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Acetylated tau destabilizes the cytoskeleton in the axon initial segment and is mislocalized to the somatodendritic compartment

Overview of attention for article published in Molecular Neurodegeneration, January 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 (84th percentile)
  • Average Attention Score compared to outputs of the same age and source

Mentioned by

news
1 news outlet
twitter
2 tweeters

Citations

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44 Dimensions

Readers on

mendeley
77 Mendeley
Title
Acetylated tau destabilizes the cytoskeleton in the axon initial segment and is mislocalized to the somatodendritic compartment
Published in
Molecular Neurodegeneration, January 2016
DOI 10.1186/s13024-016-0109-0
Pubmed ID
Authors

Sohn, Peter Dongmin, Tracy, Tara E, Son, Hye-In, Zhou, Yungui, Leite, Renata E P, Miller, Bruce L, Seeley, William W, Grinberg, Lea T, Gan, Li, Peter Dongmin Sohn, Tara E. Tracy, Hye-In Son, Yungui Zhou, Renata E. P. Leite, Bruce L. Miller, William W. Seeley, Lea T. Grinberg, Li Gan

Abstract

Neurons are highly polarized cells in which asymmetric axonal-dendritic distribution of proteins is crucial for neuronal function. Loss of polarized distribution of the axonal protein tau is an early sign of Alzheimer's disease (AD) and other neurodegenerative disorders. The cytoskeletal network in the axon initial segment (AIS) forms a barrier between the axon and the somatodentritic compartment, contributing to axonal retention of tau. Although perturbation of the AIS cytoskeleton has been implicated in neurological disorders, the molecular triggers and functional consequence of AIS perturbation are incompletely understood. Here we report that tau acetylation and consequent destabilization of the AIS cytoskeleton promote the somatodendritic mislocalization of tau. AIS cytoskeletal proteins, including ankyrin G and βIV-spectrin, were downregulated in AD brains and negatively correlated with an increase in tau acetylated at K274 and K281. AIS proteins were also diminished in transgenic mice expressing tauK274/281Q, a tau mutant that mimics K274 and K281 acetylation. In primary neuronal cultures, the tauK274/281Q mutant caused hyperdynamic microtubules (MTs) in the AIS, shown by live-imaging of MT mobility and fluorescence recovery after photobleaching. Using photoconvertible tau constructs, we found that axonal tauK274/281Q was missorted into the somatodendritic compartment. Stabilizing MTs with epothilone D to restore the cytoskeletal barrier in the AIS prevented tau mislocalization in primary neuronal cultures. Together, these findings demonstrate that tau acetylation contributes to the pathogenesis of neurodegenerative disease by compromising the cytoskeletal sorting machinery in the AIS.

Twitter Demographics

The data shown below were collected from the profiles of 2 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 77 Mendeley readers of this research output. Click here to see the associated Mendeley record.

Geographical breakdown

Country Count As %
United States 1 1%
Unknown 76 99%

Demographic breakdown

Readers by professional status Count As %
Student > Ph. D. Student 19 25%
Student > Bachelor 9 12%
Student > Doctoral Student 9 12%
Student > Master 8 10%
Researcher 4 5%
Other 17 22%
Unknown 11 14%
Readers by discipline Count As %
Biochemistry, Genetics and Molecular Biology 20 26%
Neuroscience 18 23%
Agricultural and Biological Sciences 11 14%
Medicine and Dentistry 4 5%
Unspecified 3 4%
Other 7 9%
Unknown 14 18%

Attention Score in Context

This research output has an Altmetric Attention Score of 11. 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 21 February 2018.
All research outputs
#1,555,234
of 13,785,324 outputs
Outputs from Molecular Neurodegeneration
#174
of 580 outputs
Outputs of similar age
#39,395
of 259,211 outputs
Outputs of similar age from Molecular Neurodegeneration
#4
of 8 outputs
Altmetric has tracked 13,785,324 research outputs across all sources so far. Compared to these this one has done well and is in the 88th percentile: it's in the top 25% of all research outputs ever tracked by Altmetric.
So far Altmetric has tracked 580 research outputs from this source. They typically receive more attention than average, with a mean Attention Score of 8.6. This one has gotten more attention than average, scoring higher than 70% 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 259,211 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 84% of its contemporaries.
We're also able to compare this research output to 8 others from the same source and published within six weeks on either side of this one. This one has scored higher than 4 of them.