Anti-inflammatory Effects of Glucagon-like Peptide-1 Receptor Agonists in Preclinical Models of MS and Others
Preclinical studies indicated that glucagon-like peptide-1 receptor agonists (GLP-1RAs) have anti-inflammatory effects, but clinical studies in schizophrenia and alcohol-use disorder did not show significant changes in peripheral inflammatory markers. This discrepancy highlights that preclinical findings may not directly translate to clinical relevance.
- Most relevant to
- —
- Human efficacy
- Not yet assessed
- Mechanism
- Not yet assessed
- Evidence strength
- Not yet assessed
- Outcome
- Not yet assessed
Why it matters
Understanding the anti-inflammatory potential of GLP-1RAs could help in developing treatments for neuroinflammatory conditions. However, the inconclusive human results emphasize the need for more targeted research.
What this does not prove
The clinical studies were not designed to evaluate neuroinflammatory effects, which limits their interpretability. Differences in design and methodology between preclinical and clinical studies may account for the conflicting results.
Next milestone
No next milestone was established from the available source.
Study facts
- Study design
- Systematic review
- Participants / samples
- 40 · Number of included studies
- Randomised
- No
- Controlled
- No
- Primary endpoint met
- Not reported
- Relevant MS type
- All
- Publication date
- 2026-10-16
- Evidence reviewed
- Abstract only
- Regulatory approval
- Not reported
- Research areas
- Neuroinflammation
Original sources
- Primary evidenceModulating neuroinflammation with glucagon-like peptide-1 receptor agonists: a scoping review exploring their therapeutic potential in schizophrenia. ↗DOI: 10.1016/j.pnpbp.2026.111978
Supporting passages (12)
study designThis scoping review synthesizes evidence from clinical and preclinical studies on the anti-inflammatory effects of GLP-1RAs in psychiatric, neurodegenerative and neurological disease models, identifying crucial research gaps and providing future recommendations to guide potential clinical translation.
subjectsThe literature search was conducted in PubMed, Embase and PsycINFO and included outcomes of cytokine levels within blood and brain samples.
sample sizeWithin the 40 included studies, two were clinical (schizophrenia and alcohol-use disorder) and 38 were preclinical models of psychiatric diseases, Alzheimer's -, Parkinson's Disease, Multiple Sclerosis, Epilepsy and lipopolysaccharide (LPS)-induced neuroinflammation.
sample size basisWithin the 40 included studies, two were clinical (schizophrenia and alcohol-use disorder) and 38 were preclinical models of psychiatric diseases, Alzheimer's -, Parkinson's Disease, Multiple Sclerosis, Epilepsy and lipopolysaccharide (LPS)-induced neuroinflammation.
randomizedAs these trials were not primarily designed or powered to test neuroinflammatory effects, the clinical findings remain inconclusive.
controlledAs these trials were not primarily designed or powered to test neuroinflammatory effects, the clinical findings remain inconclusive.
research categoriesTitle: Modulating neuroinflammation with glucagon-like peptide-1 receptor agonists: a scoping review exploring their therapeutic potential in schizophrenia.
relevant ms typesWithin the 40 included studies, two were clinical (schizophrenia and alcohol-use disorder) and 38 were preclinical models of psychiatric diseases, Alzheimer's -, Parkinson's Disease, Multiple Sclerosis, Epilepsy and lipopolysaccharide (LPS)-induced neuroinflammation.
publication datePublication date: 2026-10-16
interventionGlucagon-like peptide-1 receptor agonists (GLP-1RAs), clinically approved anti-diabetic and -obesity medication, have been associated with anti-inflammatory properties.
findingsPreclinical studies showed anti-(neuro)inflammatory effects of GLP-1RAs, whereas the two available clinical studies found no significant changes in peripheral inflammatory markers.
limitationsDifferences in study design, inflammatory measurements, pharmacokinetics and dosing may have contributed to the discrepancy between preclinical and clinical findings.
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