ReviewCurrent neuropharmacology2025
Myelin Repair as a Novel Mechanism for Ketamine's Sustained Antidepressant Effects.
Review in Current neuropharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
3 citing papers in PubMed.
- Low Dose Ketamine Preconditions Astrocyte Mitochondria to Achieve Antidepressant Efficacy via Adenosine, Humanin, and Melatonin Upregulation and Efflux.Alpha psychiatry · 2026Article
- Thioredoxin system: mechanisms and therapeutic potential in mental disorders.Frontiers in pharmacology · 2026Review
- Therapeutic Potentials of Anesthetics.Current neuropharmacology · 2026Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
Abstract
Depression is a prevalent mental disorder, affecting approximately 300 million people worldwide. Despite decades of research into the underlying mechanisms of depression, a consensus remains elusive. Recent studies have implicated changes in oligodendrocytes and myelin in the pathogenesis of 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 sustained antidepressant effects in treatment-resistant patients with depression. Given the association between reduced myelination and depression pathology, alterations in myelination may be a key mechanism underlying ketamine's prolonged antidepressant effects. However, the exact role of myelination in ketamine's sustained antidepressant effects remains unclear. In this review, we summarize the relationship between demyelination and depression and discuss the potential mechanisms by which ketamine may exert its antidepressant effects by repairing myelin damage, offering new insights into the role of myelination in antidepressant mechanisms.
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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.