Abstract
Depression is a prevalent mental disorder, affecting approximately 300 million peopleworldwide. Despite decades of research into the underlying mechanisms of depression, a consensusremains elusive. Recent studies have implicated changes in oligodendrocytes and myelin in the pathogenesisof depression. Conventional antidepressants may alleviate symptoms within weeks of use,but approximately one-third of patients do not respond to them. Ketamine exhibits rapid and sustainedantidepressant effects in treatment-resistant patients with depression. Given the associationbetween reduced myelination and depression pathology, alterations in myelination may be a keymechanism underlying ketamine's prolonged antidepressant effects. However, the exact role of myelinationin ketamine's sustained antidepressant effects remains unclear. In this review, we summarizethe relationship between demyelination and depression and discuss the potential mechanisms bywhich ketamine may exert its antidepressant effects by repairing myelin damage, offering new insightsinto the role of myelination in antidepressant mechanisms.
Keywords:Arketamine, enantiomer, esketamine, ketamine, depression, myelination, oligodendrocyte.
Graphical Abstract
Current Neuropharmacology
Title:Myelin Repair as a Novel Mechanism for Ketamine’s Sustained Antidepressant Effects
Volume: 23Issue: 8
Author(s):Sen Wang, Chaoli Huang, Mengyu Wang, Lingxiao Di, Cunming Liu, Kenji Hashimoto*Chun Yang*
Affiliation:
- Chiba University Center for Forensic Mental Health, Chiba, 260-8670, Japan
- Department of Anesthesiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China
Keywords:Arketamine, enantiomer, esketamine, ketamine, depression, myelination, oligodendrocyte.
Abstract: Depression is a prevalent mental disorder, affecting approximately 300 million peopleworldwide. Despite decades of research into the underlying mechanisms of depression, a consensusremains elusive. Recent studies have implicated changes in oligodendrocytes and myelin in the pathogenesisof depression. Conventional antidepressants may alleviate symptoms within weeks of use,but approximately one-third of patients do not respond to them. Ketamine exhibits rapid and sustainedantidepressant effects in treatment-resistant patients with depression. Given the associationbetween reduced myelination and depression pathology, alterations in myelination may be a keymechanism underlying ketamine's prolonged antidepressant effects. However, the exact role of myelinationin ketamine's sustained antidepressant effects remains unclear. In this review, we summarizethe relationship between demyelination and depression and discuss the potential mechanisms bywhich ketamine may exert its antidepressant effects by repairing myelin damage, offering new insightsinto the role of myelination in antidepressant mechanisms.
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Cite this article as:
Wang Sen, Huang Chaoli, Wang Mengyu, Di Lingxiao, Liu Cunming, Hashimoto Kenji*, Yang Chun*, Myelin Repair as a Novel Mechanism for Ketamine’s Sustained Antidepressant Effects, Current Neuropharmacology 2025; 23 (8) .https://dx.doi.org/10.2174/011570159X349856241213144902
| DOI https://dx.doi.org/10.2174/011570159X349856241213144902 | Print ISSN 1570-159X |
| Publisher Name Bentham Science Publisher | Online ISSN 1875-6190 |
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