ArticleMolecules (Basel, Switzerland)2017
Melatonin Treatment Reduces Oxidative Damage and Normalizes Plasma Pro-Inflammatory Cytokines in Patients Suffering from Charcot-Marie-Tooth Neuropathy: A Pilot Study in Three Children.
Article in Molecules (Basel, Switzerland), 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 35 citations in OpenAlex.
- The current status of Charcot-Marie-Tooth disease type 1 A treatment.Acta neurologica Belgica · 2025Review
- Ferroptosis and Charcot-Marie-Tooth Disease 1A: Emerging Evidence for a Pathogenic Association.Antioxidants (Basel, Switzerland) · 2025Article
- Charcot Marie Tooth disease pathology is associated with mitochondrial dysfunction and lower glutathione production.Cellular and molecular life sciences : CMLS · 2025Article
- Melatonin, an Antitumor Necrosis Factor Therapy.Journal of pineal research · 2025Review
- Review
- Charcot-Marie-Tooth-1A and sciatic nerve crush rat models: insights from proteomics.Neural regeneration research · 2023Article
- The macrophage: a key player in the pathophysiology of peripheral neuropathies.Journal of neuroinflammation · 2022Review
- New Advances on Pathophysiology of Diabetes Neuropathy and Pain Management: Potential Role of Melatonin and DPP-4 Inhibitors.Frontiers in pharmacology · 2022Review
- Age-dependent effect of continuous 'artificial light at night' on circadian rhythm in male rats: neuroprotective role of melatonin.Biogerontology · 2021Article
- Aberrant NLRP3 Inflammasome Activation Ignites the Fire of Inflammation in Neuromuscular Diseases.International journal of molecular sciences · 2021Review
- Emerging Therapies for Charcot-Marie-Tooth Inherited Neuropathies.International journal of molecular sciences · 2021Review
- The role of PPARγ in chemotherapy-evoked pain.Neuroscience letters · 2021Review
- Pharmacological agents under investigation in the treatment of coronavirus disease 2019 and the importance of melatonin.Fundamental & clinical pharmacology · 2021Review
- Metabolic and Functional Improvements in a Patient with Charcot-Marie-Tooth Disease Type 2 after EGCG Administration: A Case Report.Medicina (Kaunas, Lithuania) · 2021Article
- Disease Modeling and Therapeutic Strategies in CMT2A: State of the Art.Molecular neurobiology · 2019Review
- Regulation of Inflammatory Response and the Production of Reactive Oxygen Species by a Functional Cooked Ham Reformulated with Natural Antioxidants in a Macrophage Immunity Model.Antioxidants (Basel, Switzerland) · 2019Article
- Calcium Deregulation and Mitochondrial Bioenergetics in GDAP1-Related CMT Disease.International journal of molecular sciences · 2019Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Charcot-Marie-Tooth neuropathy (CMT) is a motor and sensory neuropathy comprising a heterogeneous group of inherited diseases. The CMT1A phenotype is predominant in the 70% of CMT patients, with nerve conduction velocity reduction and hypertrophic demyelination. These patients have elevated oxidative stress and chronic inflammation. Currently, there is no effective cure for CMT; herein, we investigated whether melatonin treatment may reduce the inflammatory and oxidative damage in CMT1A patients. Three patients, aged 8-10 years, were treated with melatonin (60 mg at 21:00 h plus 10 mg at 09:00 h), and plasma levels of lipid peroxidation (LPO), nitrites (NOx), IL-1β, IL-2, IL-6, TNF-α, INF-γ, oxidized to reduced glutathione (GSSG/GSH) ratio, and the activities of superoxide dismutase (SOD), glutathione-S transferase (GST), glutathione peroxidase (GPx), and reductase (GRd), were determined in erythrocytes at 3 and 6 months of treatment. Healthy age- and sex-matched subjects were used as controls. The results showed increased activities of SOD, GST, GPx, and GRd in CMT1A patients, which were reduced at 3 and 6 months of treatment. The GSSG/GSH ratio significantly increased in the patients, returning to control values after melatonin treatment. The inflammatory process was confirmed by the elevation of all proinflammatory cytokines measured, which were also normalized by melatonin. LPO and NOx, which also were elevated in the patients, were normalized by melatonin. The results document beneficial effects of the use of melatonin in CMT1A patients to reduce the hyperoxidative and inflammatory condition, which may correlate with a reduction of the degenerative process.
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