Multiple Sclerosis Research Studies

This study identifies novel biomarkers and pathways in multiple sclerosis using NGS data analysis and predicts potential therapeutic drugs.

The paper identifies a mechanism by which FTY720 reduces MS-like disease in an animal model through B12-TCN2-CD320 signaling in astrocytes.

This study uses lipidomic analysis to show differences in remyelination capabilities between brain and spinal cord in a mouse model of demyelination.

The paper uses in situ hybridization to track oligodendrocyte lineage cell dynamics during demyelination and remyelination in a cuprizone model, revealing early mature oligodendrocyte death and prolonged myelin-forming cell activity.

This study shows that early life stress from animal transportation worsens experimental autoimmune encephalomyelitis in mice, supporting a two-hit model for multiple sclerosis etiology.

This paper develops brain charts for people with multiple sclerosis to account for age, sex, and imaging variability, providing interpretable centile estimates of brain volume changes.

This study shows platelets modulate OPC differentiation during remyelination, with transient exposure promoting and sustained exposure inhibiting differentiation in a mouse model of MS.

The paper shows that genetically perturbed myelin increases neuroinflammation-driven axon degeneration through immune-glial interactions in mice.

This study shows that Dicer deficiency in microglia accelerates demyelination and impairs remyelination by affecting oligodendrocyte progenitor cells and microglial function.

This study shows astrocytic IFN-gamma signaling reduces inflammation in MS via PD-L1, suggesting therapeutic potential.

This study shows that people with relapsing-remitting MS have reduced muscle activation across various contraction forces after fatiguing contractions, linked to disease duration.

This study identifies a network involving oligodendroglial precursors and immune cells that drives early demyelination in EAE, showing that targeting CCL4 disrupts this cycle.

This study shows that carnosine synthase deficiency worsens neuroinflammation in MS models but not demyelination, suggesting a role in neuroinflammation regulation.

This paper models autoimmune disease flares as excitable dynamics, showing how stochastic events trigger relapses and how regulatory cells influence their frequency.

The paper uses CITE-seq to analyze B cells from vitamin D-treated MS patients, identifying NF-kB pathway inhibition as a potential mechanism for vitamin D's protective effects.

This study shows that MaR1 treatment reduces inflammation, protects neurons, and improves metabolism in a mouse model of multiple sclerosis.

This study identifies genetic correlations and causal relationships between multiple sclerosis and musculoskeletal traits using GWAS data and Mendelian Randomization.

This study shows that the 1/f spectral slope from MEG recordings correlates with E/I ratio and cognitive function in MS patients, and is affected by benzodiazepine treatment.

This study uses Mendelian randomization to investigate the causal role of lipids and statin interventions on multiple sclerosis risk and severity, finding HDL-C increases risk while RAC2 reduces it.

The paper shows that bryostatin-1, a PKC modulator, shifts microglia and CNS macrophages from pro-inflammatory to regenerative states, promoting remyelination and neuroprotection in MS.

This paper describes Wobbly hedgehog syndrome as a progressive neurodegenerative disease characterized by demyelination, remyelination, axonal degeneration, and neuronal loss, similar to progressive multiple sclerosis.

This study shows that disrupting vesicular transport in adult oligodendrocytes causes demyelination and neuroinflammation, contributing to Multiple Sclerosis.

This study models lifespan brain atrophy trajectories in MS patients and healthy controls, identifying early subcortical structures affected before clinical diagnosis.

This study shows that IRF5 regulates microglial myelin clearance and cholesterol metabolism after demyelination, with implications for remyelination in multiple sclerosis.

This study investigates working memory dysfunction in multiple sclerosis using continuous reproduction paradigms, finding increased recall error and decreased precision, and identifying decoding imprecision and swap error as key factors.

This paper develops a large animal model for demyelinating brain diseases using minipigs, demonstrating reversible and multimodally trackable lesions that mimic human pathology.

The paper identifies drug pairs for remyelination using combination screening and provides mechanistic insights into their efficacy and toxicity.

The paper challenges the view that axonal degeneration in MS results from immune-mediated damage by proposing that myelin itself increases axonal degeneration risk under inflammatory conditions.

The paper investigates DNA methylation and transcriptomic changes in chronic demyelinated MS lesions, showing hypermethylation of myelination-related genes and demonstrating reversible effects through epigenetic editing.

This study investigates the clinical relevance of dilated Virchow-Robin spaces (VRS) as an imaging biomarker in multiple sclerosis, finding they correlate with vascular pathology rather than immune cell accumulation.