Evidence map›Paper›PMID 36922861›Full record

ArticleInflammation and regeneration2023

Increased neutrophils in inflammatory bowel disease accelerate the accumulation of amyloid plaques in the mouse model of Alzheimer's disease.

Ryusei Kaneko, Ako Matsui, Mahiro Watanabe, Yoshihiro Harada, Mitsuhiro Kanamori, Natsumi Awata, Mio Kawazoe, Tomoaki Takao, Yutaro Kobayashi, Chie Kikutake and 4 more

Open access · goldFull text read
In one paragraph

Article in Inflammation and regeneration, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
3.2field-weighted citation impact, top 8% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

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  12. Amyloid, Crohn's disease, and Alzheimer's disease - are they linked?Frontiers in cellular and infection microbiology · 2024
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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

14 authors at 2 institutions in 1 country.

Ryusei Kaneko *Division of Allergy and Immunology, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
Ako Matsui *Division of Allergy and Immunology, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
Mahiro WatanabeDivision of Allergy and Immunology, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
Yoshihiro HaradaDivision of Allergy and Immunology, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
Mitsuhiro KanamoriDivision of Allergy and Immunology, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
Natsumi AwataDivision of Allergy and Immunology, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
Mio KawazoeDivision of Allergy and Immunology, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
Tomoaki TakaoDivision of Allergy and Immunology, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
Yutaro KobayashiDivision of Allergy and Immunology, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
Chie KikutakeDivision of Bioinformatics, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
Mikita SuyamaDivision of Bioinformatics, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan.
Takashi SaitoLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science (CBS), 2-1 Hirosawa, Wako-shi, Saitama, 351-0198, Japan.
Takaomi C SaidoLaboratory for Proteolytic Neuroscience, RIKEN Center for Brain Science (CBS), 2-1 Hirosawa, Wako-shi, Saitama, 351-0198, Japan.
Minako ItoDivision of Allergy and Immunology, Medical Institute of Bioregulation, Kyushu University, 3-1-1 Maidashi, Higashi-ku, Fukuoka, 812-8582, Japan. minakoito@bioreg.kyushu-u.ac.jp.ORCID http://orcid.org/0000-0002-5809-472X
Kyushu University · JPRIKEN Center for Brain Science · JP

Funding

Gesellschaft zur Förderung Kynologischer Forschung 21H02719, 21H00432, 21H05044, 21K19382Japan Agency for Medical Research and Development 21zf0127003h, 22gm6210012, 22wm0425011
6 · The paper itself

Abstract

backgroundAlzheimer's disease (AD) is one of the neurodegenerative diseases and characterized by the appearance and accumulation of amyloid-β (Aβ) aggregates and phosphorylated tau with aging. The aggregation of Aβ, which is the main component of senile plaques, is closely associated with disease progression. App

methodsWild-type and App

resultsAn increase in aggregated Aβ was observed in the brains of App

conclusionThese results suggest that neutrophils infiltrate the AD brain parenchyma when acute colitis occurs, and this infiltration is significantly related to disease progression. Therefore, we propose that neutrophil-targeted therapies could reduce Aβ accumulation observed in early AD and prevent the increased risk of AD due to colitis.

Indexed as

Alzheimer’s diseaseInflammatory bowel diseaseNeutrophils

Identifiers

PMID36922861
PMCPMC10015716
OpenAlexW4324381708

What OpenQuestion holds

Textfull text, public
LicenceCC BY
measurements read56
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.