Multiple Sclerosis Research Studies

This paper uses statistical models to estimate genetic and environmental susceptibility limits to multiple sclerosis, finding that genetic susceptibility is limited to 52% of the population and 30% of women.

The paper investigates axon initial segment alterations in multiple sclerosis, finding increased soma-axon initial segment gap in both active and inactive lesions.

This paper presents a non-human primate model of optic nerve demyelination that recapitulates key features of MS lesions, showing failed remyelination, axonal degeneration, and visual dysfunction.

This study characterizes metabolic alterations in iPSC-derived astrocytes from MS patients, identifying mitochondrial dysfunction and distinct metabolic profiles linked to disease mechanisms.

The paper compares remyelination by surviving and newly generated oligodendrocytes in MS, finding that newly generated cells produce more accurate and abundant myelin sheaths.

This study shows that iNOS deficiency in mice worsens virus-induced demyelination by altering inflammatory responses to a beta-coronavirus.

This study shows baclofen, a GABABR agonist, promotes remyelination in mouse models of demyelination, suggesting it could be a therapeutic for multiple sclerosis.

This study conducts a systematic review and meta-analysis of leptomeningeal enhancement (LME) in multiple sclerosis and other neurological diseases, finding its association with clinical and imaging features in MS.

This paper tracks the conversion of diffusely abnormal white matter to T2 lesions in MS patients, showing it occurs independently of inflammation and gadolinium enhancement.

The paper identifies mQTL effects of MS susceptibility loci on DNA methylation in CD4+ T cells, revealing both cis and trans regulatory impacts.

The paper shows that reduced CD11c+ microglia correlates with faster disease progression in a mouse model of multiple sclerosis.

This study shows that higher genetic risk burden for multiple sclerosis is associated with earlier disease onset.

The paper identifies early transcriptomic changes in brain macrophages in MS tissue, linking them to lesion development and suggesting potential therapeutic targets.

The paper shows that neuronal cholesterol synthesis is critical for remyelination in chronic demyelination models and MS patients.

This study investigates genetic correlations and causal relationships between multiple sclerosis and inflammatory bowel diseases, identifying shared SNPs and tissue-specific heritability patterns.

This study shows that CD38 in astrocytes mediates NAD+ depletion and myelin damage caused by high fat diets and demyelination, with CD38 inhibitors improving myelin regeneration.

This study analyzes transcriptomic data from Multiple Sclerosis patients to identify differentially expressed genes and their association with neurological and developmental pathways.

The paper was withdrawn by the authors due to lack of full consent, and is not intended for citation.

This study investigates how Fingolimod affects BDNF and lncRNA expression in RRMS patients, finding increased HOTAIR and decreased BDNF-AS expression.

The paper predicts combination therapies for MS by modeling patient-specific signaling networks using phosphoproteomics data and identifies TAK1 as a co-druggable target.

This study shows that chronic MS lesions exhibit fibrotic-like changes with collagen deposition, suggesting anti-fibrotic therapies may benefit progressive MS.

The paper investigates complement system involvement in synapse loss in MS hippocampus, finding C1q deposits linked to inhibitory synapse loss and impaired memory.

This study identifies a link between Epstein Barr virus and multiple sclerosis through enrichment analysis of GWAS data and biological validation.

This study shows that the hCX3CR1I249/M280 variant impairs microglial function, reducing neurogenesis and remyelination in a multiple sclerosis model.

This study investigates gene-environment interactions in Multiple Sclerosis using UK Biobank data, finding significant interaction between childhood obesity and genetic risk.

This study shows BMSCs differentiate into neurons, astrocytes, and oligodendrocytes, reducing inflammation and demyelination in EAE mice.

This study identifies SPMS-enriched microglia subsets with disrupted iron homeostasis and oxidative stress using snRNA-seq and validates findings with histology and RNA-scope.

The paper profiles small non-coding RNAs in multiple compartments of MS patients and controls, identifying distinct sncRNA expression patterns in CSF and PBMCs that suggest organ-specific regulatory mechanisms.

This study shows that infusing the TrkB agonist 7,8-dihydroxyflavone into the cerebrospinal fluid does not promote myelin repair in cuprizone or EAE models of multiple sclerosis.

This study identifies Sulf1/2 as a key inhibitor of oligodendrocyte progenitor cell recruitment and remyelination in chronic demyelination, showing that sulfatase inhibition can enhance remyelination.