ReviewAdvances in neurobiology2025
Oligodendrocyte and Myelin Pathophysiology in Multiple Sclerosis.
Review in Advances in neurobiology, 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.
- Aerobic glycolysis in Schizophrenia: Developmental rescue or energetic breakdown?Molecular psychiatry · 2026Review
- The relationship between depression, anxiety, and disability in patients with multiple sclerosis: A cross-sectional study from western Iran.PCN reports : psychiatry and clinical neurosciences · 2026Article
- Mechanism analysis and intervention strategies of the inflammatory microenvironment in traumatic spinal cord injury.Frontiers in immunology · 2025Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) is a chronic autoimmune and progressive neurodegenerative disease of the central nervous system (CNS) that has a highly variable clinical manifestation and course. MS targets primarily myelin and oligodendroglia; however, all glial cells and neurons become involved early in the pathology. Thus, inflammation, which is widely thought to be initiated peripherally, expands through the CNS, with astrocytes and microglia entering an activated state not only around and within lesions but also widespread. This chapter will emphasize the pathophysiological changes in oligodendrocytes and myelin as a consequence of the inflammatory cascade driving the disease onset and progression. Learning about the mechanisms of oligodendrocyte and myelin damage beyond the immune attack will be instrumental in protecting these two CNS compartments from damage. In turn, knowledge about the axon-myelin unit will help in devising therapies to prevent axonal degeneration, a key clinical hallmark of MS, as it strongly correlates with the progression of CNS atrophy and symptoms. Finally, exploiting paradigms of oligodendrocyte repopulation and remyelination will definitively contribute to devising treatments for tissue repair and halting MS course. This chapter aims at summarizing the state of the art in all these experimental developments including the available clinical therapies and the current clinical trials.
Indexed as
Identifiers
40500503What Socratic holds
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 Socratic graph.