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Suppression of LPS-induced tau hyperphosphorylation by serum amyloid A

Overview of attention for article published in Journal of Neuroinflammation, February 2016
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  • In the top 25% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (80th percentile)
  • Good Attention Score compared to outputs of the same age and source (72nd percentile)

Mentioned by

news
1 news outlet

Citations

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11 Dimensions

Readers on

mendeley
20 Mendeley
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Title
Suppression of LPS-induced tau hyperphosphorylation by serum amyloid A
Published in
Journal of Neuroinflammation, February 2016
DOI 10.1186/s12974-016-0493-y
Pubmed ID
Authors

Jin Liu, Ding Wang, Shu-Qin Li, Yang Yu, Richard D. Ye

Abstract

Accumulation of hyperphosphorylated tau is a major neuropathological feature of tauopathies including Alzheimer's disease (AD). Serum amyloid A (SAA), an acute-phase protein with cytokine-like property, has been implicated in amyloid deposition. It remains unclear whether SAA affects tau hyperphosphorylation. Potential involvement of SAA in tau hyperphosphorylation was examined using intracerebral injection of SAA, and in Saa3 (-/-) mice receiving systemic administration of lipopolysaccharide (LPS). Induced SAA expression and microglial activation were evaluated in these mice using real-time PCR and/or immunofluorescence staining. Cultured primary neuronal cells were treated with condition media (CM) from SAA-stimulated primary microglial cells. The alteration in tau hyperphosphorylation was determined using Western blotting. Saa3 is the predominant form of SAA proteins induced by LPS in the mouse brain that co-localizes with neurons. Overexpression of SAA by intracerebral injection attenuated tau hyperphosphorylation in the brain. Conversely, Saa3 deficiency enhanced tau phosphorylation induced by systemic LPS administration. Intracerebral injection of SAA also induced the activation of microglia in the brains. IL-10 released to CM from SAA-stimulated microglia attenuated tau hyperphosphorylation in cultured primary neurons. IL-10 neutralizing antibody reversed the effect of SAA in the attenuation of tau phosphorylation. LPS-induced expression of SAA proteins in the brain leads to the activation of microglia and release of IL-10, which in turn suppresses tau hyperphosphorylation in a mouse model of systemic inflammation.

Mendeley readers

The data shown below were compiled from readership statistics for 20 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Japan 1 5%
Unknown 19 95%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 6 30%
Other 3 15%
Student > Master 3 15%
Researcher 2 10%
Professor > Associate Professor 1 5%
Other 1 5%
Unknown 4 20%
Readers by discipline Count As %
Neuroscience 4 20%
Agricultural and Biological Sciences 4 20%
Biochemistry, Genetics and Molecular Biology 2 10%
Veterinary Science and Veterinary Medicine 2 10%
Immunology and Microbiology 2 10%
Other 2 10%
Unknown 4 20%

Attention Score in Context

This research output has an Altmetric Attention Score of 7. 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 06 February 2016.
All research outputs
#956,236
of 7,108,255 outputs
Outputs from Journal of Neuroinflammation
#166
of 934 outputs
Outputs of similar age
#57,457
of 319,312 outputs
Outputs of similar age from Journal of Neuroinflammation
#11
of 58 outputs
Altmetric has tracked 7,108,255 research outputs across all sources so far. Compared to these this one has done well and is in the 85th percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 934 research outputs from this source. They receive a mean Attention Score of 4.4. This one has done well, scoring higher than 79% 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 319,312 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 80% of its contemporaries.
We're also able to compare this research output to 58 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 72% of its contemporaries.