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Amyotrophic lateral sclerosis patient iPSC-derived astrocytes impair autophagy via non-cell autonomous mechanisms

Overview of attention for article published in Molecular Brain, June 2017
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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 (#37 of 665)
  • High Attention Score compared to outputs of the same age (85th percentile)

Mentioned by

news
1 news outlet
twitter
8 tweeters

Citations

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39 Dimensions

Readers on

mendeley
78 Mendeley
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Title
Amyotrophic lateral sclerosis patient iPSC-derived astrocytes impair autophagy via non-cell autonomous mechanisms
Published in
Molecular Brain, June 2017
DOI 10.1186/s13041-017-0300-4
Pubmed ID
Authors

Madill, Martin, McDonagh, Katya, Ma, Jun, Vajda, Alice, McLoughlin, Paul, O’Brien, Timothy, Hardiman, Orla, Shen, Sanbing, Martin Madill, Katya McDonagh, Jun Ma, Alice Vajda, Paul McLoughlin, Timothy O’Brien, Orla Hardiman, Sanbing Shen

Abstract

Amyotrophic lateral sclerosis, a devastating neurodegenerative disease, is characterized by the progressive loss of motor neurons and the accumulation of misfolded protein aggregates. The latter suggests impaired proteostasis may be a key factor in disease pathogenesis, though the underlying mechanisms leading to the accumulation of aggregates is unclear. Further, recent studies have indicated that motor neuron cell death may be mediated by astrocytes. Herein we demonstrate that ALS patient iPSC-derived astrocytes modulate the autophagy pathway in a non-cell autonomous manner. We demonstrate cells treated with patient derived astrocyte conditioned medium demonstrate decreased expression of LC3-II, a key adapter protein required for the selective degradation of p62 and ubiquitinated proteins targeted for degradation. We observed an increased accumulation of p62 in cells treated with patient conditioned medium, with a concomitant increase in the expression of SOD1, a protein associated with the development of ALS. Activation of autophagic mechanisms with Rapamycin reduces the accumulation of p62 puncta in cells treated with patient conditioned medium. These data suggest that patient astrocytes may modulate motor neuron cell death by impairing autophagic mechanisms, and the autophagy pathway may be a useful target in the development of novel therapeutics.

Twitter Demographics

The data shown below were collected from the profiles of 8 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 78 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
Unknown 78 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 21 27%
Researcher 9 12%
Student > Bachelor 9 12%
Student > Master 7 9%
Student > Doctoral Student 6 8%
Other 10 13%
Unknown 16 21%
Readers by discipline Count As %
Neuroscience 30 38%
Agricultural and Biological Sciences 16 21%
Biochemistry, Genetics and Molecular Biology 6 8%
Medicine and Dentistry 6 8%
Unspecified 1 1%
Other 1 1%
Unknown 18 23%

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 11 July 2019.
All research outputs
#1,274,342
of 14,104,163 outputs
Outputs from Molecular Brain
#37
of 665 outputs
Outputs of similar age
#37,727
of 267,848 outputs
Outputs of similar age from Molecular Brain
#1
of 2 outputs
Altmetric has tracked 14,104,163 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 665 research outputs from this source. They receive a mean Attention Score of 4.5. This one has done particularly well, scoring higher than 94% 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 267,848 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 85% of its contemporaries.
We're also able to compare this research output to 2 others from the same source and published within six weeks on either side of this one. This one has scored higher than all of them