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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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  • 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 (83rd percentile)

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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.

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Mendeley readers

Mendeley readers

The data shown below were compiled from readership statistics for 147 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Germany 2 1%
Unknown 145 99%

Demographic breakdown

Readers by professional status Count As %
Researcher 27 18%
Student > Ph. D. Student 24 16%
Student > Master 19 13%
Student > Bachelor 15 10%
Other 13 9%
Other 24 16%
Unknown 25 17%
Readers by discipline Count As %
Neuroscience 34 23%
Medicine and Dentistry 32 22%
Biochemistry, Genetics and Molecular Biology 15 10%
Immunology and Microbiology 12 8%
Agricultural and Biological Sciences 7 5%
Other 14 10%
Unknown 33 22%
Attention Score in Context

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
#2,706,949
of 22,879,161 outputs
Outputs from Journal of Neuroinflammation
#415
of 2,644 outputs
Outputs of similar age
#50,275
of 352,770 outputs
Outputs of similar age from Journal of Neuroinflammation
#9
of 56 outputs
Altmetric has tracked 22,879,161 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 2,644 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 7.6. This one has done well, scoring higher than 84% 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 352,770 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 56 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 83% of its contemporaries.