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Complement is activated in progressive multiple sclerosis cortical grey matter lesions

Overview of attention for article published in Journal of Neuroinflammation, June 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 (85th percentile)
  • High Attention Score compared to outputs of the same age and source (94th percentile)

Mentioned by

blogs
1 blog
twitter
5 tweeters

Citations

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72 Dimensions

Readers on

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133 Mendeley
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Title
Complement is activated in progressive multiple sclerosis cortical grey matter lesions
Published in
Journal of Neuroinflammation, June 2016
DOI 10.1186/s12974-016-0611-x
Pubmed ID
Authors

Lewis M. Watkins, James W. Neal, Sam Loveless, Iliana Michailidou, Valeria Ramaglia, Mark I. Rees, Richard Reynolds, Neil P. Robertson, B. Paul Morgan, Owain W. Howell

Abstract

The symptoms of multiple sclerosis (MS) are caused by damage to myelin and nerve cells in the brain and spinal cord. Inflammation is tightly linked with neurodegeneration, and it is the accumulation of neurodegeneration that underlies increasing neurological disability in progressive MS. Determining pathological mechanisms at play in MS grey matter is therefore a key to our understanding of disease progression. We analysed complement expression and activation by immunocytochemistry and in situ hybridisation in frozen or formalin-fixed paraffin-embedded post-mortem tissue blocks from 22 progressive MS cases and made comparisons to inflammatory central nervous system disease and non-neurological disease controls. Expression of the transcript for C1qA was noted in neurons and the activation fragment and opsonin C3b-labelled neurons and glia in the MS cortical and deep grey matter. The density of immunostained cells positive for the classical complement pathway protein C1q and the alternative complement pathway activation fragment Bb was significantly increased in cortical grey matter lesions in comparison to control grey matter. The number of cells immunostained for the membrane attack complex was elevated in cortical lesions, indicating complement activation to completion. The numbers of classical (C1-inhibitor) and alternative (factor H) pathway regulator-positive cells were unchanged between MS and controls, whilst complement anaphylatoxin receptor-bearing microglia in the MS cortex were found closely apposed to cortical neurons. Complement immunopositive neurons displayed an altered nuclear morphology, indicative of cell stress/damage, supporting our finding of significant neurodegeneration in cortical grey matter lesions. Complement is activated in the MS cortical grey matter lesions in areas of elevated numbers of complement receptor-positive microglia and suggests that complement over-activation may contribute to the worsening pathology that underlies the irreversible progression of MS.

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

Geographical breakdown

Country Count As %
Germany 2 2%
Unknown 131 98%

Demographic breakdown

Readers by professional status Count As %
Researcher 25 19%
Student > Ph. D. Student 20 15%
Student > Master 18 14%
Student > Bachelor 14 11%
Other 12 9%
Other 26 20%
Unknown 18 14%
Readers by discipline Count As %
Neuroscience 32 24%
Medicine and Dentistry 31 23%
Biochemistry, Genetics and Molecular Biology 14 11%
Immunology and Microbiology 12 9%
Agricultural and Biological Sciences 7 5%
Other 14 11%
Unknown 23 17%

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 11 October 2017.
All research outputs
#2,424,495
of 20,947,122 outputs
Outputs from Journal of Neuroinflammation
#353
of 2,427 outputs
Outputs of similar age
#40,450
of 276,652 outputs
Outputs of similar age from Journal of Neuroinflammation
#2
of 17 outputs
Altmetric has tracked 20,947,122 research outputs across all sources so far. Compared to these this one has done well and is in the 88th percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 2,427 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 85% 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 276,652 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 85% of its contemporaries.
We're also able to compare this research output to 17 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 94% of its contemporaries.