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Complement activation at the motor end-plates in amyotrophic lateral sclerosis

Overview of attention for article published in Journal of Neuroinflammation, April 2016
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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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49 Dimensions

Readers on

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59 Mendeley
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Title
Complement activation at the motor end-plates in amyotrophic lateral sclerosis
Published in
Journal of Neuroinflammation, April 2016
DOI 10.1186/s12974-016-0538-2
Pubmed ID
Authors

Nawal Bahia El Idrissi, Sanne Bosch, Valeria Ramaglia, Eleonora Aronica, Frank Baas, Dirk Troost

Abstract

Amyotrophic lateral sclerosis (ALS) is a fatal progressive neurodegenerative disease with no available therapy. Components of the innate immune system are activated in the spinal cord and central nervous system of ALS patients. Studies in the SOD1(G93A) mouse show deposition of C1q and C3/C3b at the motor end-plate before neurological symptoms are apparent, suggesting that complement activation precedes neurodegeneration in this model. To obtain a better understanding of the role of complement at the motor end-plates in human ALS pathology, we analyzed post-mortem tissue of ALS donors for complement activation and its regulators. Post-mortem intercostal muscle biopsies were collected at autopsy from ALS (n = 11) and control (n = 6) donors. The samples were analyzed for C1q, membrane attack complex (MAC), CD55, and CD59 on the motor end-plates, using immunofluorescence or immunohistochemistry. Here, we show that complement activation products and regulators are deposited on the motor end-plates of ALS patients. C1q co-localized with neurofilament in the intercostal muscle of ALS donors and was absent in controls (P = 0.001). In addition, C1q was found deposited on the motor end-plates in the intercostal muscle. MAC was also found deposited on motor end-plates that were innervated by nerves in the intercostal muscle of ALS donors but not in controls (P = 0.001). High levels of the regulators CD55 and CD59 were detected at the motor end-plates of ALS donors but not in controls, suggesting an attempt to counteract complement activation and prevent MAC deposition on the end-plates before they are lost. This study provides evidence that complement activation products are deposited on innervated motor end-plates in the intercostal muscle of ALS donors, indicating that complement activation may precede end-plate denervation in human ALS. This study adds to the understanding of ALS pathology in man and identifies complement as a potential modifier of the disease process.

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 59 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Australia 1 2%
Unknown 58 98%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 10 17%
Researcher 10 17%
Student > Bachelor 8 14%
Student > Master 6 10%
Student > Postgraduate 5 8%
Other 9 15%
Unknown 11 19%
Readers by discipline Count As %
Neuroscience 15 25%
Agricultural and Biological Sciences 11 19%
Medicine and Dentistry 7 12%
Biochemistry, Genetics and Molecular Biology 5 8%
Immunology and Microbiology 2 3%
Other 3 5%
Unknown 16 27%

Attention Score in Context

This research output has an Altmetric Attention Score of 13. 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
#2,235,875
of 21,454,959 outputs
Outputs from Journal of Neuroinflammation
#316
of 2,481 outputs
Outputs of similar age
#38,707
of 279,938 outputs
Outputs of similar age from Journal of Neuroinflammation
#1
of 13 outputs
Altmetric has tracked 21,454,959 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 2,481 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 7.1. 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 279,938 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 13 others from the same source and published within six weeks on either side of this one. This one has done particularly well, scoring higher than 99% of its contemporaries.