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IL-17A is implicated in lipopolysaccharide-induced neuroinflammation and cognitive impairment in aged rats via microglial activation

Overview of attention for article published in Journal of Neuroinflammation, September 2015
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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 (99th percentile)

Mentioned by

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1 news outlet
twitter
5 tweeters

Citations

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76 Dimensions

Readers on

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106 Mendeley
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Title
IL-17A is implicated in lipopolysaccharide-induced neuroinflammation and cognitive impairment in aged rats via microglial activation
Published in
Journal of Neuroinflammation, September 2015
DOI 10.1186/s12974-015-0394-5
Pubmed ID
Authors

Jie Sun, Susu Zhang, Xiang Zhang, Xiaobao Zhang, Hongquan Dong, Yanning Qian

Abstract

Neuroinflammation is considered a risk factor for impairments in neuronal function and cognition that arise with trauma, infection, and/or disease. IL-17A has been determined to be involved in neurodegenerative diseases such as multiple sclerosis. Recently, IL-17A has been shown to be upregulated in lipopolysaccharide(LPS)-induced systemic inflammation. This study aims to explore the role of IL-17A in LPS-induced neuroinflammation and cognitive impairment. Male Sprague-Dawley (SD) rats were injected intraperitoneally with LPS (500 μg/kg), and IL-17A expression in serum and in the hippocampus was examined 6, 12, 24, and 48 h later. Then, we investigated whether IL-17A-neutralizing antibodies (IL-17A Abs, 1 mg/kg) prevented neuroinflammation and memory dysfunction in aged rats that received LPS (500 μg/kg) injection. In addition, the effect of IL-17A on microglial activation in vitro was determined using ELISA and immunofluorescence. LPS injection increased the expression of IL-17A in serum and in the hippocampus. IL-17A Abs improved LPS-induced memory impairment. In addition, IL-17A Abs prevented the LPS-induced expression of TNF-α, IL-6 and inflammatory proteins, and of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) as well as the activation of microglia in the brain. IL-17A Abs also inhibited the expression of amyloid precursor protein (APP) and BACE1 and increased the expression of the synaptic marker PSD95 in the aged rats treated with LPS. In an in vitro study, we found that recombinant IL-17A could simulate microglial activation and increase production of pro-inflammatory cytokines. Taken together, our results suggest that IL-17A was involved in LPS-induced neuroinflammation and cognitive impairment in aged rats via microglial activation. Anti-IL-17A may represent a new therapeutic strategy for the treatment of endotoxemia-induced neuroinflammation and cognitive dysfunction.

Twitter Demographics

The data shown below were collected from the profiles of 5 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 106 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Japan 1 <1%
Unknown 105 99%

Demographic breakdown

Readers by professional status Count As %
Researcher 22 21%
Student > Master 15 14%
Student > Ph. D. Student 14 13%
Student > Bachelor 11 10%
Student > Doctoral Student 7 7%
Other 20 19%
Unknown 17 16%
Readers by discipline Count As %
Neuroscience 23 22%
Medicine and Dentistry 17 16%
Agricultural and Biological Sciences 15 14%
Biochemistry, Genetics and Molecular Biology 8 8%
Immunology and Microbiology 7 7%
Other 11 10%
Unknown 25 24%

Attention Score in Context

This research output has an Altmetric Attention Score of 12. 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 June 2016.
All research outputs
#2,046,835
of 19,413,723 outputs
Outputs from Journal of Neuroinflammation
#287
of 2,292 outputs
Outputs of similar age
#33,109
of 257,113 outputs
Outputs of similar age from Journal of Neuroinflammation
#1
of 6 outputs
Altmetric has tracked 19,413,723 research outputs across all sources so far. Compared to these this one has done well and is in the 89th percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 2,292 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 6.9. This one has done well, scoring higher than 87% 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 257,113 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 6 others from the same source and published within six weeks on either side of this one. This one has scored higher than all of them