Cited by 54Alzheimer's disease research and treatmentsDementia and Cognitive Impairment ResearchNeuroinflammation and Neurodegeneration Mechanisms

Glucagon-like peptide 1 (GLP-1) receptor agonists in experimental Alzheimer’s disease models: a systematic review and meta-analysis of preclinical studies

Open access
Kong, Fanjing, Wu, Tianyu, Dai, Jingyi, Zhai, Zhenwei, Cai, Jie, Zhu, Zhishan, Xu, Ying, Sun, Tao·2023·Frontiers in Pharmacology

Abstract

Alzheimer’s disease (AD) is a degenerative disease of the nervous system. Glucagon-like peptide-1 receptor agonists (GLP-1 RAs), a drug used to treat type 2 diabetes, have been shown to have neuroprotective effects. This systematic review and meta-analysis evaluated the effects and potential mechanisms of GLP-1 RAs in AD animal models. 26 studies were included by searching relevant studies from seven databases according to a predefined search strategy and inclusion criteria. Methodological quality was assessed using SYRCLE’s risk of bias tool, and statistical analysis was performed using ReviewManger 5.3. The results showed that, in terms of behavioral tests, GLP-1 RAs could improve the learning and memory abilities of AD rodents; in terms of pathology, GLP-1 RAs could reduce Aβ deposition and phosphorylated tau levels in the brains of AD rodents. The therapeutic potential of GLP-1 RAs in AD involves a range of mechanisms that work synergistically to enhance the alleviation of various pathological manifestations associated with the condition. A total of five clinical trials were retrieved from ClinicalTrials.gov . More large-scale and high-quality preclinical trials should be conducted to more accurately assess the therapeutic effects of GLP-1 RAs on AD.

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.3389/fphar.2023.1205207

Cites

174 of 174 references verified0 citation errors · 0 not checkable

Statistics

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

  • Preclinical studies have shown that GLP-1RAs exert neurocognitive protection by reducing amyloid-β deposition, tau hyperphosphorylation, neuroinflammation, and oxidative stress, while also improving cognitive function in murine Alzheimer disease and human brain organoid models.

    “Preclinical studies have shown that GLP-1RAs exert neurocognitive protection by reducing amyloid-β deposition, tau hyperphosphorylation, neuroinflammation, and oxidative stress, while also improving cognitive function in murine Alzheimer disease 24,25 and human brain organoid models.26”
  • Substantial preclinical evidence supports the neuroprotective effects of GLP-1R agonists on cognition in AD, attributed to reducing Aβ pathology, tau phosphorylation, glial activation, and neuroinflammation.

    “Substantial preclinical evidence supports the neuroprotective effects of GLP-1R agonists on cognition in AD, which is attributed to the ability to reduce Aβ pathology, tau phosphorylation, glial activation, and neuroinflammation.”

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Cites

1 retracted

Flagged first, then by citations

Research works printed but not linked: 9

  1. Bomfim T. R. Forny-Germano L. Sathler L. B. Brito-Moreira J. Houzel J. C. Decker H. (2012a). An anti-diabetes agent protects the mouse brain from defective insulin signaling caused by Alzheimer’s disease-associated A beta oligomers. J. Clin. Investigation 122, 1339– 1353. 10.1172/jci57256 PMC3314445 22476196 · DOI
  2. Harr S. D. Simonian N. A. Hyman B. T. (1995). Functional alterations in Alzheimer’s disease: decreased glucose transporter 3 immunoreactivity in the perforant pathway terminal zone. J. Neuropathol. Exp. Neurol. 54, 38– 41. 10.1097/00005072-199501000-00005 7815078 · DOI
  3. Hölscher C. Li L. (2010). New roles for insulin-like hormones in neuronal signalling and protection: new hopes for novel treatments of Alzheimer’s disease? Neurobiol. Aging 31, 1495– 1502. 10.1016/j.neurobiolaging.2008.08.023 18930564 · DOI
  4. Janhavi P. Divyashree S. Sanjailal K. P. Muthukumar S. P. (2022). DoseCal: a virtual calculator for dosage conversion between human and different animal species. Arch. Physiol. Biochem. 128, 426– 430. 10.1080/13813455.2019.1687523 31746232 · DOI
  5. Lu C. Li X. Sun Y. Liu L. Wei Y. (2019). The effect and mechanism of Glucagon like peptide 1(GLP-1)in improving cognitive function of Alzheimer’s disease rat model. Stroke Nerv. Dis. 26, 193– 197. 10.3969/j.issn.1007-0478.2019.02.015 · DOI
  6. Oddo S. Caccamo A. Shepherd J. D. Murphy M. P. Golde T. E. Kayed R. (2003). Triple-transgenic model of Alzheimer’s disease with plaques and tangles: intracellular Abeta and synaptic dysfunction. Neuron 39, 409– 421. 10.1016/s0896-6273(03)00434-3 12895417 · DOI · Paper page
  7. Watson G. S. Craft S. (2003). The role of insulin resistance in the pathogenesis of Alzheimer’s disease: implications for treatment. CNS Drugs 17, 27– 45. 10.2165/00023210-200317010-00003 12467491 · DOI
  8. Zhang Z. (2019). Protective effects of geniposide on behavioral and pathologic changes in APP/PS1 mice and exploration of molecular mechanism:down regulation of mTOR signal pathway and enhancement of autophagy. Dissertation. Taiyuan, Shanxi: Shanxi Medical University.
  9. Zheng J. (2022). Cerebral glucose metabolic phenotype mediates cognitive improving effect of glucagon like peptide-1 analogue in Alzheimer’s disease. Dissertation. Fuzhou, Fujian: Fujian Medical University.

Cited by

Sorted by citations

Authors
Kong, F., Wu, T., Dai, J., Zhai, Z., Cai, J., Zhu, Z., Xu, Y., & Sun, T.
Affiliations
Chengdu University of Traditional Chinese Medicine (CN)
Corresponding author
  • Xu, Ying
  • Sun, Tao
Venue
Frontiers in Pharmacology
Published
2023-09-13
Volume
14
Pages
1205207-1205207
ISSN
1663-9812 (ISSN-L)
OpenAlex
W4386708321
Cited by
54
References
174
Citations by year
2026: 19 · 2025: 20 · 2024: 14 · 2023: 1
FWCI
1.92
Type
journal article
Language
en
Open access
Locations
  • Frontiers in Pharmacology (publishedVersion, cc-by)
  • PubMed Central (publishedVersion, cc-by)
  • PubMed (publishedVersion)
  • DOAJ (DOAJ: Directory of Open Access Journals) (submittedVersion, cc-by-sa)
Funders
  • Chengdu University of Traditional Chinese Medicine
  • Jiangxi University of Traditional Chinese Medicine
  • Chengdu University
  • Maryland Population Research Center, University of Maryland
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
Keywords
Alzheimer's disease, GLP-1 receptor agonists, GLP-1 receptor, neuroprotection, amyloid-beta deposition, tau phosphorylation, learning and memory, animal models of Alzheimer's 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 ›

Are you an author, or do you see a problem with this page? Request a review