ArticleJCI insight2022
Biological aging of CNS-resident cells alters the clinical course and immunopathology of autoimmune demyelinating disease.
Article in JCI insight, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Caspase-11-mediated hyperinflammation impairs CD8+ T cell immunity and viral clearance in severe SARS-CoV-2 infection.JCI insight · 2026Article
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- Anti-aging and Anti-inflammatory Dietary Interventions in Multiple Sclerosis: A Narrative Review.Neurology and therapy · 2026Review
- Article
- Oligodendrocyte progenitor cell responses to inflammatory demyelination with aging.Research square · 2025Article
- MHC class I and II expression and induction in oligodendrocytes varies with age.Scientific reports · 2025Article
- Disease Aggravation With Age in an Experimental Model of Multiple Sclerosis: Role of Immunosenescence.Aging cell · 2025Article
- Experimental autoimmune encephalomyelitis pathogenesis alters along animal age: impact of S100B expression.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2025Article
- Senescent cell reduction does not improve recovery in mice under experimental autoimmune encephalomyelitis (EAE) induced demyelination.Journal of neuroinflammation · 2025Article
- Engineered immunological niche directs therapeutic development in models of progressive multiple sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Cellular Senescence in Glial Cells: Implications for Multiple Sclerosis.Journal of neurochemistry · 2025Review
- Targeting senescent microglia in progressive multiple sclerosis: a geroscience-informed approach.Frontiers in immunology · 2025Article
- Disease-modifying therapies for Parkinson disease: lessons from multiple sclerosis.Nature reviews. Neurology · 2024Review
- Senolytic treatment diminishes microglia and decreases severity of experimental autoimmune encephalomyelitis.Journal of neuroinflammation · 2024Article
- The neuropathobiology of multiple sclerosis.Nature reviews. Neuroscience · 2024Review
- What Jane Jacobs has taught me about neuroimmunology.Nature immunology · 2024Article
- Impact of aging on treatment considerations for multiple sclerosis patients.Frontiers in neurology · 2023Review
- Age-dependent gray matter demyelination is associated with leptomeningeal neutrophil accumulation.JCI insight · 2022Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Biological aging is the strongest factor associated with the clinical phenotype of multiple sclerosis (MS). Relapsing-remitting MS typically presents in the third or fourth decade, whereas the mean age of presentation of progressive MS (PMS) is 45 years old. Here, we show that experimental autoimmune encephalomyelitis (EAE), induced by the adoptive transfer of encephalitogenic CD4+ Th17 cells, was more severe, and less likely to remit, in middle-aged compared with young adult mice. Donor T cells and neutrophils were more abundant, while B cells were relatively sparse, in CNS infiltrates of the older mice. Experiments with reciprocal bone marrow chimeras demonstrated that radio-resistant, nonhematopoietic cells played a dominant role in shaping age-dependent features of the neuroinflammatory response, as well as the clinical course, during EAE. Reminiscent of PMS, EAE in middle-aged adoptive transfer recipients was characterized by widespread microglial activation. Microglia from older mice expressed a distinctive transcriptomic profile suggestive of enhanced chemokine synthesis and antigen presentation. Collectively, our findings suggest that drugs that suppress microglial activation, and acquisition or expression of aging-associated properties, may be beneficial in the treatment of progressive forms of inflammatory demyelinating disease.
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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.