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TNF signaling inhibition in the CNS: implications for normal brain function and neurodegenerative disease

Overview of attention for article published in Journal of Neuroinflammation, January 2008
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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 (80th percentile)
  • High Attention Score compared to outputs of the same age and source (83rd percentile)

Mentioned by

twitter
1 tweeter
patent
1 patent
wikipedia
1 Wikipedia page

Citations

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597 Dimensions

Readers on

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486 Mendeley
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Title
TNF signaling inhibition in the CNS: implications for normal brain function and neurodegenerative disease
Published in
Journal of Neuroinflammation, January 2008
DOI 10.1186/1742-2094-5-45
Pubmed ID
Authors

Melissa K McCoy, Malú G Tansey

Abstract

The role of tumor necrosis factor (TNF) as an immune mediator has long been appreciated but its function in the brain is still unclear. TNF receptor 1 (TNFR1) is expressed in most cell types, and can be activated by binding of either soluble TNF (solTNF) or transmembrane TNF (tmTNF), with a preference for solTNF; whereas TNFR2 is expressed primarily by microglia and endothelial cells and is preferentially activated by tmTNF. Elevation of solTNF is a hallmark of acute and chronic neuroinflammation as well as a number of neurodegenerative conditions including ischemic stroke, Alzheimer's (AD), Parkinson's (PD), amyotrophic lateral sclerosis (ALS), and multiple sclerosis (MS). The presence of this potent inflammatory factor at sites of injury implicates it as a mediator of neuronal damage and disease pathogenesis, making TNF an attractive target for therapeutic development to treat acute and chronic neurodegenerative conditions. However, new and old observations from animal models and clinical trials reviewed here suggest solTNF and tmTNF exert different functions under normal and pathological conditions in the CNS. A potential role for TNF in synaptic scaling and hippocampal neurogenesis demonstrated by recent studies suggest additional in-depth mechanistic studies are warranted to delineate the distinct functions of the two TNF ligands in different parts of the brain prior to large-scale development of anti-TNF therapies in the CNS. If inactivation of TNF-dependent inflammation in the brain is warranted by additional pre-clinical studies, selective targeting of TNFR1-mediated signaling while sparing TNFR2 activation may lessen adverse effects of anti-TNF therapies in the CNS.

Twitter Demographics

The data shown below were collected from the profile of 1 tweeter 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 486 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 9 2%
Germany 3 <1%
United Kingdom 3 <1%
Brazil 2 <1%
Japan 2 <1%
Canada 2 <1%
Mexico 2 <1%
Iran, Islamic Republic of 1 <1%
Singapore 1 <1%
Other 7 1%
Unknown 454 93%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 117 24%
Researcher 86 18%
Student > Master 79 16%
Student > Bachelor 64 13%
Student > Doctoral Student 25 5%
Other 75 15%
Unknown 40 8%
Readers by discipline Count As %
Agricultural and Biological Sciences 177 36%
Medicine and Dentistry 77 16%
Neuroscience 65 13%
Biochemistry, Genetics and Molecular Biology 44 9%
Immunology and Microbiology 17 3%
Other 47 10%
Unknown 59 12%

Attention Score in Context

This research output has an Altmetric Attention Score of 7. 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 08 July 2019.
All research outputs
#2,867,463
of 15,397,971 outputs
Outputs from Journal of Neuroinflammation
#525
of 1,867 outputs
Outputs of similar age
#54,891
of 289,170 outputs
Outputs of similar age from Journal of Neuroinflammation
#7
of 42 outputs
Altmetric has tracked 15,397,971 research outputs across all sources so far. Compared to these this one has done well and is in the 81st percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 1,867 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 5.9. This one has gotten more attention than average, scoring higher than 71% 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 289,170 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 42 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.