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Amyloid-beta-dependent phosphorylation of collapsin response mediator protein-2 dissociates kinesin in Alzheimer's disease

Overview of attention for article published in Neural Regeneration Research, January 2018
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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 (#39 of 1,532)
  • High Attention Score compared to outputs of the same age (87th percentile)
  • High Attention Score compared to outputs of the same age and source (88th percentile)

Mentioned by

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2 news outlets
twitter
1 tweeter

Readers on

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21 Mendeley
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Title
Amyloid-beta-dependent phosphorylation of collapsin response mediator protein-2 dissociates kinesin in Alzheimer's disease
Published in
Neural Regeneration Research, January 2018
DOI 10.4103/1673-5374.233451
Pubmed ID
Authors

SaraH Mokhtar, MinJoung Kim, KylieA Magee, PeiMun Aui, Speros Thomas, MahaM Bakhuraysah, AmaniA Alrehaili, JaeYoung Lee, DavidL Steer, Rachel Kenny, Catriona McLean, MichaelF Azari, Antonis Birpanagos, Ewlina Lipiec, Philip Heraud, Bayden Wood, Steven Petratos

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder characterized by accumulation of amyloid plaques and neurofibrillary tangles. Prior to the development of these characteristic pathological hallmarks of AD, anterograde axonal transport is impaired. However, the key proteins that initiate these intracellular impairments remain elusive. The collapsin response mediator protein-2 (CRMP-2) plays an integral role in kinesin-1-dependent axonal transport and there is evidence that phosphorylation of CRMP-2 releases kinesin-1. Here, we tested the hypothesis that amyloid-beta (Aβ)-dependent phosphorylation of CRMP-2 disrupts its association with the kinesin-1 (an anterograde axonal motor transport protein) in AD. We found that brain sections and lysates from AD patients demonstrated elevated phosphorylation of CRMP-2 at the T555 site. Additionally, in the transgenic Tg2576 mouse model of familial AD (FAD) that exhibits Aβ accumulation in the brain with age, we found substantial co-localization of pT555CRMP-2 and dystrophic neurites. In SH-SY5Y differentiated neuronal cultures, Aβ-dependent phosphorylation of CRMP-2 at the T555 site was also elevated and this reduced the CRMP-2 association with kinesin-1. The overexpression of an unphosphorylatable form of CRMP-2 in neurons promoted the re-establishment of CRMP-2-kinesin association and axon elongation. These data suggest that Aβ-dependent phosphorylation of CRMP-2 at the T555 site may directly impair anterograde axonal transport protein function, leading to neuronal defects.

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

Geographical breakdown

Country Count As %
Unknown 21 100%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 5 24%
Student > Bachelor 3 14%
Researcher 2 10%
Student > Doctoral Student 2 10%
Professor 2 10%
Other 3 14%
Unknown 4 19%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 7 33%
Neuroscience 5 24%
Agricultural and Biological Sciences 1 5%
Medicine and Dentistry 1 5%
Pharmacology, Toxicology and Pharmaceutical Science 1 5%
Other 1 5%
Unknown 5 24%

Attention Score in Context

This research output has an Altmetric Attention Score of 17. 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 04 April 2019.
All research outputs
#1,068,486
of 14,568,570 outputs
Outputs from Neural Regeneration Research
#39
of 1,532 outputs
Outputs of similar age
#34,289
of 273,599 outputs
Outputs of similar age from Neural Regeneration Research
#1
of 9 outputs
Altmetric has tracked 14,568,570 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 1,532 research outputs from this source. They receive a mean Attention Score of 4.1. This one has done particularly well, scoring higher than 97% 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 273,599 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 9 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