ArticleExperimental neurology2020
Synaptic alterations and immune response are sexually dimorphic in a non-pertussis toxin model of experimental autoimmune encephalomyelitis.
Article in Experimental neurology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
What it found
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Who cites it
19 citing papers in PubMed, 22 citations in OpenAlex.
- Understanding the Role of Hypothalamic-Pituitary-Gonadal Axis in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis.Biomedicines · 2026Review
- TNFR2 Agonism as a Sex-Specific Therapy for Novel Osteoarthritis-Induced Cardiac Dysfunction.bioRxiv : the preprint server for biology · 2026Article
- EAE models of neuropathic pain in multiple sclerosis do not require pertussis toxin.Brain research · 2026Article
- Advancing EAE Modeling: Establishment of a Non-Pertussis Immunization Protocol for Multiple Sclerosis.Bio-protocol · 2026Article
- Sex-chromosome complement and Activin-A shape the therapeutic potential of TNFR2 activation in a model of MS and CNP.Proceedings of the National Academy of Sciences of the United States of America · 2025Article
- Investigating mechanisms underlying the development of paralysis symptom in a model of MS.Brain research bulletin · 2025Article
- Plasticity of Mouse Dorsal Root Ganglion Neurons by Innate Immune Activation Is Influenced by Electrophysiological Activity.Journal of neurochemistry · 2025Article
- TNFR1/p38αMAPK signaling in Nex + supraspinal neurons regulates estrogen-dependent chronic neuropathic pain.Brain, behavior, and immunity · 2024Article
- Tumor necrosis factor receptor 2 activation elicits sex-specific effects on cortical myelin proteins and functional recovery in a model of multiple sclerosis.Brain research bulletin · 2024Article
- Potential biological contributers to the sex difference in multiple sclerosis progression.Frontiers in immunology · 2023Article
- Immune Cell Contributors to the Female Sex Bias in Multiple Sclerosis and Experimental Autoimmune Encephalomyelitis.Current topics in behavioral neurosciences · 2023Article
- Involvement of TLR2-TLR4, NLRP3, and IL-17 in pain induced by a novel Sprague-Dawley rat model of experimental autoimmune encephalomyelitis.Frontiers in pain research (Lausanne, Switzerland) · 2022Article
- Conquering the host:Frontiers in microbiology · 2022Review
- Review
- Phagocyte-mediated synapse removal in cortical neuroinflammation is promoted by local calcium accumulation.Nature neuroscience · 2021Article
- Toll-like receptor 2 and 4 antagonism for the treatment of experimental autoimmune encephalomyelitis (EAE)-related pain.Brain, behavior, and immunity · 2021Article
- TNFα in MS and Its Animal Models: Implications for Chronic Pain in the Disease.Frontiers in neurology · 2021Review
- Network Pharmacology-Based Strategy for Elucidating the Molecular Basis Forthe Pharmacologic Effects of Licorice (Frontiers in pharmacology · 2021Article
- Article
Corrections and comments
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Multiple sclerosis is an autoimmune disorder of the central nervous system (CNS) characterized by locomotor impairments, cognitive deficits, affective disorders, and chronic pain. Females are predominately affected by MS compared to males and develop motor symptoms earlier. However, key symptoms affect all patients regardless of sex. Previous studies have shown that demyelination and axonal damage play key roles in symptom development, but it is unclear why sex differences exist in MS onset, and effective symptom treatment is still lacking. We here used a non-pertussis toxin (nPTX) experimental autoimmune encephalomyelitis (EAE) model in C57BL/6 mice, to explore chronic symptoms and sex differences in CNS autoimmunity. We observed that, like in humans, female mice developed motor disease earlier than males. Further, changes in pre- and post-synaptic protein expression levels were observed in a sexually dimorphic manner with an overall shift towards excitatory signaling. Our data suggest that this shift towards excitatory signaling is achieved through different mechanisms in males and females. Altogether, our study helps to better understand sex-specific disease mechanisms to ultimately develop better diagnostic and treatment tools.
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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.