ArticleF1000prime reports2013
Pathoetiology of multiple sclerosis: are we barking up the wrong tree?
Article in F1000prime reports, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 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
18 citing papers in PubMed, 45 citations in OpenAlex.
- Oligodendrocytes Are Active Participants in the Pathogenesis of Multiple Sclerosis and Its Animal Models.International journal of molecular sciences · 2026Review
- Multiple sclerosis and autoimmunity: a reappraisal of the evidence.Frontiers in immunology · 2026Review
- Review
- TGFα controls checkpoints in CNS resident and infiltrating immune cells to promote resolution of inflammation.Nature communications · 2025Article
- Newly Identified Deficiencies in the Multiple Sclerosis Central Nervous System and Their Impact on the Remyelination Failure.Biomedicines · 2022Review
- Identification of viral-mediated pathogenic mechanisms in neurodegenerative diseases using network-based approaches.Briefings in bioinformatics · 2021Article
- Cerebrospinal fluid proteome shows disrupted neuronal development in multiple sclerosis.Scientific reports · 2021Article
- Engine Failure in Axo-Myelinic Signaling: A Potential Key Player in the Pathogenesis of Multiple Sclerosis.Frontiers in cellular neuroscience · 2021Review
- New Epidermal-Growth-Factor-Related Insights Into the Pathogenesis of Multiple Sclerosis: Is It Also Epistemology?Frontiers in neurology · 2021Review
- The Neuroimmunology of Multiple Sclerosis: Fictions and Facts.Frontiers in neurology · 2021Review
- Revisiting the Pathoetiology of Multiple Sclerosis: Has the Tail Been Wagging the Mouse?Frontiers in immunology · 2020Review
- CD8 T-cell Recruitment Into the Central Nervous System of Cuprizone-Fed Mice: Relevance to Modeling the Etiology of Multiple Sclerosis.Frontiers in cellular neuroscience · 2020Article
- Article
- Corticohippocampal Dysfunction In The OBiden Mouse Model Of Primary Oligodendrogliopathy.Scientific reports · 2018Article
- A comparison between the pathophysiology of multiple sclerosis and normal pressure hydrocephalus: is pulse wave encephalopathy a component of MS?Fluids and barriers of the CNS · 2016Article
- Absence of CCL2 and CCL3 Ameliorates Central Nervous System Grey Matter But Not White Matter Demyelination in the Presence of an Intact Blood-Brain Barrier.Molecular neurobiology · 2016Article
- Deletion of mitochondrial anchoring protects dysmyelinating shiverer: implications for progressive MS.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Hemoglobin as a source of iron overload in multiple sclerosis: does multiple sclerosis share risk factors with vascular disorders?Cellular and molecular life sciences : CMLS · 2014Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
1 author at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Despite a century of intensive investigation, the underlying cause of multiple sclerosis has eluded us. It is clear that there exists a prominent progressive degenerative phenotype together with an important autoimmune inflammatory component, and careful histopathological examination always shows, to a greater or lesser degree, concomitant degeneration/demyelination and adaptive T cell-dependent immune responses. Given this picture, it is difficult, if not impossible, to definitively say whether degeneration or autoimmunity is the initiator of the disease. In this review, I put forward the evidence for and against both models and speculate that, in contrast to the accepted view, it is equally likely that multiple sclerosis may be a degenerative disease that secondarily elicits an autoimmune response, and suggest how this might influence therapeutic approaches.
Identifiers
What OpenQuestion 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 OpenQuestion graph.