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Inflammatory pre-conditioning restricts the seeded induction of α-synuclein pathology in wild type mice

Overview of attention for article published in Molecular Neurodegeneration, January 2017
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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 (83rd percentile)
  • Average Attention Score compared to outputs of the same age and source

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1 news outlet
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1 tweeter

Citations

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19 Dimensions

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31 Mendeley
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Title
Inflammatory pre-conditioning restricts the seeded induction of α-synuclein pathology in wild type mice
Published in
Molecular Neurodegeneration, January 2017
DOI 10.1186/s13024-016-0142-z
Pubmed ID
Authors

Emily J. Koller, Mieu M. T. Brooks, Todd E. Golde, Benoit I. Giasson, Paramita Chakrabarty

Abstract

Cell-to-cell transmission of α-synuclein (αSyn) is hypothesized to play an important role in disease progression in synucleinopathies. This process involves cellular uptake of extracellular amyloidogenic αSyn seeds followed by seeding of endogenous αSyn. Though it is well known that αSyn is an immunogenic protein that can interact with immune receptors, the role of innate immunity in regulating induction of αSyn pathology in vivo is unknown. Herein, we explored whether altering innate immune activation affects induction of αSyn pathology in wild type mice. We have previously demonstrated that recombinant adeno-associated virus (AAV) mediated expression of the inflammatory cytokine, Interleukin (IL)-6, in neonatal wild type mice brains leads to widespread immune activation in the brain without overt neurodegeneration. To investigate how IL-6 expression affects induction of αSyn pathology, we injected mouse wild type αSyn fibrils in the hippocampus of AAV-IL-6 expressing mice. Control mice received AAV containing an Empty vector (EV) construct. Two separate cohorts of AAV-IL-6 and AAV-EV mice were analyzed in this study: 4 months or 2 months following intrahippocampal αSyn seeding. Here, we show that IL-6 expression resulted in widespread gliosis and concurrently reduced αSyn inclusion pathology induced by a single intra-hippocampal injection of exogenous amyloidogenic αSyn. The reduction in αSyn inclusion pathology in IL-6 expressing mice was time-dependent. Suppression of αSyn pathology was accompanied by reductions in both argyrophilic and p62 immunoreactive inclusions. Our data supports a beneficial role of inflammatory priming of the CNS in wild type mice challenged with exogenous αSyn. A likely mechanism is efficient astroglial scavenging of exogenous αSyn, at least early in the disease process, and in the absence of human αSyn transgene overexpression. Given evidence that a pro-inflammatory environment may restrict seeding of αSyn pathology, this can be used to design anti-αSyn immunobiotherapies by harnessing innate immune function.

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 31 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Italy 1 3%
Germany 1 3%
Unknown 29 94%

Demographic breakdown

Readers by professional status Count As %
Researcher 8 26%
Student > Ph. D. Student 7 23%
Professor 5 16%
Professor > Associate Professor 3 10%
Student > Bachelor 2 6%
Other 1 3%
Unknown 5 16%
Readers by discipline Count As %
Agricultural and Biological Sciences 11 35%
Neuroscience 8 26%
Medicine and Dentistry 4 13%
Biochemistry, Genetics and Molecular Biology 1 3%
Chemistry 1 3%
Other 0 0%
Unknown 6 19%

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 01 June 2017.
All research outputs
#1,169,950
of 11,218,844 outputs
Outputs from Molecular Neurodegeneration
#149
of 494 outputs
Outputs of similar age
#51,303
of 316,924 outputs
Outputs of similar age from Molecular Neurodegeneration
#12
of 27 outputs
Altmetric has tracked 11,218,844 research outputs across all sources so far. Compared to these this one has done well and is in the 89th percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 494 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 7.9. This one has gotten more attention than average, scoring higher than 66% 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 316,924 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 83% of its contemporaries.
We're also able to compare this research output to 27 others from the same source and published within six weeks on either side of this one. This one is in the 40th percentile – i.e., 40% of its contemporaries scored the same or lower than it.