong Pill relieves CPZ-induced demyelination by improving the microenvironment in the brain.Heliyon · 2022Article
- New insights into the immunologic role of oligodendrocyte lineage cells in demyelination diseases.Journal of biomedical research · 2022Article
- A Brief Overview on BDNF-Trk Pathway in the Nervous System: A Potential Biomarker or Possible Target in Treatment of Multiple Sclerosis?Frontiers in neurology · 2022Review
- Presentation and integration of multiple signals that modulate oligodendrocyte lineage progression and myelination.Frontiers in cellular neuroscience · 2022Review
- Alzheimer's disease: Pathophysiology and dental pulp stem cells therapeutic prospects.Frontiers in cell and developmental biology · 2022Review
- Analysis of platelet-derived growth factor receptor A and oligodendrocyte transcription factor 2 markers following Hydroxychloroquine administration in animal induced multiple sclerosis model.Metabolic brain disease · 2021Article
- Oligodendroglial GABAergic Signaling: More Than Inhibition!Neuroscience bulletin · 2021Review
- Exploratory study on neurochemical effects of low-intensity pulsed ultrasound in brains of mice.Medical & biological engineering & computing · 2021Article
- Cross-Talk of the CNS With Immune Cells and Functions in Health and Disease.Frontiers in neurology · 2021Review
- Noninvasive Brain Delivery and Efficacy of BDNF to Stimulate Neuroregeneration and Suppression of Disease Relapse in EAE Mice.Molecular pharmaceutics · 2020Article
- Loss of Adaptive Myelination Contributes to Methotrexate Chemotherapy-Related Cognitive Impairment.Neuron · 2019Article
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
Brain-derived neurotrophic factor (BDNF) is a member of the neurotrophin family of growth factors that through its neurotrophic tyrosine kinase, receptor, type 2 (TrkB) receptor, increases 5-bromo-2-deoxyuridine incorporation in oligodendrocyte progenitor cells (OPCs) in culture. Roles in vivo are less well understood; however, increases in numbers of OPCs are restricted in BDNF+/- mice following cuprizone-elicited demyelination. Here, we investigate whether these blunted increases in OPCs are associated with changes in proliferation. BDNF+/+ and BDNF+/- mice were fed cuprizone-containing or control feed. To assess effects on OPC numbers, platelet-derived growth factor receptor alpha (PDGFRα)+ or NG2+ cells were counted. To monitor DNA synthesis, 5-ethynyl-2'-deoxyuridine (EdU) was injected intraperitoneally and colocalized with PDGFRα+ cells. Alternatively, proliferating cell nuclear antigen (PCNA) was colocalized with PDGFRα or NG2. Labeling indices were determined in the BDNF+/+ and BDNF+/- animals. After 4 or 5 weeks of control feed, BDNF+/- mice exhibit similar numbers of OPCs compared with BDNF+/+ animals. The labeling indices for EdU and PCNA also were not significantly different, suggesting that neither the DNA synthesis phase (S phase) nor the proliferative pool size was different between genotypes. In contrast, when mice were challenged by cuprizone for 4 or 5 weeks, increases in OPCs observed in BDNF+/+ mice were reduced in the BDNF+/- mice. This difference in elevations in cell number was accompanied by decreases in EdU labeling and PCNA labeling without changes in cell death, indicating a reduction in the DNA synthesis and the proliferative pool. Therefore, levels of BDNF influence the proliferation of OPCs resulting from a demyelinating lesion.
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