Evidence map›Paper›PMID 32138327›Full record

ArticleInternational journal of molecular sciences2020

Liraglutide Suppresses Tau Hyperphosphorylation, Amyloid Beta Accumulation through Regulating Neuronal Insulin Signaling and BACE-1 Activity.

Salinee Jantrapirom, Wutigri Nimlamool, Nipon Chattipakorn, Siriporn Chattipakorn, Piya Temviriyanukul, Woorawee Inthachat, Piyarat Govitrapong, Saranyapin Potikanond

Open access · goldAbstract read
In one paragraph

Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 36 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
36citing papers in PubMed, 1 pooled it
4.7field-weighted citation impact, top 4% 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

36 citing papers in PubMed, 1 synthesis or guideline pooled it, 57 citations in OpenAlex.

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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

8 authors at 2 institutions in 1 country.

Salinee JantrapiromDepartment of Pharmacology, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand.ORCID 0000-0002-3111-5658
Wutigri NimlamoolDepartment of Pharmacology, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand.
Nipon ChattipakornNeurophysiology Unit, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand.
Siriporn ChattipakornNeurophysiology Unit, Cardiac Electrophysiology Research and Training Center, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand.
Piya TemviriyanukulInstitute of Nutrition, Mahidol University, Salaya, Phuttamonthon, Nakhon Pathom 73170, Thailand.ORCID 0000-0002-7590-7024
Woorawee InthachatInstitute of Nutrition, Mahidol University, Salaya, Phuttamonthon, Nakhon Pathom 73170, Thailand.
Piyarat GovitrapongDepartment of Pharmacology, Faculty of Science, Mahidol University, Bangkok 10400, Thailand.
Saranyapin PotikanondDepartment of Pharmacology, Faculty of Medicine, Chiang Mai University, Chiang Mai 50200, Thailand.ORCID 0000-0001-8951-8532
Chiang Mai University · THMahidol University · TH

Funding

Faculty of Medicine, Chiang Mai University 85/2556Thailand Research Fund MRG6180078
6 · The paper itself

Abstract

Neuronal insulin resistance is a significant feature of Alzheimer's disease (AD). Accumulated evidence has revealed the possible neuroprotective mechanisms of antidiabetic drugs in AD. Liraglutide, a glucagon-like peptide-1 (GLP-1) analog and an antidiabetic agent, has a benefit in improving a peripheral insulin resistance. However, the neuronal effect of liraglutide on the model of neuronal insulin resistance with Alzheimer's formation has not been thoroughly investigated. The present study discovered that liraglutide alleviated neuronal insulin resistance and reduced beta-amyloid formation and tau hyperphosphorylation in a human neuroblostoma cell line, SH-SY5Y. Liraglutide could effectively reverse deleterious effects of insulin overstimulation. In particular, the drug reversed the phosphorylation status of insulin receptors and its major downstream signaling molecules including insulin receptor substrate 1 (IRS-1), protein kinase B (AKT), and glycogen synthase kinase 3 beta (GSK-3β). Moreover, liraglutide reduced the activity of beta secretase 1 (BACE-1) enzyme, which then decreased the formation of beta-amyloid in insulin-resistant cells. This indicated that liraglutide can reverse the defect of phosphorylation status of insulin signal transduction but also inhibit the formation of pathogenic Alzheimer's proteins like Aβ in neuronal cells. We herein provided the possibility that the liraglutide-based therapy may be able to reduce such deleterious effects caused by insulin resistance. In view of the beneficial effects of liraglutide administration, these findings suggest that the use of liraglutide may be a promising therapy for AD with insulin-resistant condition.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAmyloid Precursor Protein SecretasesAspartic Acid EndopeptidasesBlotting, WesternCell Line, TumorCell SurvivalGlucagon-Like Peptide 1Glycogen Synthase Kinase 3 betaHumansImmunoprecipitationInsulinInsulin Receptor Substrate ProteinsLiraglutidePhosphorylationProto-Oncogene Proteins c-aktAmyloid beta-PeptidesAmyloid Precursor Protein SecretasesAspartic Acid EndopeptidasesBACE1 protein, humanGlucagon-Like Peptide 1Glycogen Synthase Kinase 3 betaInsulinInsulin Receptor Substrate ProteinsLiraglutideProto-Oncogene Proteins c-akttau ProteinsAlzheimer’s diseaseBACE-1beta-amyloidinsulin resistanceliraglutideSH-SY5Ytau

Identifiers

PMID32138327
PMCPMC7084306
OpenAlexW3009642639

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.