ReviewBrain sciences2017
Contribution of the Degeneration of the Neuro-Axonal Unit to the Pathogenesis of Multiple Sclerosis.
Review in Brain sciences, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 1 of them a synthesis that pooled it.
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
13 citing papers in PubMed, 1 synthesis or guideline pooled it, 27 citations in OpenAlex.
- Multiple Sclerosis in Pregnancy and its Role in Female Fertility: A Systematic Review.JBRA assisted reproduction · 2021Pooled it
- Multiple sclerosis, urinary tract infections and infertility: a comprehensive scoping review.Journal of the Turkish German Gynecological Association · 2025Article
- Implementation of Dialyzable Leukocyte Extract to Treat Multiple Sclerosis: A Clinical Case.Clinical case reports · 2024Article
- Investigating the Mitoprotective Effects of S1P Receptor Modulators Ex Vivo Using a Novel Semi-Automated Live Imaging Set-Up.International journal of molecular sciences · 2023Article
- Synapse Dysfunctions in Multiple Sclerosis.International journal of molecular sciences · 2023Review
- hnRNP A/B Proteins: An Encyclopedic Assessment of Their Roles in Homeostasis and Disease.Biology · 2021Review
- The Potential Contribution of Dysfunctional RNA-Binding Proteins to the Pathogenesis of Neurodegeneration in Multiple Sclerosis and Relevant Models.International journal of molecular sciences · 2020Review
- Optical Coherence Tomography and Optical Coherence Tomography Angiography Findings After Optic Neuritis in Multiple Sclerosis.Frontiers in neurology · 2020Article
- Idiosyncrasies of hnRNP A1-RNA recognition: Can binding mode influence function.Seminars in cell & developmental biology · 2019Review
- Identification of novel non-myelin biomarkers in multiple sclerosis using an improved phage-display approach.PloS one · 2019Article
- Localization of near-infrared labeled antibodies to the central nervous system in experimental autoimmune encephalomyelitis.PloS one · 2019Article
- Sequential phases of RGC axonal and somatic injury in EAE mice examined using DTI and OCT.Multiple sclerosis and related disorders · 2019Article
- Pathophysiology and Imaging Diagnosis of Demyelinating Disorders.Brain sciences · 2018Article
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 at 3 institutions in 2 countries.
Funding
Abstract
Multiple sclerosis (MS) is a demyelinating, autoimmune disease of the central nervous system. In recent years, it has become more evident that neurodegeneration, including neuronal damage and axonal injury, underlies permanent disability in MS. This manuscript reviews some of the mechanisms that could be responsible for neurodegeneration and axonal damage in MS and highlights the potential role that dysfunctional heterogeneous nuclear ribonucleoprotein A1 (hnRNP A1) and antibodies to hnRNP A1 may play in MS pathogenesis.
Indexed as
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.