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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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  • In the top 25% of all research outputs scored by Altmetric
  • High Attention Score compared to outputs of the same age (87th percentile)
  • Good Attention Score compared to outputs of the same age and source (72nd percentile)

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1 news outlet
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7 X users

Citations

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141 Dimensions

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118 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.

X Demographics

X Demographics

The data shown below were collected from the profiles of 7 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 118 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 1 <1%
Unknown 117 99%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 23 19%
Researcher 21 18%
Student > Bachelor 13 11%
Student > Master 10 8%
Other 8 7%
Other 18 15%
Unknown 25 21%
Readers by discipline Count As %
Neuroscience 30 25%
Medicine and Dentistry 17 14%
Agricultural and Biological Sciences 13 11%
Biochemistry, Genetics and Molecular Biology 13 11%
Immunology and Microbiology 5 4%
Other 10 8%
Unknown 30 25%
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 15 April 2016.
All research outputs
#2,240,068
of 22,860,626 outputs
Outputs from Molecular Neurodegeneration
#255
of 849 outputs
Outputs of similar age
#38,812
of 301,058 outputs
Outputs of similar age from Molecular Neurodegeneration
#5
of 18 outputs
Altmetric has tracked 22,860,626 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 849 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 14.2. This one has gotten more attention than average, scoring higher than 69% 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 301,058 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 18 others from the same source and published within six weeks on either side of this one. This one has gotten more attention than average, scoring higher than 72% of its contemporaries.