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Age exacerbates the CCR2/5-mediated neuroinflammatory response to traumatic brain injury

Overview of attention for article published in Journal of Neuroinflammation, 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 (80th percentile)
  • Above-average Attention Score compared to outputs of the same age and source (53rd percentile)

Mentioned by

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9 tweeters
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1 patent

Citations

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27 Dimensions

Readers on

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39 Mendeley
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Title
Age exacerbates the CCR2/5-mediated neuroinflammatory response to traumatic brain injury
Published in
Journal of Neuroinflammation, April 2016
DOI 10.1186/s12974-016-0547-1
Pubmed ID
Authors

Josh M. Morganti, Lara-Kirstie Riparip, Austin Chou, Sharon Liu, Nalin Gupta, Susanna Rosi

Abstract

Traumatic brain injury (TBI) is a major risk factor for the development of multiple neurodegenerative diseases, including Alzheimer's disease (AD) and numerous recent reports document the development of dementia after TBI. Age is a significant factor in both the risk of and the incidence of acquired brain injury. TBI-induced inflammatory response is associated with activation of brain resident microglia and accumulation of infiltrating monocytes, which plays a pivotal role in chronic neurodegeneration and loss of neurological function after TBI. Despite the extensive clinical evidence implicating neuroinflammation with the TBI-related sequelae, the specific role of these different myeloid cells and the influence of age on TBI-initiated innate immune response remain unknown and poorly studied. We used gene profiling and pathway analysis to define the effect of age on inflammatory response at the time of injury. The recruitment of peripheral CCR2(+) macrophages was delineated using the CX3CR1 (GFP/+) CCR2 (RFP/+) reporter mouse. These responses were examined in the context of CCR2/5 antagonism using cenicriviroc. Unsupervised gene clustering and pathway analysis revealed that age predisposes exacerbated inflammatory response related to the recruitment and activation of peripheral monocytes to the injured brain. Using a unique reporter animal model able to discriminate resident versus peripherally derived myeloid cells, we demonstrate that in the aged brain, there is an increased accumulation of peripherally derived CCR2(+) macrophages after TBI compared to young animals. Exaggerated recruitment of this population of cells was associated with an augmented inflammatory response in the aged TBI animals. Targeting this cellular response with cenicriviroc, a dual CCR2/5 antagonist, significantly ameliorated injury-induced sequelae in the aged TBI animals. Importantly, these findings demonstrate that peripheral monocytes play a non-redundant and contributing role to the etiology of trauma-induced inflammatory sequelae in the aged brain.

Twitter Demographics

The data shown below were collected from the profiles of 9 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 39 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 39 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 10 26%
Researcher 8 21%
Student > Doctoral Student 6 15%
Student > Master 5 13%
Other 5 13%
Other 3 8%
Unknown 2 5%
Readers by discipline Count As %
Neuroscience 8 21%
Agricultural and Biological Sciences 8 21%
Medicine and Dentistry 7 18%
Biochemistry, Genetics and Molecular Biology 6 15%
Psychology 4 10%
Other 3 8%
Unknown 3 8%

Attention Score in Context

This research output has an Altmetric Attention Score of 9. 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 10 December 2019.
All research outputs
#2,261,614
of 14,923,543 outputs
Outputs from Journal of Neuroinflammation
#369
of 1,797 outputs
Outputs of similar age
#50,048
of 263,484 outputs
Outputs of similar age from Journal of Neuroinflammation
#12
of 26 outputs
Altmetric has tracked 14,923,543 research outputs across all sources so far. Compared to these this one has done well and is in the 84th percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 1,797 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.5. This one has done well, scoring higher than 79% 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 263,484 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 80% of its contemporaries.
We're also able to compare this research output to 26 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 53% of its contemporaries.