Multiple Sclerosis Research Studies

The paper uses multiomic single nucleus RNA/ATAC sequencing to show ependymal cell dysregulation correlates with periventricular pathology in MS and identifies IFNγ as a driver.

This study shows that MCT2 is essential for oligodendrocyte myelin maintenance and axonal support, and its loss leads to myelin and axonal damage, which can be mitigated by a ketogenic diet.

This study uses deep learning and normative modeling to analyze MRI data from MS patients and identify subcortical volume deviations that improve understanding of disease progression.

This paper investigates the 1/f slope modulation during cognitive tasks in MS patients and healthy controls, finding it as a paradigm-independent marker of cognitive control and E/I balance, with reduced modulation in benzodiazepine-treated MS patients.

The paper analyzes gene expression dynamics in a remyelinating microenvironment using single nucleus RNA sequencing in mice, revealing shifts in microglial, astrocytic, and fibroblast activities linked to oligodendrocyte differentiation.

This study identifies a gut microbiome-derived peptide that mimics a myelin antigen and induces experimental autoimmune encephalomyelitis in mice.

This study identifies inflammatory gene expression changes in oligodendroglial lineage cells during EAE using RiboTag-based RNA-Seq, revealing their role in neuroinflammation.

The paper uses single nuclei RNAseq to identify distinct glial gene expression patterns in MS patients, revealing subgroup-specific pathological processes and suggesting precision medicine approaches.

This study identifies proteomic differences in neutrophils from MS patients compared to healthy donors, highlighting dysregulated granule proteins and MAVS signaling, and impaired T cell suppression.

This study identifies 236 MS susceptibility variants and highlights neuronal and glial dysfunction as key factors in MS susceptibility.

This paper uses TDE-HMM to analyze MEG data from a working memory task in MS patients, identifying altered activation patterns in specific brain networks linked to cognitive impairment and treatment effects.

The paper analyzes gene expression and alternative splicing in MS using RNA-seq data to identify differentially expressed genes, spliced transcripts, and SNVs associated with disease pathways and potential therapeutic targets.

This study demonstrates that TCR-like antibodies targeting the MOG35-55 epitope can prevent and regress EAE by blocking TCR-MHC interactions and modulating APCs.

This study shows that senolytic treatment reduces microglia and alleviates EAE symptoms in mice, suggesting senescent glia contribute to neuroinflammation.

The paper uses spatial transcriptomics to study meningeal inflammation in a mouse model, identifying inflammatory gene signatures in adjacent brain parenchyma and highlighting candidate pathways in grey matter pathology.

This paper develops a novel mouse model of cerebral adrenoleukodystrophy (cALD) that replicates human disease features and highlights NLRP3 inflammasome activation in lesion pathogenesis.

The paper shows that indole lactate (ILA), reduced in MS, restores gut microbiome metabolic balance, promoting remyelination and reducing neuroinflammation.

The paper identifies microglial states associated with lesion expansion and remyelination in multiple sclerosis using spatial transcriptomics on human brain tissue.

This study shows that iron accumulates abnormally in the spinal cord of MS patients, correlating with oxidative stress and neurodegeneration, but not with demyelination or iron-rimmed lesions.

This study shows that remyelination protects neurons from DLK-mediated neurodegeneration by preventing apoptosis and inflammation in a mouse model of demyelination.

This study analyzes T cell receptor repertoires in MS patients and controls to explore the relationship between EBV-specific and myelin-specific immune responses, finding distinct patterns associated with MS.

This study identifies increased cholesterol synthesis in PMS patient-derived neural progenitor cells as a driver of neurotoxicity, which can be mitigated by simvastatin.

This study uses genetically diverse mice to identify genetic loci associated with different disease progression patterns in multiple sclerosis.

This study shows that microglia-specific Brd4 knockout reduces T cell reactivation and EAE pathology by impairing microglia-T cell interactions and neuroinflammation.

This study measures DAMPs in SPMS patients and finds elevated levels of Annexin A1, calreticulin, and HMGB1, suggesting potential immunogenic cell death in MS.

The paper uses iPSC-derived glia cultures from MS patients to identify glia-intrinsic disease mechanisms and potential therapeutic targets.

This study identifies TAF1-dependent transcriptional dysregulation as a mechanism underlying multiple sclerosis progression and presents an in vivo model for therapeutic development.

This study identifies immune gene expression signatures in neurons from MS patients and EAE mice, revealing shared pathways and potential roles for IRF5 and STAT1 in neuronal inflammation.

This study shows that low intensity repetitive transcranial magnetic stimulation (LI-rTMS) enhances remyelination by increasing myelin production from new and surviving oligodendrocytes in a mouse model of demyelination.

This study develops a glia-enriched 3D brain model from human iPSCs that mimics MS-related neurodegenerative phenotypes and intercellular communication.