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

Overview of attention for article published in Molecular Neurodegeneration, April 2017
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About this Attention Score

  • In the top 25% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (86th percentile)
  • High Attention Score compared to outputs of the same age and source (84th percentile)

Mentioned by

news
1 news outlet
twitter
6 tweeters
facebook
1 Facebook page
googleplus
1 Google+ user

Citations

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10 Dimensions

Readers on

mendeley
23 Mendeley
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Title
Amelioration of amyloid-β-induced deficits by DcR3 in an Alzheimer’s disease model
Published in
Molecular Neurodegeneration, April 2017
DOI 10.1186/s13024-017-0173-0
Pubmed ID
Authors

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

Abstract

Microglia 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. We 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. We 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(+)YM1(+) M2a-like microglia that reduces Aβ-induced proinflammatory cytokines and promotes phagocytosis ability of microglia. The 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.

Twitter Demographics

The data shown below were collected from the profiles of 6 tweeters who shared this research output. Click here to find out more about how the information was compiled.

Mendeley readers

The data shown below were compiled from readership statistics for 23 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 23 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 5 22%
Researcher 3 13%
Student > Bachelor 2 9%
Student > Master 2 9%
Student > Postgraduate 2 9%
Other 3 13%
Unknown 6 26%
Readers by discipline Count As %
Neuroscience 5 22%
Agricultural and Biological Sciences 3 13%
Medicine and Dentistry 3 13%
Biochemistry, Genetics and Molecular Biology 2 9%
Immunology and Microbiology 1 4%
Other 2 9%
Unknown 7 30%

Attention Score in Context

This research output has an Altmetric Attention Score of 14. This is our high-level measure of the quality and quantity of online attention that it has received. This Attention Score, as well as the ranking and number of research outputs shown below, was calculated when the research output was last mentioned on 23 February 2018.
All research outputs
#1,005,430
of 12,552,783 outputs
Outputs from Molecular Neurodegeneration
#63
of 546 outputs
Outputs of similar age
#35,063
of 258,972 outputs
Outputs of similar age from Molecular Neurodegeneration
#3
of 19 outputs
Altmetric has tracked 12,552,783 research outputs across all sources so far. Compared to these this one has done particularly well and is in the 91st percentile: it's in the top 10% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 546 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.1. This one has done well, scoring higher than 88% of its peers.
Older research outputs will score higher simply because they've had more time to accumulate mentions. To account for age we can compare this Altmetric Attention Score to the 258,972 tracked outputs that were published within six weeks on either side of this one in any source. This one has done well, scoring higher than 86% of its contemporaries.
We're also able to compare this research output to 19 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 84% of its contemporaries.