ArticleActa neuropathologica communications2024
IFNγ drives neuroinflammation, demyelination, and neurodegeneration in a mouse model of multiple system atrophy.
Article in Acta neuropathologica communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 18 citations in OpenAlex.
- Transcriptional dysregulation in the cerebellum triggered by oligodendroglial α-synucleinopathy: insights from a transgenic mouse into the early disease mechanisms of MSA.Journal of neural transmission (Vienna, Austria : 1996) · 2026Article
- Cytotoxic T cell recognition of α-synuclein drives pathogenic immune responses in multiple system atrophy.Proceedings of the National Academy of Sciences of the United States of America · 2026Article
- Chaperone-mediated autophagy sustains pericyte stemness necessary for brain tissue homeostasis.Journal of advanced research · 2026Article
- Effects of West Nile Virus on behavioral and cognitive performance, circadian body temperatures, cortical Aβ and p-tau pathology, and immune measures in human apoE and human amyloid precursor protein NL-G-F/human apoE mice.Frontiers in immunology · 2026Article
- Multiple system atrophy: advances in pathogenesis and emerging therapeutic strategies.Journal of neurology · 2025Review
- Review
- Tau, amyloid-β and α-synuclein co-pathologies synergistically enhance neuroinflammation and neuropathology.bioRxiv : the preprint server for biology · 2025Article
- Exosomes in Regulating miRNAs for Biomarkers of Neurodegenerative Disorders.Molecular neurobiology · 2025Review
- Oligodendrocyte-specific overexpression of human alpha-synuclein results in elevated MBP levels and inflammatory responses in TgM83 mice, mimicking the pathological features of multiple system atrophy.Acta neuropathologica communications · 2025Article
- Interplay of Neuroinflammation and Gut Microbiota Dysbiosis in Alzheimer's Disease Using Diffusion Kurtosis Imaging Biomarker in 3 × Tg-AD Mouse Models.ACS chemical neuroscience · 2025Article
- Fibrinogen degradation products exacerbate alpha-synuclein aggregation by inhibiting autophagy via downregulation of Beclin1 in multiple system atrophy.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025Article
- A dual role for pleiotrophin in modulating inflammation and myelination in the presence of chondroitin sulfate proteoglycans after nervous system injury.Frontiers in cellular neuroscience · 2025Article
- Serum cytokine profiles at near term-equivalent age and their association with neurodevelopmental outcomes in preterm infants: an exploratory study.Frontiers in pediatrics · 2025Article
- Glyphosate exposure exacerbates neuroinflammation and Alzheimer's disease-like pathology despite a 6-month recovery period in mice.Journal of neuroinflammation · 2024Article
- Assessing the Benefit of Dietary Choline Supplementation Throughout Adulthood in the Ts65Dn Mouse Model of Down Syndrome.Nutrients · 2024Article
- Tissue resident memory CD8+ T cells are present but not critical for demyelination and neurodegeneration in a mouse model of multiple system atrophy.bioRxiv : the preprint server for biology · 2024Article
- Inflammation and heterogeneity in synucleinopathies.Frontiers in immunology · 2024Review
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
Abstract
Multiple system atrophy (MSA) is a rare and fatal synucleinopathy characterized by insoluble alpha-synuclein (α-syn) cytoplasmic inclusions located within oligodendroglia. Neuroinflammation, demyelination, and neurodegeneration are correlated with areas of glia cytoplasmic inclusions (GCI) pathology, however it is not known what specifically drives disease pathogenesis. Recent studies have shown that disease pathologies found in post-mortem tissue from MSA patients can be modeled in rodents via a modified AAV overexpressing α-syn, Olig001-SYN, which has a 95% tropism for oligodendrocytes. In the Olig001-SYN mouse model, CD4+ T cells have been shown to drive neuroinflammation and demyelination, however the mechanism by which this occurs remains unclear. In this study we use genetic and pharmacological approaches in the Olig001-SYN model of MSA to show that the pro-inflammatory cytokine interferon gamma (IFNγ) drives neuroinflammation, demyelination, and neurodegeneration. Furthermore, using an IFNγ reporter mouse, we found that infiltrating CD4+ T cells were the primary producers of IFNγ in response to α-syn overexpression in oligodendrocytes. Results from these studies indicate that IFNγ expression from CD4+ T cells drives α-syn-mediated neuroinflammation, demyelination, and neurodegeneration. These results indicate that targeting IFNγ expression may be a potential disease modifying therapeutic strategy for MSA.
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