Evidence map›Paper›PMID 40051115›Full record

ArticleNeurogastroenterology and motility2025

Gastrointestinal Dysfunction and Low-Grade Inflammation Associate With Enteric Neuronal Amyloid-β in a Model for Amyloid Pathology.

Kinga Réka Tasnády, Reindert Jehoul, Manuel Gutiérrez de Ravé, Marion J Gijbels, Bert Brône, Ilse Dewachter, Veerle Melotte, Werend Boesmans

Abstract read
In one paragraph

Article in Neurogastroenterology and motility, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. Review
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.

Kinga Réka TasnádyBiomedical Research Institute (BIOMED), Hasselt University, Diepenbeek, Belgium.ORCID https://orcid.org/0000-0002-8406-9106
Reindert JehoulBiomedical Research Institute (BIOMED), Hasselt University, Diepenbeek, Belgium.ORCID https://orcid.org/0000-0002-6929-4129
Manuel Gutiérrez de RavéBiomedical Research Institute (BIOMED), Hasselt University, Diepenbeek, Belgium.ORCID https://orcid.org/0000-0001-8545-1166
Marion J GijbelsDepartment of Pathology, NUTRIM Institute of Nutrition and Translational Research in Metabolism, Maastricht University Medical Centre, Maastricht, the Netherlands.ORCID https://orcid.org/0000-0002-4906-0384
Bert BrôneBiomedical Research Institute (BIOMED), Hasselt University, Diepenbeek, Belgium.ORCID https://orcid.org/0000-0002-4851-9480
Ilse DewachterBiomedical Research Institute (BIOMED), Hasselt University, Diepenbeek, Belgium.ORCID https://orcid.org/0000-0001-7202-515X
Veerle MelotteDepartment of Pathology, GROW-Research Institute for Oncology and Reproduction, Maastricht University Medical Centre, Maastricht, the Netherlands.ORCID https://orcid.org/0000-0002-9459-123X
Werend BoesmansBiomedical Research Institute (BIOMED), Hasselt University, Diepenbeek, Belgium.ORCID https://orcid.org/0000-0002-2426-0451

Funding

Dutch Research Council 016.196.367Research Foundation Flanders G036320NResearch Foundation Flanders W001620NWB acknowledges additional funding from the Francqui Foundation
6 · The paper itself

Abstract

backgroundPatients suffering from Alzheimer's disease, a progressive neurodegenerative disorder involving cognitive decline and memory impairment, often present with gastrointestinal comorbidities. Accumulating data also indicate that alterations in the gut can modulate Alzheimer's disease pathology, highlighting the need to better understand the link between gastrointestinal abnormalities and neurodegeneration in the brain.

methodsTo disentangle the pathophysiology of gastrointestinal dysfunction in Alzheimer's disease, we conducted a detailed pathological characterization of the gastrointestinal tract of 5xFAD mice by performing histological analyses, gene expression studies, immunofluorescence labeling and gut function assays.

resultsWe found that 5xFAD mice have elevated levels of intestinal amyloid precursor protein and accumulate amyloid-β in enteric neurons. Histopathology revealed that this is associated with mild intestinal inflammation and fibrosis and accompanied by increased expression of proinflammatory cytokines. While overall enteric nervous system composition and organization appeared unaffected, 5xFAD mice have faster gastrointestinal transit.

conclusionOur findings indicate that amyloid-β accumulation in enteric neurons is associated with low-grade intestinal inflammation and altered motility and suggest that peripheral pathology may cause gastrointestinal dysfunction in Alzheimer's disease patients.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesEnteric Nervous SystemGastrointestinal DiseasesInflammationNeuronsAmyloid beta-Protein PrecursorAnimalsDisease Models, AnimalMaleMiceMice, TransgenicAmyloid beta-PeptidesAmyloid beta-Protein Precursorenteric gliaenteric nervous systemgut functionintestinal motilityneuroinflammation

Identifiers

PMID40051115
PMCPMC11996054

What OpenQuestion holds

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Registered trials

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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.