Role of glucagon-like peptide-1 receptor agonists in Alzheimer’s disease and Parkinson’s disease
Open accessAbstract
Neurodegenerative diseases, including Alzheimer's Disease (AD) and Parkinson's Disease (PD) are common complications of diabetes, arising from insulin resistance, inflammation, and other pathological processes in the central nervous system. The potential of numerous antidiabetic agents to modify neurodegenerative disease progression, both preclinically and clinically, has been assessed. These agents may provide additional therapeutic benefits beyond glycemic control. Introduced in the twenty-first century, glucagon-like peptide-1 receptor agonists (GLP-1RAs) are a class of antidiabetic drugs noted not only for their potent glucose-lowering effects but also for their cardiovascular and renal protective benefits. Various GLP-1RAs have been demonstrated to have significant benefits in in vitro and in vivo models of neurodegenerative diseases through modulating a variety of pathogenic mechanisms, including neuroinflammation, autophagy, mitochondrial dysfunction, and the abnormal phosphorylation of pathognomonic proteins. These agents also have substantial protective effects on cognitive and behavioral functions, such as motor function. However, clinical trials investigating GLP-1RAs in diseases such as AD, PD, mild cognitive impairment, psychiatric disorders, and diabetes have yielded mixed results for cognitive and motor function. This review examines the link between diabetes and neurodegenerative diseases, explores the effects of antidiabetic agents on neurodegeneration, provides a concise overview of the GLP-1 pathway, and discusses both preclinical and clinical trial outcomes of GLP-1RAs for neurodegenerative diseases, including their effects on cognition in AD and PD. This review also proposed new strategies for the design of future clinical trials on GLP-1 RAs for both AD and PD.
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Type 2 diabetes and obesity, characterized by insulin resistance, oxidative stress, and chronic inflammation, contribute to neurodegeneration.
“These metabolic disorders, characterized by insulin resistance, oxidative stress, and chronic inflammation, contribute to neurodegeneration. 2”
From Neurodegeneration and Stroke After Semaglutide and Tirzepatide in Patients With Diabetes and Obesity (2025) · cites this paper as [2]
The “Diabetes and neurodegenerative diseases” section links diabetes to neurodegeneration through insulin resistance and inflammation; the figure caption in “Diabetes and pathogeneses of AD and PD” also identifies oxidative stress. These passages describe the mechanism as believed or postulated, and they do not establish the same claim for obesity. Page numbers are unavailable in our copy. (LLM, conf=0.86)
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- Authors
- Hong, C.-T., Chen, J.-H., & Hu, C.-J.
- Affiliations
- Taipei Medical University-Shuang Ho Hospital (TW)
- Corresponding author
- Hu, Chaur-Jong
- Venue
- Journal of Biomedical Science
- Published
- 2024-11-05
- Volume
- 31
- Issue
- 1
- Pages
- 102-102
- ISSN
- 1021-7770 (ISSN-L)
- 1423-0127
- PMC
- PMC11539687
- OpenAlex
- W4404054638
- Cited by
- 78
- References
- 108
- Citations by year
- 2026: 42 · 2025: 34 · 2024: 2
- FWCI
- 4.45
- Type
- journal article
- Language
- en
- Open access
- diamond
- doi.org
- Locations
- Journal of Biomedical Science (publishedVersion, cc-by)
- PubMed Central (publishedVersion, cc-by)
- PubMed (publishedVersion)
- DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion)
- Funders
- Ministry of Education (MOE) in Taiwan. (Higher Education Sprout Project)
- Topics
- Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- GLP-1 receptor agonists, Alzheimer's disease, Parkinson's disease, neurodegenerative diseases, diabetes mellitus, insulin resistance, neuroinflammation, autophagy, mitochondrial dysfunction, cognitive function, motor function, antidiabetic drugs, clinical trial design
- MeSH terms
- Glucagon-Like Peptide-1 Receptor, Glucagon-Like Peptide-1 Receptor Agonists, Alzheimer Disease, Animals, Humans, Hypoglycemic Agents, Parkinson Disease
About these checks
Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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