Evidence map›Paper›PMID 20308787›Full record

ArticleJournal of Alzheimer's disease : JAD2010

GLP-1 receptor stimulation reduces amyloid-beta peptide accumulation and cytotoxicity in cellular and animal models of Alzheimer's disease.

Yazhou Li, Kara B Duffy, Mary Ann Ottinger, Balmiki Ray, Jason A Bailey, Harold W Holloway, David Tweedie, Tracyann Perry, Mark P Mattson, Dimitrios Kapogiannis and 3 more

Abstract read
In one paragraph

Article in Journal of Alzheimer's disease : JAD, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 161 papers, 4 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
161citing papers in PubMed, 4 pooled it
13.7field-weighted citation impact, top 1% of its field
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

161 citing papers in PubMed, 4 syntheses or guidelines pooled it, 320 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Pooled it
  4. GLP-1 receptor agonists for Parkinson's disease.The Cochrane database of systematic reviews · 2020
    Pooled it
  5. Trial
  6. Article
  7. Article
  8. Review
  9. Review
  10. Review
  11. Review
  12. Review
  13. Sleep and circadian effects on the incretin system.Current sleep medicine reports · 2025
    Article
  14. Review
  15. From metabolism to mind: The expanding role of the GLP-1 receptor in neurotherapeutics.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2025
    Review
  16. Article
  17. Article
  18. Review
  19. Article
  20. Review

101 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

13 authors at 5 institutions in 1 country.

Yazhou LiLaboratory of Neurosciences, Intramural Research Program, National Institute on Aging, Baltimore, MD, USA.
Kara B Duffy
Mary Ann Ottinger
Balmiki Ray
Jason A Bailey
Harold W Holloway
David Tweedie
Tracyann Perry
Mark P Mattson
Dimitrios Kapogiannis
Kumar Sambamurti
Debomoy K Lahiri
Nigel H Greig
National Institute on Aging · USIndiana University – Purdue University Indianapolis · USUniversity of Maryland, College Park · USIndiana University School of MedicineMedical University of South Carolina · US

Funding

Research Education ComponentP30AG010133 · NIA · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI SAYKIN, ANDREW J · 1991 to 2020
$37.3M
Studies in Dementia and Neurodegenerative DiseasesZIAAG000975 · NIA · NATIONAL INSTITUTE ON AGING · PI KAPOGIANNIS, DIMITRIOS · 2009 to 2025
$31.5M
Design And Development Of Experimental Therapeutics ((Systemic & Neurodegenerative Disorders and Alzheimer's Disease)ZIAAG000311 · NIA · NATIONAL INSTITUTE ON AGING · PI GREIG, NIGEL H. · 2009 to 2025
$16.0M
Neuroprotective role of GLP-1 receptor agonists (Neurodegenerative disorders & Alzheimer's disease)ZIAAG000333 · NIA · NATIONAL INSTITUTE ON AGING · PI GREIG, NIGEL H. · 2009 to 2025
$10.9M
Neuroprotective And Neurorestorative Signaling Mechanisms in Alzheimer's DiseaseZIAAG000314 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$6.7M
Cellular And Molecular Pathogenesis Of Alzheimer's DiseaseZIAAG000312 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$6.4M
Apoptosis In Neurodegenerative DisordersZIAAG000313 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$6.4M
Hormesis/Adaptive Stress Responses and AgingZIAAG000331 · NIA · NATIONAL INSTITUTE ON AGING · PI MATTSON, MARK · 2009 to 2018
$5.0M
Regulation of APP Pathway Gene Promoters in Alzheimer'sR01AG018379 · NIA · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI LAHIRI, DEBOMOY K · 2000 to 2011
$3.1M
Mechanisms of Cholinesterase Inhibitors on Beta-amyloidR01AG018884 · NIA · INDIANA UNIV-PURDUE UNIV AT INDIANAPOLIS · PI LAHIRI, DEBOMOY K · 2002 to 2012
$2.9M
Cholesterol and amyloidogenesisR01AG022103 · NIA · UNIVERSITY OF SOUTH ALABAMA · PI SAMBAMURTI, KUMAR · 2003 to 2007
$1.7M
Design And Development Of Experimental TherapeuticsZ01AG000311 · NIA · NATIONAL INSTITUTE ON AGING · PI GREIG, NIGEL H. · 2001 to 2008
$1.7M
Intramural NIH HHS Z01 AG000311Intramural NIH HHS Z99 AG999999Intramural NIH HHS ZIA AG000975NIA NIH HHS AG023055NIA NIH HHS P30-AG10133NIA NIH HHS R01 AG018379NIA NIH HHS R01 AG018884NIA NIH HHS R01 AG022103NIA NIH HHS R01 AG023055NIA NIH HHS R01-AG18379NIA NIH HHS R01-AG18884NIA NIH HHS U01-AG21380-03
6 · The paper itself

Abstract

Type 2 (T2) diabetes mellitus (DM) has been associated with an increased incidence of neurodegenerative disorders, including Alzheimer's disease (AD). Several pathological features are shared between diabetes and AD, including dysfunctional insulin signaling and a dysregulation of glucose metabolism. It has therefore been suggested that not only may the two conditions share specific molecular mechanisms but also that agents with proven efficacy in one may be useful against the other. Hence, the present study characterized the effects of a clinically approved long-acting analogue, exendin-4 (Ex-4), of the endogenous insulin releasing incretin, glucagon-like peptide-1 (GLP-1), on stress-induced toxicity in neuronal cultures and on amyloid-beta protein (Abeta) and tau levels in triple transgenic AD (3xTg-AD) mice with and without streptozocin (STZ)-induced diabetes. Ex-4 ameliorated the toxicity of Abeta and oxidative challenge in primary neuronal cultures and human SH-SY5Y cells in a concentration-dependent manner. When 11 to 12.5 month old female 3xTg AD mice were challenged with STZ or saline, and thereafter treated with a continuous subcutaneous infusion of Ex-4 or vehicle, Ex-4 ameliorated the diabetic effects of STZ in 3xTg-AD mice, elevating plasma insulin and lowering both plasma glucose and hemoglobin A1c (HbA1c) levels. Furthermore, brain levels of Abeta protein precursor and Abeta, which were elevated in STZ 3xTg-AD mice, were significantly reduced in Ex-4 treated mice. Brain tau levels were unaffected following STZ challenge, but showed a trend toward elevation that was absent following Ex-4 treatment. Together, these results suggest a potential value of Ex-4 in AD, particularly when associated with T2DM or glucose intolerance.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainDiabetes Mellitus, Type 2Disease Models, AnimalFemaleGlucagon-Like Peptide-1 ReceptorMiceMice, TransgenicOxidative StressReceptors, Glucagontau ProteinsAmyloid beta-PeptidesGLP1R protein, humanGlp1r protein, mouseGlucagon-Like Peptide-1 ReceptorReceptors, Glucagontau Proteins

Identifiers

PMID20308787
PMCPMC2948479
OpenAlexW2152355721

What OpenQuestion holds

Textmetadata
LicenceTDM
Read underepoch 390

Registered trials

None linked

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 OpenQuestion graph.