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Accumulation of amyloid-β by astrocytes result in enlarged endosomes and microvesicle-induced apoptosis of neurons

Overview of attention for article published in Molecular Neurodegeneration, May 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 (86th percentile)
  • Above-average Attention Score compared to outputs of the same age and source (55th percentile)

Mentioned by

news
1 news outlet
twitter
1 tweeter
wikipedia
2 Wikipedia pages

Citations

dimensions_citation
54 Dimensions

Readers on

mendeley
110 Mendeley
Title
Accumulation of amyloid-β by astrocytes result in enlarged endosomes and microvesicle-induced apoptosis of neurons
Published in
Molecular Neurodegeneration, May 2016
DOI 10.1186/s13024-016-0098-z
Pubmed ID
Authors

Sofia Söllvander, Elisabeth Nikitidou, Robin Brolin, Linda Söderberg, Dag Sehlin, Lars Lannfelt, Anna Erlandsson

Abstract

Despite the clear physical association between activated astrocytes and amyloid-β (Aβ) plaques, the importance of astrocytes and their therapeutic potential in Alzheimer's disease remain elusive. Soluble Aβ aggregates, such as protofibrils, have been suggested to be responsible for the widespread neuronal cell death in Alzheimer's disease, but the mechanisms behind this remain unclear. Moreover, ineffective degradation is of great interest when it comes to the development and progression of neurodegeneration. Based on our previous results that astrocytes are extremely slow in degrading phagocytosed material, we hypothesized that astrocytes may be an important player in these processes. Hence, the aim of this study was to clarify the role of astrocytes in clearance, spreading and neuronal toxicity of Aβ. To examine the role of astrocytes in Aβ pathology, we added Aβ protofibrils to a co-culture system of primary neurons and glia. Our data demonstrates that astrocytes rapidly engulf large amounts of Aβ protofibrils, but then store, rather than degrade the ingested material. The incomplete digestion results in a high intracellular load of toxic, partly N-terminally truncated Aβ and severe lysosomal dysfunction. Moreover, secretion of microvesicles containing N-terminally truncated Aβ, induce apoptosis of cortical neurons. Taken together, our results suggest that astrocytes play a central role in the progression of Alzheimer's disease, by accumulating and spreading toxic Aβ species.

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

Geographical breakdown

Country Count As %
Spain 1 <1%
United States 1 <1%
Denmark 1 <1%
Unknown 107 97%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 23 21%
Student > Master 17 15%
Student > Bachelor 17 15%
Researcher 16 15%
Other 9 8%
Other 19 17%
Unknown 9 8%
Readers by discipline Count As %
Neuroscience 31 28%
Agricultural and Biological Sciences 24 22%
Biochemistry, Genetics and Molecular Biology 23 21%
Medicine and Dentistry 7 6%
Chemistry 5 5%
Other 7 6%
Unknown 13 12%

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 02 October 2019.
All research outputs
#1,321,843
of 14,079,291 outputs
Outputs from Molecular Neurodegeneration
#108
of 590 outputs
Outputs of similar age
#34,230
of 264,365 outputs
Outputs of similar age from Molecular Neurodegeneration
#3
of 9 outputs
Altmetric has tracked 14,079,291 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 590 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.9. 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 264,365 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 86% of its contemporaries.
We're also able to compare this research output to 9 others from the same source and published within six weeks on either side of this one. This one has scored higher than 6 of them.