Evidence map›Paper›PMID 31847859›Full record

ArticleJournal of neuroinflammation2019

Genetic deletion of soluble epoxide hydrolase delays the progression of Alzheimer's disease.

Hsueh-Te Lee, Kuan-I Lee, Chia-Hui Chen, Tzong-Shyuan Lee

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of neuroinflammation, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
48citing papers in PubMed, 1 pooled it
3.9field-weighted citation impact, top 6% 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

48 citing papers in PubMed, 1 synthesis or guideline pooled it, 72 citations in OpenAlex.

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  19. Maternal pre-conceptional glyphosate exposure impacts the offspring hepatic and ovarian proteome.Toxicological sciences : an official journal of the Society of Toxicology · 2023
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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

4 authors at 2 institutions in 1 country.

Hsueh-Te LeeInstitute of Anatomy and Cell Biology, National Yang-Ming University, Taipei, Taiwan.
Kuan-I LeeDepartment of Physiology, National Yang-Ming University, Taipei, Taiwan.
Chia-Hui ChenGraduate Institute and Department of Physiology, College of Medicine, National Taiwan University, Taipei, 10051, Taiwan.
Tzong-Shyuan LeeGraduate Institute and Department of Physiology, College of Medicine, National Taiwan University, Taipei, 10051, Taiwan. ntutslee@ntu.edu.tw.ORCID http://orcid.org/0000-0002-9593-4062
National Taiwan University · TWNational Yang Ming Chiao Tung University · TW

Funding

Cheng Hsin General Hospital CY10606 and CY10708Ministry of Science and Technology, Taiwan 105-2320-B-010-036, 105-2811-B-010-022, 106-2320-B-002-057-MY3, 106-2320-B-002-056, 106-2811-B-002-146, 104-2320-B-010 -041-MY3 and 108-2320-B-002-032-MY3Yen Tjing Ling Medical Foundation CI -105 -15
6 · The paper itself

Abstract

backgroundSoluble epoxide hydrolase (sEH) is a bifunctional enzyme with COOH-terminal hydrolase and NH2-terminal lipid phosphatase activities. It is expressed in various cell types in the brain and is involved in the pathogenesis of inflammatory and neurodegenerative diseases. Alzheimer's disease (AD) is a progressive neuroinflammatory and neurodegenerative disease. However, the pathological significance of sEH and underlying molecular mechanism in AD remain unclear.

methodsTo examine the role of sEH in pathogenesis of AD, we used wild-type (WT) mice, soluble epoxide hydrolase deficient (sEH

resultsWe demonstrated that the level of sEH was increased in the brain and predominantly appeared in hippocampal astrocytes of APP/PS1 Tg mice. Genetic ablation of sEH in APP/PS1 Tg mice delayed the progression of AD as evidenced by the alleviation in behavior outcomes and Aβ plaque deposition. In addition, loss of the function of sEH in APP/PS1 Tg mice increased astrogliosis and the production of astrocyte-derived anti-inflammatory cytokines including IL-1β, IL-4, and IL-10, as well as the activity of NF-kB and NFAT. Moreover, analysis of gene ontology in the AD brain revealed that important signaling pathways and processes related to AD pathogenesis such as translational regulation, oxidative stress, cytoskeleton reorganization, and small GTPase signal transduction were altered in APP/PS1 Tg/sEH

conclusionOur results suggest that sEH is a crucial regulator in the progression of AD and might be a potential therapeutic target for the treatment of AD.

Indexed as

Alzheimer DiseaseAnimalsBehavior, AnimalBrainDisease Models, AnimalDisease ProgressionEpoxide HydrolasesMiceMice, TransgenicEpoxide HydrolasesAlzheimer’s diseaseAstrocyteInflammationSoluble epoxide hydrolase

Identifiers

PMID31847859
PMCPMC6916033
OpenAlexW2995956111

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.