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Inhibition of the classical pathway of the complement cascade prevents early dendritic and synaptic degeneration in glaucoma

Overview of attention for article published in Molecular Neurodegeneration, 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 (87th percentile)
  • High Attention Score compared to outputs of the same age and source (80th percentile)

Mentioned by

news
1 news outlet
twitter
8 tweeters

Citations

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80 Dimensions

Readers on

mendeley
90 Mendeley
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Title
Inhibition of the classical pathway of the complement cascade prevents early dendritic and synaptic degeneration in glaucoma
Published in
Molecular Neurodegeneration, April 2016
DOI 10.1186/s13024-016-0091-6
Pubmed ID
Authors

Pete A. Williams, James R. Tribble, Keating W. Pepper, Stephen D. Cross, B Paul Morgan, James E. Morgan, Simon W. M. John, Gareth R. Howell

Abstract

Glaucoma is a complex, multifactorial disease characterised by the loss of retinal ganglion cells and their axons leading to a decrease in visual function. The earliest events that damage retinal ganglion cells in glaucoma are currently unknown. Retinal ganglion cell death appears to be compartmentalised, with soma, dendrite and axon changes potentially occurring through different mechanisms. There is mounting evidence from other neurodegenerative diseases suggesting that neuronal dendrites undergo a prolonged period of atrophy, including the pruning of synapses, prior to cell loss. In addition, recent evidence has shown the role of the complement cascade in synaptic pruning in glaucoma and other diseases. Using a genetic (DBA/2J mouse) and an inducible (rat microbead) model of glaucoma we first demonstrate that there is loss of retinal ganglion cell synapses and dendrites at time points that precede axon or soma loss. We next determine the role of complement component 1 (C1) in early synaptic loss and dendritic atrophy during glaucoma. Using a genetic knockout of C1qa (D2.C1qa (-/-) mouse) or pharmacological inhibition of C1 (in the rat bead model) we show that inhibition of C1 is sufficient to preserve dendritic and synaptic architecture. This study further supports assessing the potential for complement-modulating therapeutics for the prevention of retinal ganglion cell degeneration in glaucoma.

Twitter Demographics

The data shown below were collected from the profiles of 8 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 90 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 1 1%
Unknown 89 99%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 19 21%
Researcher 19 21%
Student > Master 10 11%
Student > Bachelor 10 11%
Student > Doctoral Student 5 6%
Other 16 18%
Unknown 11 12%
Readers by discipline Count As %
Neuroscience 26 29%
Medicine and Dentistry 14 16%
Agricultural and Biological Sciences 12 13%
Biochemistry, Genetics and Molecular Biology 11 12%
Immunology and Microbiology 5 6%
Other 7 8%
Unknown 15 17%

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 15 April 2016.
All research outputs
#1,422,199
of 15,814,274 outputs
Outputs from Molecular Neurodegeneration
#102
of 639 outputs
Outputs of similar age
#32,541
of 265,963 outputs
Outputs of similar age from Molecular Neurodegeneration
#1
of 5 outputs
Altmetric has tracked 15,814,274 research outputs across all sources so far. Compared to these this one has done particularly well and is in the 90th percentile: it's in the top 10% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 639 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 9.8. This one has done well, scoring higher than 83% 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 265,963 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 87% of its contemporaries.
We're also able to compare this research output to 5 others from the same source and published within six weeks on either side of this one. This one has scored higher than all of them