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Amyloid-β 1–24 C-terminal truncated fragment promotes amyloid-β 1–42 aggregate formation in the healthy brain

Overview of attention for article published in Acta Neuropathologica Communications, October 2016
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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 (84th percentile)
  • Good Attention Score compared to outputs of the same age and source (70th percentile)

Mentioned by

news
1 news outlet
twitter
3 tweeters

Citations

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13 Dimensions

Readers on

mendeley
42 Mendeley
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Title
Amyloid-β 1–24 C-terminal truncated fragment promotes amyloid-β 1–42 aggregate formation in the healthy brain
Published in
Acta Neuropathologica Communications, October 2016
DOI 10.1186/s40478-016-0381-9
Pubmed ID
Authors

Sonia Mazzitelli, Fabia Filipello, Marco Rasile, Eliana Lauranzano, Chiara Starvaggi-Cucuzza, Matteo Tamborini, Davide Pozzi, Isabella Barajon, Toni Giorgino, Antonino Natalello, Michela Matteoli

Abstract

Substantial data indicate that amyloid-β (Aβ), the major component of senile plaques, plays a central role in Alzheimer's Disease and indeed the assembly of naturally occurring amyloid peptides into cytotoxic aggregates is linked to the disease pathogenesis. Although Aβ42 is a highly aggregating form of Aβ, the co-occurrence of shorter Aβ peptides might affect the aggregation potential of the Aβ pool. In this study we aimed to assess whether the structural behavior of human Aβ42 peptide inside the brain is influenced by the concomitant presence of N-terminal fragments produced by the proteolytic activity of glial cells. We show that the occurrence of the human C-terminal truncated 1-24 Aβ fragment impairs Aβ42 clearance through blood brain barrier and promotes the formation of Aβ42 aggregates even in the healthy brain. By showing that Aβ1-24 has seeding properties for aggregate formation in intracranially injected wild type mice, our study provide the proof-of-concept that peptides produced upon Aβ42 cleavage by activated glial cells may cause phenotypic defects even in the absence of genetic mutations associated with Alzheimer's Disease, possibly contributing to the development of the sporadic form of the pathology.

Twitter Demographics

The data shown below were collected from the profiles of 3 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 42 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 42 100%

Demographic breakdown

Readers by professional status Count As %
Researcher 8 19%
Student > Bachelor 7 17%
Student > Master 5 12%
Student > Doctoral Student 5 12%
Student > Ph. D. Student 4 10%
Other 7 17%
Unknown 6 14%
Readers by discipline Count As %
Neuroscience 10 24%
Physics and Astronomy 5 12%
Chemistry 3 7%
Biochemistry, Genetics and Molecular Biology 3 7%
Agricultural and Biological Sciences 2 5%
Other 9 21%
Unknown 10 24%

Attention Score in Context

This research output has an Altmetric Attention Score of 11. 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 19 September 2017.
All research outputs
#1,121,655
of 11,794,580 outputs
Outputs from Acta Neuropathologica Communications
#93
of 508 outputs
Outputs of similar age
#40,442
of 260,380 outputs
Outputs of similar age from Acta Neuropathologica Communications
#8
of 27 outputs
Altmetric has tracked 11,794,580 research outputs across all sources so far. Compared to these this one has done particularly well and is in the 90th percentile: it's in the top 10% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 508 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 7.7. This one has done well, scoring higher than 80% 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 260,380 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 27 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 70% of its contemporaries.