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GLP-1 receptor agonists in delirium and encephalopathies: a neuroprotective scoping review
Francisco Mercado, Michaela Kop, Michelle Trinh. Discover Medicine, 2025-07-31
Topic: Brain proteins, microglia and lab models
Abstract Background and Purpose Delirium and encephalopathy are frequent causes of hospitalization leading to functional disability and cognitive impairment. Recent studies have suggested that glucagon-like peptide-1 receptor agonists (GLP-1 RAs) may protect against neurodegeneration in conditions such as Alzheimer's dementia and Parkinson’s disease. However, there is limited literature on their benefits in delirium and encephalopathy. This scoping review explores the mechanisms of GLP-1 RAs in relation to delirium and encephalopathy based on animal studies, and presents current clinical evidence on their potential benefits for managing these neurological disorders. Methodology A literature search was conducted on PubMed, Embase, Google Scholar,Web of Science, and APA PsycInfo using search terms related to GLP-1 RAs, delirium, and encephalopathy, in which GLP-1 RAs may have potential benefits. In accordance with the Prisma-Scr guidelines, a total of 38 articles were included in the scoping review. Results This review focuses on several key brain dysfunctions in which GLP-1 RAs may offer potential benefits. These include postoperative delirium, sepsis-associated encephalopathy, hepatic encephalopathy, hypoxia-induced encephalopathy, diabetic encephalopathy, and alcohol withdrawal syndrome. Both preclinical and clinical studies suggest that GLP-1 RAs may provide neuroprotective benefits, including anti-apoptotic, anti-inflammatory, and cognitive-enhancing properties. These neuroprotective effects are supported by the molecular and pathophysiological pathways that could serve as potential targets for GLP-1 RAs. Conclusion GLP-1 RAs may offer neuroprotective benefits in patients with postoperative delirium and encephalopathies.. Cellular benefits involve pathophysiological or molecular pathways that are shared with other biological systems. While the current evidence is based on preclinical and clinical studies, more research involving human subjects is needed to clarify the role of GLP-1 RAs in various brain dysfunctions.
Cite this study APA, Vancouver, BibTeX · download .bib or .ris
APA 7th
Mercado, F., Kop, M., & Trinh, M. (2025). GLP-1 receptor agonists in delirium and encephalopathies: a neuroprotective scoping review. Discover Medicine. https://doi.org/10.1007/s44337-025-00428-0
Vancouver
Mercado F, Kop M, Trinh M. GLP-1 receptor agonists in delirium and encephalopathies: a neuroprotective scoping review. Discover Medicine. 2025. doi:10.1007/s44337-025-00428-0.
BibTeX
@article{mercado2025-1839cdb4,
author = {Mercado, Francisco and Kop, Michaela and Trinh, Michelle},
title = {{GLP-1 receptor agonists in delirium and encephalopathies: a neuroprotective scoping review}},
journal = {Discover Medicine},
year = {2025},
doi = {10.1007/s44337-025-00428-0},
url = {https://doi.org/10.1007/s44337-025-00428-0}
}
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Key findings
- Recent studies have suggested that glucagon-like peptide-1 receptor agonists (GLP-1 RAs) may protect against neurodegeneration in conditions such as Alzheimer's dementia and Parkinson’s disease.
- Results This review focuses on several key brain dysfunctions in which GLP-1 RAs may offer potential benefits.
- Both preclinical and clinical studies suggest that GLP-1 RAs may provide neuroprotective benefits, including anti-apoptotic, anti-inflammatory, and cognitive-enhancing properties.
Why it matters
This scoping review of animal and clinical studies suggests GLP-1 receptor agonists may offer neuroprotective benefits such as anti-apoptotic, anti-inflammatory and cognitive-enhancing properties in delirium and encephalopathy. The authors note there is limited literature on their benefits in these conditions.
Study details
- Participants38
- Evidence strengthLow
How this study scored 35/100
Published in a peer-reviewed journal. Scored zero for study design, effect reported and randomised / blinded because the record does not state it. We have no data on senior author's track record, so that was left out: it earned 34 of the 96 points we could judge it on, which is 35 out of 100.
| Component | Points | Why |
|---|---|---|
| Journal tier | 7 / 10 | Tier 3 — peer-reviewed journal (Discover Medicine) |
| Journal's citation record | 0 / 4 | Discover Medicine: journal h-index 14 (OpenAlex, 2026-10-29) |
| Study design | 0 / 12 | No study design recorded — scores zero, not guessed (not stated in the record — scored 0) |
| Strength of evidence | 1 / 5 | Rated “low” in our summary |
| Peer-review validation | 10 / 10 | Peer-reviewed. Published as an article in a named peer-reviewed journal. |
| How recent | 4 / 5 | 2025 — within 3 year(s) of the newest study here |
| Sample size | 1 / 4 | 38 participants |
| Effect reported | 0 / 3 | No effect size reported — scores zero (not stated in the record — scored 0) |
| Studied in people | 3 / 3 | Studied in people (participant count stated) |
| Randomised / blinded | 0 / 2 | No randomisation or blinding stated — scores zero (not stated in the record — scored 0) |
| Times cited | 1 / 7 | Cited 2 times (OpenAlex, 2026-10-10) |
| Citations per year | 0 / 5 | 0.7 citations a year over 3 year(s) since 2025 |
| Impact for its field and year | 2 / 6 | Cited 1.5× the average for papers of its field and year (OpenAlex FWCI) |
| Cited by studies here | 0 / 6 | No other study in this library cites it |
| Still being cited | 0 / 4 | Cited 2 times in 2024–2026 (2026 still in progress; OpenAlex) |
| Senior author's track record | — / 4 | OpenAlex's profile for last-listed author Michelle Trinh holds only 3 work(s), too few to judge a track record — left out of this score |
| Institution's track record | 1 / 3 | University of Hawaiʻi at Mānoa: institution h-index 816 (OpenAlex) |
| Multi-centre collaboration | 1 / 3 | OpenAlex lists 3 institution(s) in 1 country |
| Indexed in PubMed | 1 / 2 | Not in PubMed, but has a DOI |
| Free to read | 2 / 2 | Free to read |
| Points | 34 / 96 | Scored on 19 of 20 parts. We have no data for the rest, so they are left out: 34 of the 96 points we could judge it on is 35 out of 100. |
| Total | 35 / 100 | — |
What each of these 20 components measures, and what this score is not →
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