Evidence map›Paper›PMID 37830152›Full record

ArticleInternational journal of molecular medicine2023

Intestinal changes in permeability, tight junction and mucin synthesis in a mouse model of Alzheimer's disease.

Jing He, Yuanjie Liu, Junhua Li, Yueyang Zhao, Hanxiao Jiang, Shifang Luo, Guiqiong He

Open access · hybridAbstract read
In one paragraph

Article in International journal of molecular medicine, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
3.9field-weighted citation impact, top 5% 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

23 citing papers in PubMed, 32 citations in OpenAlex.

  1. Effects ofFoods (Basel, Switzerland) · 2026
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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

7 authors at 2 institutions in 1 country.

Jing He *Institute of Neuroscience, School of Basic Medical Sciences, Chongqing Medical University, Chongqing 400016, P.R. China.
Yuanjie Liu *Institute of Neuroscience, School of Basic Medical Sciences, Chongqing Medical University, Chongqing 400016, P.R. China.
Junhua LiInstitute of Neuroscience, School of Basic Medical Sciences, Chongqing Medical University, Chongqing 400016, P.R. China.
Yueyang ZhaoInstitute of Neuroscience, School of Basic Medical Sciences, Chongqing Medical University, Chongqing 400016, P.R. China.
Hanxiao JiangDepartment of Neurology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing 400010, P.R. China.
Shifang LuoInstitute of Neuroscience, School of Basic Medical Sciences, Chongqing Medical University, Chongqing 400016, P.R. China.
Guiqiong HeInstitute of Neuroscience, School of Basic Medical Sciences, Chongqing Medical University, Chongqing 400016, P.R. China.
Chongqing Medical University · CNDalian Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by the accumulation of amyloid‑β (Aβ) in the brain. The gut/brain axis may serve a role in AD pathogenesis. The present study investigated deposition of Aβ in the intestinal epithelium and its potential effects on intestinal barrier function in a transgenic mouse model of AD. To investigate alterations in the structure and functionality of the intestinal mucosal barrier in AD model mice, hematoxylin and eosin staining for Paneth cell count, Alcian blue‑periodic acid Schiff staining for goblet cells, immunohistochemistry and immunofluorescence for mucin (MUC)2 and wheat germ agglutin expression, transmission electron microscopy for mucosal ultrastructure, FITC‑labeled dextran assay for intestinal permeability, quantitative PCR for goblet cell precursor expression and western blot analysis for tight junction proteins, MUC2 and inflammatory cytokine detection were performed. The results showed that AD model mice exhibited excessive Aβ deposition in the intestinal epithelium, which was accompanied by increased intestinal permeability, inflammatory changes and decreased expression of tight junction proteins. These alterations in the intestinal barrier led to an increased proliferation of goblet and Paneth cells and increased mucus synthesis. Dysfunction of gut barrier occurs in AD and may contribute to its etiology. Future therapeutic strategies to reverse AD pathology may involve early manipulation of gut physiology and its microbiota.

Indexed as

Alzheimer DiseaseMucinsAnimalsIntestinal MucosaMiceMice, TransgenicPermeabilityTight Junction ProteinsTight JunctionsMucinsTight Junction ProteinsAlzheimer's diseaseamyloid‑βgoblet cellintestinal barrierMUC2Notch signaling pathway

Identifiers

PMID37830152
PMCPMC10599350
OpenAlexW4387460481

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
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.