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Increased levels of Stress-inducible phosphoprotein-1 accelerates amyloid-β deposition in a mouse model of Alzheimer’s disease

Overview of attention for article published in Acta Neuropathologica Communications, August 2020
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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 (87th percentile)
  • Good Attention Score compared to outputs of the same age and source (77th percentile)

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1 news outlet
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15 X users
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2 Facebook pages

Citations

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14 Dimensions

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30 Mendeley
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Title
Increased levels of Stress-inducible phosphoprotein-1 accelerates amyloid-β deposition in a mouse model of Alzheimer’s disease
Published in
Acta Neuropathologica Communications, August 2020
DOI 10.1186/s40478-020-01013-5
Pubmed ID
Authors

Rachel E. Lackie, Jose Marques-Lopes, Valeriy G. Ostapchenko, Sarah Good, Wing-Yiu Choy, Patricija van Oosten-Hawle, Stephen H. Pasternak, Vania F. Prado, Marco A. M. Prado

Abstract

Molecular chaperones and co-chaperones, which are part of the protein quality control machinery, have been shown to regulate distinct aspects of Alzheimer's Disease (AD) pathology in multiple ways. Notably, the co-chaperone STI1, which presents increased levels in AD, can protect mammalian neurons from amyloid-β toxicity in vitro and reduced STI1 levels worsen Aβ toxicity in C. elegans. However, whether increased STI1 levels can protect neurons in vivo remains unknown. We determined that overexpression of STI1 and/or Hsp90 protected C. elegans expressing Aβ(3-42) against Aβ-mediated paralysis. Mammalian neurons were also protected by elevated levels of endogenous STI1 in vitro, and this effect was mainly due to extracellular STI1. Surprisingly, in the 5xFAD mouse model of AD, by overexpressing STI1, we find increased amyloid burden, which amplifies neurotoxicity and worsens spatial memory deficits in these mutants. Increased levels of STI1 disturbed the expression of Aβ-regulating enzymes (BACE1 and MMP-2), suggesting potential mechanisms by which amyloid burden is increased in mice. Notably, we observed that STI1 accumulates in dense-core AD plaques in both 5xFAD mice and human brain tissue. Our findings suggest that elevated levels of STI1 contribute to Aβ accumulation, and that STI1 is deposited in AD plaques in mice and humans. We conclude that despite the protective effects of STI1 in C. elegans and in mammalian cultured neurons, in vivo, the predominant effect of elevated STI1 is deleterious in AD.

X Demographics

X Demographics

The data shown below were collected from the profiles of 15 X users 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 30 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 30 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 5 17%
Student > Bachelor 3 10%
Student > Postgraduate 3 10%
Researcher 3 10%
Student > Doctoral Student 2 7%
Other 5 17%
Unknown 9 30%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 5 17%
Neuroscience 3 10%
Unspecified 2 7%
Nursing and Health Professions 2 7%
Pharmacology, Toxicology and Pharmaceutical Science 1 3%
Other 7 23%
Unknown 10 33%
Attention Score in Context

Attention Score in Context

This research output has an Altmetric Attention Score of 19. 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 27 February 2021.
All research outputs
#1,799,456
of 23,881,329 outputs
Outputs from Acta Neuropathologica Communications
#205
of 1,452 outputs
Outputs of similar age
#49,334
of 401,345 outputs
Outputs of similar age from Acta Neuropathologica Communications
#15
of 62 outputs
Altmetric has tracked 23,881,329 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 1,452 research outputs from this source. They typically receive a lot more attention than average, with a mean Attention Score of 13.4. This one has done well, scoring higher than 85% 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 401,345 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 87% of its contemporaries.
We're also able to compare this research output to 62 others from the same source and published within six weeks on either side of this one. This one has done well, scoring higher than 77% of its contemporaries.