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Expression of endogenous mouse APP modulates β-amyloid deposition in hAPP-transgenic mice

Overview of attention for article published in Acta Neuropathologica Communications, June 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 (80th percentile)
  • Average Attention Score compared to outputs of the same age and source

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Title
Expression of endogenous mouse APP modulates β-amyloid deposition in hAPP-transgenic mice
Published in
Acta Neuropathologica Communications, June 2017
DOI 10.1186/s40478-017-0448-2
Pubmed ID
Authors

Johannes Steffen, Markus Krohn, Christina Schwitlick, Thomas Brüning, Kristin Paarmann, Claus U. Pietrzik, Henrik Biverstål, Baiba Jansone, Oliver Langer, Jens Pahnke

Abstract

Amyloid-β (Aβ) deposition is one of the hallmarks of the amyloid hypothesis in Alzheimer's disease (AD). Mouse models using APP-transgene overexpression to generate amyloid plaques have shown to model only certain parts of the disease. The extent to which the data from mice can be transferred to man remains controversial. Several studies have shown convincing treatment results in reducing Aβ and enhancing cognition in mice but failed totally in human. One model-dependent factor has so far been almost completely neglected: the endogenous expression of mouse APP and its effects on the transgenic models and the readout for therapeutic approaches.Here, we report that hAPP-transgenic models of amyloidosis devoid of endogenous mouse APP expression (mAPP-knockout / mAPPko) show increased amounts and higher speed of Aβ deposition than controls with mAPP. The number of senile plaques and the level of aggregated hAβ were elevated in mAPPko mice, while the deposition in cortical blood vessels was delayed, indicating an alteration in the general aggregation propensity of hAβ together with endogenous mAβ. Furthermore, the cellular response to Aβ deposition was modulated: mAPPko mice developed a pronounced and age-dependent astrogliosis, while microglial association to amyloid plaques was diminished. The expression of human and murine aggregation-prone proteins with differing amino acid sequences within the same mouse model might not only alter the extent of deposition but also modulate the route of pathogenesis, and thus, decisively influence the study outcome, especially in translational research.

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

Geographical breakdown

Country Count As %
Unknown 55 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 10 18%
Student > Bachelor 8 15%
Researcher 7 13%
Student > Master 7 13%
Professor > Associate Professor 4 7%
Other 8 15%
Unknown 11 20%
Readers by discipline Count As %
Neuroscience 13 24%
Agricultural and Biological Sciences 7 13%
Biochemistry, Genetics and Molecular Biology 4 7%
Chemistry 2 4%
Veterinary Science and Veterinary Medicine 1 2%
Other 11 20%
Unknown 17 31%
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 30 June 2017.
All research outputs
#3,262,867
of 22,982,639 outputs
Outputs from Acta Neuropathologica Communications
#706
of 1,391 outputs
Outputs of similar age
#61,768
of 316,841 outputs
Outputs of similar age from Acta Neuropathologica Communications
#14
of 23 outputs
Altmetric has tracked 22,982,639 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 1,391 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 12.8. This one is in the 46th percentile – i.e., 46% of its peers scored the same or lower than it.
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 316,841 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 23 others from the same source and published within six weeks on either side of this one. This one is in the 39th percentile – i.e., 39% of its contemporaries scored the same or lower than it.