Evidence map›Paper›PMID 35970890›Full record

ArticleScientific reports2022

A GLP1 receptor agonist diabetes drug ameliorates neurodegeneration in a mouse model of infantile neurometabolic disease.

L Poupon-Bejuit, M P Hughes, W Liu, A Geard, N Faour-Slika, S Whaler, G Massaro, A A Rahim

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed, 2 pooled it
1.3field-weighted citation impact, top 20% 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

13 citing papers in PubMed, 2 syntheses or guidelines pooled it, 15 citations in OpenAlex.

  1. Genotype-Phenotype Relations for the Dystonia-Parkinsonism GenesInternational journal of molecular sciences · 2025
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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 1 institution in 1 country.

L Poupon-Bejuit *UCL School of Pharmacy, University College London, London, UK.
M P Hughes *UCL School of Pharmacy, University College London, London, UK.
W LiuUCL School of Pharmacy, University College London, London, UK.
A GeardUCL School of Pharmacy, University College London, London, UK.
N Faour-SlikaUCL School of Pharmacy, University College London, London, UK.
S WhalerUCL School of Pharmacy, University College London, London, UK.
G MassaroUCL School of Pharmacy, University College London, London, UK. giulia.massaro.13@ucl.ac.uk.
A A RahimUCL School of Pharmacy, University College London, London, UK. a.rahim@ucl.ac.uk.
University College London · GB

Funding

Department of Health 562868Medical Research Council MR/N026101/1Medical Research Council MR/R015325/1Medical Research Council MR/R025134/1Medical Research Council MR/S009434/1Medical Research Council MR/S036784/1Medical Research Council MR/T044853/1Wellcome TrustWellcome Trust 204841/Z/16/ZWellcome Trust 562646
6 · The paper itself

Abstract

Infantile neuroaxonal dystrophy (INAD) is a rare paediatric neurodegenerative condition caused by mutations in the PLA2G6 gene, which is also the causative gene for PARK14-linked young adult-onset dystonia parkinsonism. INAD patients usually die within their first decade of life, and there are currently no effective treatments available. GLP1 receptor (GLP-1R) agonists are licensed for treating type 2 diabetes mellitus but have also demonstrated neuroprotective properties in a clinical trial for Parkinson's disease. Therefore, we evaluated the therapeutic efficacy of a new recently licensed GLP-1R agonist diabetes drug in a mouse model of INAD. Systemically administered high-dose semaglutide delivered weekly to juvenile INAD mice improved locomotor function and extended the lifespan. An investigation into the mechanisms underlying these therapeutic effects revealed that semaglutide significantly increased levels of key neuroprotective molecules while decreasing those involved in pro-neurodegenerative pathways. The expression of mediators in both the apoptotic and necroptotic pathways were also significantly reduced in semaglutide treated mice. A reduction of neuronal loss and neuroinflammation was observed. Finally, there was no obvious inflammatory response in wild-type mice associated with the repeated high doses of semaglutide used in this study.

Indexed as

Diabetes Mellitus, Type 2Neuroaxonal DystrophiesParkinsonian DisordersAnimalsDisease Models, AnimalDystonic DisordersGroup VI Phospholipases A2MiceGroup VI Phospholipases A2Pla2g6 protein, mouse

Identifiers

PMID35970890
PMCPMC9378686
OpenAlexW4291552694

What Socratic 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 Socratic graph.