ReviewMolecular neurobiology2025
Unlocking the Therapeutic Potential of RGMa: A New Frontier in Neurological Disorder Treatment.
Review in Molecular neurobiology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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
1 citing paper in PubMed.
- TRIM21 promotes astrocyte-mediated neuroinflammation in experimental autoimmune encephalomyelitis by stabilizing RGMa via K33-linked ubiquitination.Journal of neuroinflammation · 2026Article
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
Finding new biomolecules to target upstream signaling in neurological disorders is a state-of-the-art research strategy. Axon guidance molecules (AGMs) play vital roles in development; however, evidence suggests that these molecules are involved in the pathogenesis of several neurological diseases. Recent studies have shown that repulsive guidance molecule A (RGMa), a member of AGMs, can be targeted as a novel therapeutic option. This molecule has been implicated in several diseases, and inhibiting it improves the outcomes. For example, in various pathological conditions such as multiple sclerosis, neuromyelitis optica, optic nerve crush model, focal cerebral ischemia, traumatic brain injury, and vascular dementia the expression of RGMa is significantly elevated. RGMa has been detected on amyloid plaques and in the glial scar in brains impacted by Alzheimer's disease. Furthermore, RGMa is elevated by activated astrocytes after exposure to TGFβ. Since the role of RGMa in the development of neurological disorders is crucial, inhibiting RGMa can lead to positive outcomes such as axonal regeneration, neuronal repair, and behavioral improvement. Our review explores the impact of RGMa and outlines the positive results achieved by targeting it in preclinical studies. Based on this information, it is clear that RGMa has significant potential as both a predictive biomarker and a therapeutic option.
Indexed as
Identifiers
41299145What Socratic 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 Socratic graph.