ArticleClinical and experimental immunology2023
The pathogenesis of multiple sclerosis: a series of unfortunate events.
Article in Clinical and experimental immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed.
- Azetidine-2-carboxylic acid-induced oligodendrogliopathy in vitro and the pathogenesis of multiple sclerosis.Journal of neuropathology and experimental neurology · 2026Article
- Longitudinal Changes in Neutrophil-to-Lymphocyte and Monocyte-to-Lymphocyte Ratios During Multiple Sclerosis Relapse.Journal of clinical medicine · 2026Article
- Exploring the Link Between IL-6 rs1800795 G > C SNP and the Severity of Epstein-Barr Virus-Associated Multiple Sclerosis: Potential Impact on Cognitive Impairment.Molecular neurobiology · 2025Article
- Chloroindazole based estrogen receptor β ligands with favorable pharmacokinetics promote functional remyelination and visual recovery.Scientific reports · 2025Article
- Precision Nutrition and Gut-Brain Axis Modulation in the Prevention of Neurodegenerative Diseases.Nutrients · 2025Review
- Dual Targeting of TLR9 and cGAS-STING Pathways Attenuates Astrocyte Inflammatory Activation: Potential Implication in Multiple Sclerosis.Neurochemical research · 2025Article
- The case for targeting latent and lytic Epstein-Barr virus infection in multiple sclerosis.Brain : a journal of neurology · 2025Review
- Decreased mitochondrial activity in the demyelinating cerebellum of progressive multiple sclerosis and chronic EAE contributes to Purkinje cell loss.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Beyond weight loss: exploring the neurological ramifications of altered gut microbiota post-bariatric surgery.Journal of translational medicine · 2025Review
- Pyroptosis the Emerging Link Between Gut Microbiota and Multiple Sclerosis.Drug design, development and therapy · 2024Review
Corrections and comments
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Authors and funding
4 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) is characterized by the chronic inflammatory destruction of myelinated axons in the central nervous system. Several ideas have been put forward to clarify the roles of the peripheral immune system and neurodegenerative events in such destruction. Yet, none of the resulting models appears to be consistent with all the experimental evidence. They also do not answer the question of why MS is exclusively seen in humans, how Epstein-Barr virus contributes to its development but does not immediately trigger it, and why optic neuritis is such a frequent early manifestation in MS. Here we describe a scenario for the development of MS that unifies existing experimental evidence as well as answers the above questions. We propose that all manifestations of MS are caused by a series of unfortunate events that usually unfold over a longer period of time after a primary EBV infection and involve periodic weakening of the blood-brain barrier, antibody-mediated CNS disturbances, accumulation of the oligodendrocyte stress protein αB-crystallin and self-sustaining inflammatory damage.
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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.