ReviewMolecular neurobiology2016
Transcriptional Regulation of Brain-Derived Neurotrophic Factor (BDNF) by Methyl CpG Binding Protein 2 (MeCP2): a Novel Mechanism for Re-Myelination and/or Myelin Repair Involved in the Treatment of Multiple Sclerosis (MS).
Review in Molecular neurobiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 39 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
39 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.
- Uncovering the Causal Link Between Obesity-Associated Genes and Multiple Sclerosis: A Systematic Literature Review.Brain and behavior · 2025Pooled it
- Smoldering neuroinflammation in progressive multiple sclerosis: mechanisms, imaging biomarkers, and therapeutic opportunities.Frontiers in immunology · 2026Review
- BDNF levels in serum and CSF are associated with clinicoradiological characteristics of aggressive disease in MS patients.Journal of neurology · 2025Article
- Early Growth Response Gene-1 Deficiency Interrupts TGFβ1 Signaling Activation and Aggravates Neurodegeneration in Experimental Autoimmune Encephalomyelitis Mice.Neuroscience bulletin · 2024Article
- Impact of physical exercise on the regulation of brain-derived neurotrophic factor in people with neurodegenerative diseases.Frontiers in neurology · 2024Review
- The relevance of BDNF for neuroprotection and neuroplasticity in multiple sclerosis.Frontiers in neurology · 2024Review
- Cerebrospinal fluid camk2a levels at baseline predict long-term progression in multiple sclerosis.Clinical proteomics · 2023Article
- Article
- Role of primary aging hallmarks in Alzheimer´s disease.Theranostics · 2023Review
- Nucleic Acids as Novel Therapeutic Modalities to Address Multiple Sclerosis Onset and Progression.Cellular and molecular neurobiology · 2022Review
- Whole Exome Sequencing in Multi-Incident Families Identifies Novel Candidate Genes for Multiple Sclerosis.International journal of molecular sciences · 2022Article
- Ketogenic and Modified Mediterranean Diet as a Tool to Counteract Neuroinflammation in Multiple Sclerosis: Nutritional Suggestions.Nutrients · 2022Review
- Dysregulated cortical synaptic plasticity under methyl-CpG binding protein 2 deficiency and its implication in motor impairments.World journal of psychiatry · 2022Review
- AcuteNeurorehabilitation and neural repair · 2021Article
- Inhibition of DNA methylation during chronic obstructive bladder disease (COBD) improves function, pathology and expression.Scientific reports · 2021Article
- MeCP2 deficiency exacerbates the neuroinflammatory setting and autoreactive response during an autoimmune challenge.Scientific reports · 2021Article
- Spatiotemporal Regulation of Transcript Isoform Expression in the Hippocampus.Frontiers in molecular neuroscience · 2021Article
- The Relation of the Brain-Derived Neurotrophic Factor with MicroRNAs in Neurodegenerative Diseases and Ischemic Stroke.Molecular neurobiology · 2021Review
- AD7c-NTP Impairs Adult Striatal Neurogenesis by Affecting the Biological Function of MeCP2 in APP/PSl Transgenic Mouse Model of Alzheimer's Disease.Frontiers in aging neuroscience · 2020Article
- Resveratrol Mitigates Sevoflurane-Induced Neurotoxicity by the SIRT1-Dependent Regulation of BDNF Expression in Developing Mice.Oxidative medicine and cellular longevity · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) is a chronic progressive, neurological disease characterized by the targeted immune system-mediated destruction of central nervous system (CNS) myelin. Autoreactive CD4+ T helper cells have a key role in orchestrating MS-induced myelin damage. Once activated, circulating Th1-cells secrete a variety of inflammatory cytokines that foster the breakdown of blood-brain barrier (BBB) eventually infiltrating into the CNS. Inside the CNS, they become reactivated upon exposure to the myelin structural proteins and continue to produce inflammatory cytokines such as tumor necrosis factor α (TNFα) that leads to direct activation of antibodies and macrophages that are involved in the phagocytosis of myelin. Proliferating oligodendrocyte precursors (OPs) migrating to the lesion sites are capable of acute remyelination but unable to completely repair or restore the immune system-mediated myelin damage. This results in various permanent clinical neurological disabilities such as cognitive dysfunction, fatigue, bowel/bladder abnormalities, and neuropathic pain. At present, there is no cure for MS. Recent remyelination and/or myelin repair strategies have focused on the role of the neurotrophin brain-derived neurotrophic factor (BDNF) and its upstream transcriptional repressor methyl CpG binding protein (MeCP2). Research in the field of epigenetic therapeutics involving histone deacetylase (HDAC) inhibitors and lysine acetyl transferase (KAT) inhibitors is being explored to repress the detrimental effects of MeCP2. This review will address the role of MeCP2 and BDNF in remyelination and/or myelin repair and the potential of HDAC and KAT inhibitors as novel therapeutic interventions for MS.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.