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Tauopathy in transgenic (SHR72) rats impairs function of central noradrenergic system and promotes neuroinflammation

Overview of attention for article published in Journal of Neuroinflammation, January 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 (84th percentile)
  • Good Attention Score compared to outputs of the same age and source (74th percentile)

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Title
Tauopathy in transgenic (SHR72) rats impairs function of central noradrenergic system and promotes neuroinflammation
Published in
Journal of Neuroinflammation, January 2016
DOI 10.1186/s12974-016-0482-1
Pubmed ID
Authors

Boris Mravec, Katarina Lejavova, Peter Vargovic, Katarina Ondicova, Lubica Horvathova, Petr Novak, Georg Manz, Peter Filipcik, Michal Novak, Richard Kvetnansky

Abstract

Brain norepinephrine (NE) plays an important role in the modulation of stress response and neuroinflammation. Recent studies indicate that in Alzheimer's disease (AD), the tau neuropathology begins in the locus coeruleus (LC) which is the main source of brain NE. Therefore, we investigated the changes in brain NE system and also the immune status under basal and stress conditions in transgenic rats over-expressing the human truncated tau protein. Brainstem catecholaminergic cell groups (LC, A1, and A2) and forebrain subcortical (nucleus basalis of Meynert), hippocampal (cornu ammonis, dentate gyrus), and neocortical areas (frontal and temporal association cortices) were analyzed for NE and interleukin 6 (IL-6) mRNA levels in unstressed rats and also in rats exposed to single or repeated immobilization. Moreover, gene expression of NE-biosynthetic enzyme, tyrosine hydroxylase (TH), and several pro- and anti-inflammatory mediators were determined in the LC. It was found that tauopathy reduced basal NE levels in forebrain areas, while the gene expression of IL-6 was increased in all selected areas at the same time. The differences between wild-type and transgenic rats in brain NE and IL-6 mRNA levels were observed in stressed animals as well. Tauopathy increased also the gene expression of TH in the LC. In addition, the LC exhibited exaggerated expression of pro- and anti-inflammatory mediators (IL-6, TNFα, inducible nitric oxide synthases 2 (iNOS2), and interleukin 10 (IL-10)) in transgenic rats suggesting that tauopathy affects also the immune background in LC. Positive correlation between NE and IL-6 mRNA levels in cornu ammonis in stressed transgenic animals indicated the reduction of anti-inflammatory effect of NE. Our data thus showed that tauopathy alters the functions of LC further leading to the reduction of NE levels and exaggeration of neuroinflammation in forebrain. These findings support the assumption that tau-related dysfunction of LC activates the vicious circle perpetuating neurodegeneration leading to the development of AD.

X Demographics

X Demographics

The data shown below were collected from the profile of 1 X user 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 27 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 27 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 8 30%
Student > Bachelor 3 11%
Professor 3 11%
Student > Master 3 11%
Student > Ph. D. Student 3 11%
Other 4 15%
Unknown 3 11%
Readers by discipline Count As %
Medicine and Dentistry 9 33%
Neuroscience 8 30%
Nursing and Health Professions 2 7%
Agricultural and Biological Sciences 2 7%
Pharmacology, Toxicology and Pharmaceutical Science 1 4%
Other 0 0%
Unknown 5 19%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 10. 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 29 January 2016.
All research outputs
#3,237,908
of 22,840,638 outputs
Outputs from Journal of Neuroinflammation
#643
of 2,639 outputs
Outputs of similar age
#59,525
of 394,766 outputs
Outputs of similar age from Journal of Neuroinflammation
#19
of 83 outputs
Altmetric has tracked 22,840,638 research outputs across all sources so far. Compared to these this one has done well and is in the 85th percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 2,639 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 7.6. This one has gotten more attention than average, scoring higher than 73% 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 394,766 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 84% of its contemporaries.
We're also able to compare this research output to 83 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 74% of its contemporaries.