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Prion-like propagation of human brain-derived alpha-synuclein in transgenic mice expressing human wild-type alpha-synuclein

Overview of attention for article published in Acta Neuropathologica Communications, November 2015
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About this Attention Score

  • In the top 25% of all research outputs scored by Altmetric
  • Among the highest-scoring outputs from this source (#34 of 363)
  • High Attention Score compared to outputs of the same age (89th percentile)
  • High Attention Score compared to outputs of the same age and source (82nd percentile)

Mentioned by

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1 news outlet
twitter
5 tweeters

Citations

dimensions_citation
87 Dimensions

Readers on

mendeley
151 Mendeley
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2 CiteULike
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Title
Prion-like propagation of human brain-derived alpha-synuclein in transgenic mice expressing human wild-type alpha-synuclein
Published in
Acta Neuropathologica Communications, November 2015
DOI 10.1186/s40478-015-0254-7
Pubmed ID
Authors

Maria E. Bernis, Julius T. Babila, Sara Breid, Katharina Annick Wüsten, Ullrich Wüllner, Gültekin Tamgüney

Abstract

Parkinson's disease (PD) and multiple system atrophy (MSA) are neurodegenerative diseases that are characterized by the intracellular accumulation of alpha-synuclein containing aggregates. Recent increasing evidence suggests that Parkinson's disease and MSA pathology spread throughout the nervous system in a spatiotemporal fashion, possibly by prion-like propagation of alpha-synuclein positive aggregates between synaptically connected areas. Concurrently, intracerebral injection of pathological alpha-synuclein into transgenic mice overexpressing human wild-type alpha-synuclein, or human alpha-synuclein with the familial A53T mutation, or into wild-type mice causes spreading of alpha-synuclein pathology in the CNS. Considering that wild-type mice naturally also express a threonine at codon 53 of alpha-synuclein, it has remained unclear whether human wild-type alpha-synuclein alone, in the absence of endogenously expressed mouse alpha-synuclein, would support a similar propagation of alpha-synuclein pathology in vivo. Here we show that brain extracts from two patients with MSA and two patients with probable incidental Lewy body disease (iLBD) but not phosphate-buffered saline induce prion-like spreading of pathological alpha-synuclein after intrastriatal injection into mice expressing human wild-type alpha-synuclein. Mice were sacrificed at 3, 6, and 9 months post injection and analyzed neuropathologically and biochemically. Mice injected with brain extracts from patients with MSA or probable iLBD both accumulated intraneuronal inclusion bodies, which stained positive for phosphorylated alpha-synuclein and appeared predominantly within the injected brain hemisphere after 6 months. After 9 months these intraneuronal inclusion bodies had spread to the contralateral hemisphere and more rostral and caudal areas. Biochemical analysis showed that brains of mice injected with brain extracts from patients with MSA and probable iLBD contained hyperphosphorylated alpha-synuclein that also seeded aggregation of recombinant human wild-type alpha-synuclein in a Thioflavin T binding assay. Our results indicate that human wild-type alpha-synuclein supports the prion-like spreading of alpha-synuclein pathology in the absence of endogenously expressed mouse alpha-synuclein in vivo.

Twitter Demographics

The data shown below were collected from the profiles of 5 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 151 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
France 1 <1%
Unknown 150 99%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 39 26%
Researcher 28 19%
Student > Master 19 13%
Student > Bachelor 18 12%
Student > Postgraduate 6 4%
Other 20 13%
Unknown 21 14%
Readers by discipline Count As %
Neuroscience 41 27%
Agricultural and Biological Sciences 32 21%
Biochemistry, Genetics and Molecular Biology 28 19%
Medicine and Dentistry 10 7%
Chemistry 4 3%
Other 9 6%
Unknown 27 18%

Attention Score in Context

This research output has an Altmetric Attention Score of 13. 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 28 May 2016.
All research outputs
#622,467
of 7,822,782 outputs
Outputs from Acta Neuropathologica Communications
#34
of 363 outputs
Outputs of similar age
#31,432
of 291,864 outputs
Outputs of similar age from Acta Neuropathologica Communications
#5
of 28 outputs
Altmetric has tracked 7,822,782 research outputs across all sources so far. Compared to these this one has done particularly well and is in the 92nd percentile: it's in the top 10% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 363 research outputs from this source. They typically receive a little more attention than average, with a mean Attention Score of 7.2. This one has done particularly well, scoring higher than 90% 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 291,864 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 89% of its contemporaries.
We're also able to compare this research output to 28 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 82% of its contemporaries.