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Complement components are upregulated and correlate with disease progression in the TDP-43Q331K mouse model of amyotrophic lateral sclerosis

Overview of attention for article published in Journal of Neuroinflammation, June 2018
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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 (84th percentile)
  • High Attention Score compared to outputs of the same age and source (88th percentile)

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1 news outlet
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6 X users

Citations

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45 Dimensions

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69 Mendeley
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Title
Complement components are upregulated and correlate with disease progression in the TDP-43Q331K mouse model of amyotrophic lateral sclerosis
Published in
Journal of Neuroinflammation, June 2018
DOI 10.1186/s12974-018-1217-2
Pubmed ID
Authors

John D. Lee, Samantha C. Levin, Emily F. Willis, Rui Li, Trent M. Woodruff, Peter G. Noakes

Abstract

Components of the innate immune complement system have been implicated in the pathogenesis of amyotrophic lateral sclerosis (ALS) specifically using hSOD1 transgenic animals; however, a comprehensive examination of complement expression in other transgenic ALS models has not been performed. This study therefore aimed to determine the expression of several key complement components and regulators in the lumbar spinal cord and tibialis anterior muscle of TDP-43Q331K mice during different disease ages. Non-transgenic, TDP-43WT and TDP-43Q331K mice were examined at three different ages of disease progression. Expression of complement components and their regulators were examined using real-time quantitative PCR and enzyme-linked immunosorbent assay. Localisation of terminal complement component receptor C5aR1 within the lumbar spinal cord was also investigated using immunohistochemistry. Altered levels of several major complement factors, including C5a, in the spinal cord and tibialis anterior muscle of TDP-43Q331K mice were observed as disease progressed, suggesting overall increased complement activation in TDP-43Q331K mice. C5aR1 increased during disease progression, with immuno-localisation demonstrating expression on motor neurons and expression on microglia surrounding the regions of motor neuron death. There was a strong negative linear relationship between spinal cord C1qB, C3 and C5aR1 mRNA levels with hind-limb grip strength. These results indicate that similar to SOD1 transgenic animals, local complement activation and increased expression of C5aR1 may contribute to motor neuron death and neuromuscular junction denervation in the TDP-43Q331K mouse ALS model. This further validates C5aR1 as a potential therapeutic target for ALS.

X Demographics

X Demographics

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

Mendeley readers

The data shown below were compiled from readership statistics for 69 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 69 100%

Demographic breakdown

Readers by professional status Count As %
Student > Bachelor 12 17%
Student > Ph. D. Student 11 16%
Researcher 9 13%
Student > Master 8 12%
Student > Doctoral Student 6 9%
Other 13 19%
Unknown 10 14%
Readers by discipline Count As %
Neuroscience 17 25%
Medicine and Dentistry 11 16%
Biochemistry, Genetics and Molecular Biology 9 13%
Pharmacology, Toxicology and Pharmaceutical Science 6 9%
Agricultural and Biological Sciences 4 6%
Other 10 14%
Unknown 12 17%
Attention Score in Context

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 01 January 2022.
All research outputs
#2,622,610
of 25,537,395 outputs
Outputs from Journal of Neuroinflammation
#369
of 2,960 outputs
Outputs of similar age
#52,427
of 343,255 outputs
Outputs of similar age from Journal of Neuroinflammation
#10
of 80 outputs
Altmetric has tracked 25,537,395 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 2,960 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.7. 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 343,255 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 84% of its contemporaries.
We're also able to compare this research output to 80 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 88% of its contemporaries.