ArticleMolecular neurobiology2026
CD44 as a Conserved Biomarker and Functional Modulator of Neuroinflammation in Multiple Sclerosis and Beyond.
Article in Molecular neurobiology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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
0 citing papers in PubMed.
No citing paper in PubMed yet.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
19 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) characterized by demyelination, blood-brain barrier disruption, and leukocyte infiltration. The transmembrane glycoprotein cluster of differentiation 44 (CD44) has been implicated in neuroinflammation, but its functional role remains unclear. Here, we examined CD44 expression and function across both non-immune-mediated and immune-mediated MS animal models, including cuprizone-induced demyelination, experimental autoimmune encephalomyelitis (EAE), and combined cuprizone/EAE (Cup/EAE), as well as in human MS tissue and cerebrospinal fluid (CSF), using immunohistochemistry, flow cytometry and enzyme-linked immunosorbent assay. CD44 expression increased in parallel with demyelination and was most pronounced in the forebrain of Cup/EAE mice, where it localized to perivascular cuffs and lesion-associated parenchyma. CD44 expression co-localized to IBA1⁺ microglia/monocytes and CD3⁺ T cells. Flow cytometry analyses revealed high CD44 expression on myeloid-derived suppressor cells and regulatory T cells, which further increased upon immune activation. On the functional level, Cd44-deficient mice exhibited exacerbated disease severity in EAE, accompanied by increased immune cell infiltration and tissue damage. In human MS samples, CD44 expression and soluble CD44 levels in CSF were significantly elevated. Notably, CD44 upregulation was also observed in other neurological disease models, including ischemic stroke and APPswe/PS1dE9 mice, a model of Alzheimer's disease. Together, these findings identify CD44 as a conserved marker of neuroinflammatory activity and a context-dependent regulator of neuroinflammation with partially protective functions, rather than an exclusively pro-inflammatory molecule, highlighting its potential relevance in MS and related neurological disorders.
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.