Evidence map›Paper›PMID 32264971›Full record

ArticleJournal of neuroinflammation2020

Deterioration of cognitive function after transient cerebral ischemia with amyloid-β infusion-possible amelioration of cognitive function by AT

Li-Juan Min, Jun Iwanami, Masachika Shudou, Hui-Yu Bai, Bao-Shuai Shan, Akinori Higaki, Masaki Mogi, Masatsugu Horiuchi

Open access · goldAbstract read
In one paragraph

Article in Journal of neuroinflammation, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.

0numbers the graph read from it
0cells of the map it votes in
9citing papers in PubMed
1.2field-weighted citation impact, top 22% 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

9 citing papers in PubMed, 14 citations in OpenAlex.

  1. Trial
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  3. Review
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  9. Defective mitophagy in Alzheimer's disease.Ageing research reviews · 2020
    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 at 1 institution in 1 country.

Li-Juan MinDepartment of Molecular Cardiovascular Biology and Pharmacology, Ehime University, Graduate School of Medicine, Shitsukawa, Tohon, Ehime, 791-0295, Japan. minchen@m.ehime-u.ac.jp.
Jun IwanamiDepartment of Molecular Cardiovascular Biology and Pharmacology, Ehime University, Graduate School of Medicine, Shitsukawa, Tohon, Ehime, 791-0295, Japan.
Masachika ShudouDivision of Analytical Bio-Medicine, Advanced Research Support Center (ADRES), Ehime University, Graduate School of Medicine, Tohon, Ehime, 791-0295, Japan.
Hui-Yu BaiDepartment of Molecular Cardiovascular Biology and Pharmacology, Ehime University, Graduate School of Medicine, Shitsukawa, Tohon, Ehime, 791-0295, Japan.
Bao-Shuai ShanDepartment of Molecular Cardiovascular Biology and Pharmacology, Ehime University, Graduate School of Medicine, Shitsukawa, Tohon, Ehime, 791-0295, Japan.
Akinori HigakiDepartment of Molecular Cardiovascular Biology and Pharmacology, Ehime University, Graduate School of Medicine, Shitsukawa, Tohon, Ehime, 791-0295, Japan.
Masaki MogiDepartment of Pharmacology, Ehime University, Graduate School of Medicine, Tohon, Ehime, 791-0295, Japan.
Masatsugu HoriuchiDepartment of Molecular Cardiovascular Biology and Pharmacology, Ehime University, Graduate School of Medicine, Shitsukawa, Tohon, Ehime, 791-0295, Japan.
Ehime University · JP

Funding

JSPS KAKENHI Grant Number 17K10835JSPS KAKENHI Grant Number 25462220JSPS KAKENHI Grant Number 26860567
6 · The paper itself

Abstract

backgroundTo promote understanding of the pathogenesis of cognitive impairment or dementia, we explored the potential interaction between transient cerebral ischemia and amyloid-β (Aβ) infusion in mediating cognitive decline and examined the possible ameliorative effect of angiotensin II type 2 (AT

methodsAdult male wild-type mice (WT) and mice with VSMC-specific AT

resultsAβ injection in WT induced a cognitive decline, whereas BCCAO did not cause a significant cognitive deficit. In contrast, WT with BCCAO following Aβ injection exhibited more marked cognitive decline compared to Aβ injection alone, in concert with increases in superoxide anion production, nicotinamide adenine dinucleotide phosphate (NADPH) oxidase activity, and expression of p22phox, p40phox, monocyte chemoattractant protein (MCP)-1 and interleukin (IL)-1β in the hippocampus, and upregulation of RAGE (receptor for advanced glycation end product), an Aβ transporter. BCCAO following Aβ injection further enhanced neuronal pyknosis in the hippocampus, compared with BCCAO or Aβ injection alone. In contrast, smAT

conclusionsTransient cerebral ischemia might worsen Aβ infusion-mediated cognitive decline and vice versa, with possible involvement of amplified oxidative stress and inflammation and impairment of the RAGE-mediated Aβ clearance system, contributing to exaggerated neuronal degeneration. AT

Indexed as

Amyloid beta-PeptidesAnimalsCognitionCognitive DysfunctionIschemic Attack, TransientMaleMiceMice, Inbred C57BLMuscle, Smooth, VascularMyocytes, Smooth MuscleOxidative StressReceptor, Angiotensin, Type 2Amyloid beta-PeptidesReceptor, Angiotensin, Type 2Amyloid-β peptideAT2 receptor activationCerebral ischemiaCerebral protectionCerebrovascular damageCognitive impairmentNeuroinflammationNeuronal degeneration

Identifiers

PMID32264971
PMCPMC7140348
OpenAlexW3014510158

What OpenQuestion holds

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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 OpenQuestion graph.