Evidence map›Paper›PMID 30858535›Full record

ArticleScientific reports2019

Establishment of Novel Murine Model showing Vascular Inflammation-derived Cognitive Dysfunction.

Tsuyoshi Hashizume, Bo-Kyung Son, Sakiko Taniguchi, Koichi Ito, Yoshihiro Noda, Tamao Endo, Michiko Nanao-Hamai, Sumito Ogawa, Masahiro Akishita

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.

0numbers the graph read from it
0cells of the map it votes in
5citing papers in PubMed
0.9field-weighted citation impact, top 24% 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

5 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Article
  3. Review
  4. Review
  5. Article
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

9 authors at 2 institutions in 1 country.

Tsuyoshi HashizumeDepartment of Geriatric Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Bo-Kyung SonDepartment of Geriatric Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Sakiko TaniguchiDepartment of Food and Physiological Models, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan.
Koichi ItoDepartment of Food and Physiological Models, Graduate School of Agricultural and Life Sciences, The University of Tokyo, Tokyo, Japan.
Yoshihiro NodaAnimal Facility, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.ORCID 0000-0002-2657-2555
Tamao EndoAnimal Facility, Tokyo Metropolitan Institute of Gerontology, Tokyo, Japan.
Michiko Nanao-HamaiDepartment of Geriatric Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Sumito OgawaDepartment of Geriatric Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.
Masahiro AkishitaDepartment of Geriatric Medicine, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan. akishita-tky@umin.ac.jp.
The University of Tokyo · JPTokyo Metropolitan Institute of Gerontology · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Inflammation is a critical feature of aging and its related diseases, including cardiovascular diseases. Recent epidemiological studies demonstrated that abdominal aortic aneurysm (AAA), an aging-related vascular pathological condition, is associated with cognitive decline. However, the underlying mechanism, especially the role of vascular inflammation, is largely unknown because of lack of an available animal model. In this study, we examined whether vascular inflammation affects synaptic and cognitive dysfunction, using an AAA mouse model. In young (3 months) and middle-aged (12 months) C57BL/6J mice, AAA was induced by angiotensin II infusion with calcium chloride application. After 4 weeks of induction, aortic diameter was significantly increased and excessive Mac3-positive inflammatory cells infiltrated the destroyed aorta in middle-aged mice. AAA-induced middle-aged mice further exhibited cognitive impairment. Neuronal loss was observed in the CA3 region of the hippocampus. IBA1/MHCII-double-positive microglia activation was also seen in the hippocampus, suggesting that vascular inflammation drives neuroinflammation and subsequent cognitive dysfunction. Furthermore, we found that senescence-accelerated mice prone 8 exhibited robust AAA formation and a marked decrease of cognitive and synaptic function in the hippocampus mediated by inflammation. In conclusion, this novel murine model convincingly suggested the occurrence of vascular inflammation-derived cognitive dysfunction.

Indexed as

Disease Models, AnimalMice, Inbred C57BLAgingAngiotensin IIAnimalsAntigens, DifferentiationAorta, AbdominalAortic Aneurysm, AbdominalCalcium-Binding ProteinsCalcium ChlorideCognitive DysfunctionGenes, MHC Class IIHippocampusInflammationMacrophage ActivationMaleAif1 protein, mouseAngiotensin IIAntigens, DifferentiationCalcium-Binding ProteinsCalcium ChlorideMicrofilament Proteinsmonocyte-macrophage differentiation antigen

Identifiers

PMID30858535
PMCPMC6411753
OpenAlexW2921785128

What OpenQuestion holds

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LicenceCC BY
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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.