Evidence map›Paper›PMID 28438208›Full record

ArticleMolecular neurodegeneration2017

Amelioration of amyloid-β-induced deficits by DcR3 in an Alzheimer's disease model.

Yi-Ling Liu, Wei-Ting Chen, Yu-Yi Lin, Po-Hung Lu, Shie-Liang Hsieh, Irene Han-Juo Cheng

Open access · goldAbstract read
In one paragraph

Article in Molecular neurodegeneration, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 23% 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

17 citing papers in PubMed, 29 citations in OpenAlex.

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  8. Research Progress of DcR3 in the Diagnosis and Treatment of Sepsis.International journal of molecular sciences · 2023
    Review
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  11. Suppression of HIV-associated Macrophage Activation by a p75 Neurotrophin Receptor Ligand.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2022
    Article
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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

6 authors at 2 institutions in 1 country.

Yi-Ling LiuInstitute of Brain Science, National Yang-Ming University, Taipei, Taiwan.
Wei-Ting ChenBrain Research Center, National Yang-Ming University, Taipei, Taiwan.
Yu-Yi LinInstitute of Brain Science, National Yang-Ming University, Taipei, Taiwan.
Po-Hung LuInstitute of Brain Science, National Yang-Ming University, Taipei, Taiwan.
Shie-Liang HsiehGenomics Research Center, Academia Sinica, Taipei, Taiwan. slhsieh@gate.sinica.edu.tw.
Irene Han-Juo ChengInstitute of Brain Science, National Yang-Ming University, Taipei, Taiwan. hjcheng@ym.edu.tw.
National Yang Ming Chiao Tung University · TWGenomics Research Center, Academia Sinica · TW

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundMicroglia mediate amyloid-beta peptide (Aβ)-induced neuroinflammation, which is one of the key events in the pathogenesis of Alzheimer's disease (AD). Decoy receptor 3 (DcR3)/TNFRSF6B is a pleiotropic immunomodulator that promotes macrophage differentiation toward the M2 anti-inflammatory phenotype. Based on its role as an immunosupressor, we examined whether DcR3 could alleviate neuroinflammation and AD-like deficits in the central nervous system.

methodWe crossed human APP transgenic mice (line J20) with human DcR3 transgenic mice to generate wild-type, APP, DcR3, and APP/DcR3 mice for pathological analysis. The Morris water maze, fear conditioning test, open-field, and elevated-plus maze were used to access their cognitive behavioral changes. Furthermore, the pathological and immune profiles were examined by immunostaining, ELISA, Q-PCR, and IP. In vitro assays were designed to examine DcR3-mediated innate cytokine profile alteration and the potential protective mechanism.

resultsWe reported that DcR3 ameliorates hippocampus-dependent memory deficits and reduces amyloid plaque deposition in APP transgenic mouse. The protective mechanism of DcR3 mediates through interacting with heparan sulfate proteoglycans and activating IL-4

conclusionThe neuroprotective effect of DcR3 is mediated via modulating microglia activation into anti-inflammatory M2a phenotype, and upregulating DcR3 expression in the brain may be a potential therapeutic approach for AD.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainCytokinesDisease Models, AnimalMemory DisordersMice, TransgenicMicrogliaPlaque, AmyloidReceptors, Tumor Necrosis Factor, Member 6bAmyloid beta-PeptidesCytokinesReceptors, Tumor Necrosis Factor, Member 6bAlzheimer's DiseaseDecoy Receptor 3M2a microgliaNeuroinflammation

Identifiers

PMID28438208
PMCPMC5402663
OpenAlexW2607534205

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.