ReviewInternational journal of molecular sciences2021
Microglia: The Missing Link to Decipher and Therapeutically Control MS Progression?
Review in International journal of molecular sciences, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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
22 citing papers in PubMed, 42 citations in OpenAlex.
- Investigations of remibrutinib in models pertinent to multiple sclerosis.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2026Article
- Microglia-associated progression of multiple sclerosis: target identification and therapeutic engagement in human in vitro models.Experimental & molecular medicine · 2026Review
- Siponimod inhibits disease-associated microglia-T cell interactions in chronic experimental autoimmune encephalomyelitis.Acta neuropathologica communications · 2025Article
- Multiple sclerosis: molecular pathogenesis and therapeutic intervention.Signal transduction and targeted therapy · 2025Review
- Glial Cytokine and Metabolic Networks in Progressive Multiple Sclerosis: From Pathophysiology to Biomarkers and Therapeutic Strategies.International journal of molecular sciences · 2025Review
- Inhibition of Bruton's tyrosine kinase restricts neuroinflammation following intracerebral hemorrhage.Theranostics · 2025Article
- BTK inhibition limits microglia-perpetuated CNS inflammation and promotes myelin repair.Acta neuropathologica · 2024Article
- Characterizing microglial gene expression in a model of secondary progressive multiple sclerosis.Glia · 2023Article
- The therapeutic value of treatment for multiple sclerosis: analysis of health technology assessments of three European countries.Frontiers in pharmacology · 2023Article
- Microglia in the context of multiple sclerosis.Frontiers in neurology · 2023Review
- Neurodegeneration and its potential markers in the diagnosing of secondary progressive multiple sclerosis. A review.Frontiers in molecular neuroscience · 2023Review
- Bruton's Tyrosine Kinase Inhibitors: The Next Frontier of B-Cell-Targeted Therapies for Cancer, Autoimmune Disorders, and Multiple Sclerosis.Journal of clinical medicine · 2022Review
- Choroid plexus volume in multiple sclerosis predicts expansion of chronic lesions and brain atrophy.Annals of clinical and translational neurology · 2022Article
- Bruton's Tyrosine Kinase Inhibitors in Multiple Sclerosis: Pioneering the Path Towards Treatment of Progression?CNS drugs · 2022Review
- A Narrative Review on Axonal Neuroprotection in Multiple Sclerosis.Neurology and therapy · 2022Review
- Neuroinflammation Is Associated with GFAP and sTREM2 Levels in Multiple Sclerosis.Biomolecules · 2022Article
- Integration of Genetic and Immune Infiltration Insights into Data Mining of Multiple Sclerosis Pathogenesis.Computational intelligence and neuroscience · 2022Article
- The Role of Microglia in the Development of Neurodegenerative Diseases.Biomedicines · 2021Review
- Oligodendrocytes and Microglia: Key Players in Myelin Development, Damage and Repair.Biomolecules · 2021Review
- Demyelination of the Optic Nerve: An Underlying Factor in Glaucoma?Frontiers in aging neuroscience · 2021Review
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 at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Therapeutically controlling chronic progression in multiple sclerosis (MS) remains a major challenge. MS progression is defined as a steady loss of parenchymal and functional integrity of the central nervous system (CNS), occurring independent of relapses or focal, magnetic resonance imaging (MRI)-detectable inflammatory lesions. While it clinically surfaces in primary or secondary progressive MS, it is assumed to be an integral component of MS from the very beginning. The exact mechanisms causing progression are still unknown, although evolving evidence suggests that they may substantially differ from those driving relapse biology. To date, progression is assumed to be caused by an interplay of CNS-resident cells and CNS-trapped hematopoietic cells. On the CNS-resident cell side, microglia that are phenotypically and functionally related to cells of the monocyte/macrophage lineage may play a key role. Microglia function is highly transformable. Depending on their molecular signature, microglia can trigger neurotoxic pathways leading to neurodegeneration, or alternatively exert important roles in promoting neuroprotection, downregulation of inflammation, and stimulation of repair. Accordingly, to understand and to possibly alter the role of microglial activation during MS disease progression may provide a unique opportunity for the development of suitable, more effective therapeutics. This review focuses on the current understanding of the role of microglia during disease progression of MS and discusses possible targets for therapeutic intervention.
Indexed as
Identifiers
What 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.