ReviewNature reviews. Neuroscience2024
The neuropathobiology of multiple sclerosis.
Review in Nature reviews. Neuroscience, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 108 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
108 citing papers in PubMed, 1 synthesis or guideline pooled it.
- MS Fatigue Post High-Efficacy Treatment.European journal of neurology · 2025Pooled it
- Trial
- Vitamin D3 Supplementation Modulates Inflammatory Protein CHI3L1/YKL-40 and Oxidative Stress Status in Multiple Sclerosis.Neuropsychopharmacology reports · 2025Trial
- Polypharmacy, Potential Drug-Drug Interactions and Medication Non-Adherence in Patients with Multiple Sclerosis: A Longitudinal Study.Neurology and therapy · 2026Article
- The transcriptional cortical response to daily torpor inLife science alliance · 2026Article
- Review
- Article
- The potential and therapeutic advances of the integrin family in neurological disorders.Neural regeneration research · 2026Article
- Multiancestry genome-wide association and multiomics analyses elucidate spatiocellular features of multiple sclerosis genetics.Nature genetics · 2026Article
- The Neurovascular Niche: A Gathering Venue for Neuroinflammation and Remyelination in Multiple Sclerosis.Acta physiologica (Oxford, England) · 2026Review
- Genome-wide association analyses highlight the neuronal contribution to multiple sclerosis susceptibility.Nature genetics · 2026Article
- The Neuroimmune Duality of CD4⁺ T Cells: Drivers of Damage and Repair in the Brain.Molecular neurobiology · 2026Review
- Hydrogels: current biomedical applications and future directions.Molecular biomedicine · 2026Review
- Akkermansia muciniphila : A next-generation gut probiotic supporting neurorepair and functional recovery.Neural regeneration research · 2026Article
- TREM2 in neurodegenerative diseases and acute neurological injuries: mechanisms to targeted therapies.Cell communication and signaling : CCS · 2026Review
- Personality Traits and Their Association With Medication Non-Adherence in Patients With Multiple Sclerosis.CNS neuroscience & therapeutics · 2026Article
- Increased Ih Current Is Associated with Reduced Hippocampal CA1 Excitability in a Mouse Model of Multiple Sclerosis.eNeuro · 2026Article
- Abnormal B-Cell Exosome Proapoptotic and Antiapoptotic Cargo in Multiple Sclerosis: Potential Implication in Progressive Disease Biology.Neurology(R) neuroimmunology & neuroinflammation · 2026Article
- 25+ Years of TRPV4: From Discovery to Translational Horizons.Research square · 2026Article
- Neuroglial P2YJournal of neuroinflammation · 2026Article
48 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Chronic low-grade inflammation and neuronal deregulation are two components of a smoldering disease activity that drives the progression of disability in people with multiple sclerosis (MS). Although several therapies exist to dampen the acute inflammation that drives MS relapses, therapeutic options to halt chronic disability progression are a major unmet clinical need. The development of such therapies is hindered by our limited understanding of the neuron-intrinsic determinants of resilience or vulnerability to inflammation. In this Review, we provide a neuron-centric overview of recent advances in deciphering neuronal response patterns that drive the pathology of MS. We describe the inflammatory CNS environment that initiates neurotoxicity by imposing ion imbalance, excitotoxicity and oxidative stress, and by direct neuro-immune interactions, which collectively lead to mitochondrial dysfunction and epigenetic dysregulation. The neuronal demise is further amplified by breakdown of neuronal transport, accumulation of cytosolic proteins and activation of cell death pathways. Continuous neuronal damage perpetuates CNS inflammation by activating surrounding glia cells and by directly exerting toxicity on neighbouring neurons. Further, we explore strategies to overcome neuronal deregulation in MS and compile a selection of neuronal actuators shown to impact neurodegeneration in preclinical studies. We conclude by discussing the therapeutic potential of targeting such neuronal actuators in MS, including some that have already been tested in interventional clinical trials.
Indexed as
Identifiers
38789516What OpenQuestion holds
Registered trials
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.