Evidence map›Paper›PMID 26198811›Full record

ArticleNature communications2015

HDAC6 and RhoA are novel players in Abeta-driven disruption of neuronal polarity.

Hanako Tsushima, Marco Emanuele, Alice Polenghi, Alessandro Esposito, Massimo Vassalli, Andrea Barberis, Francesco Difato, Evelina Chieregatti

Open access · goldAbstract read
PubMed Publisher
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed
3.6field-weighted citation impact, top 7% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

47 citing papers in PubMed, 71 citations in OpenAlex.

  1. Article
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  11. Extracellular Tau Oligomers Damage the Axon Initial Segment.Journal of Alzheimer's disease : JAD · 2023
    Article
  12. ACS chemical biology · 2022
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  13. Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Review
  19. Review
  20. Meet the editor series-Massimo Vassalli.Biophysical reviews · 2021
    Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 2 institutions in 1 country.

Hanako TsushimaDepartment of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genoa 16163, Italy.
Marco EmanueleDepartment of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genoa 16163, Italy.
Alice PolenghiDepartment of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genoa 16163, Italy.
Alessandro EspositoDepartment of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genoa 16163, Italy.
Massimo VassalliInstitute of Biophysics, National Research Council of Italy, Genoa, Italy.
Andrea BarberisDepartment of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genoa 16163, Italy.
Francesco DifatoDepartment of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genoa 16163, Italy.
Evelina ChieregattiDepartment of Neuroscience and Brain Technologies, Istituto Italiano di Tecnologia, Genoa 16163, Italy.
Italian Institute of Technology · ITNational Research Council · IT

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Maintenance of neuronal polarity and regulation of cytoskeletal dynamics are vital during development and to uphold synaptic activity in neuronal networks. Here we show that soluble β-amyloid (Aβ) disrupts actin and microtubule (MT) dynamics via activation of RhoA and inhibition of histone deacetylase 6 (HDAC6) in cultured hippocampal neurons. The contact of Aβ with the extracellular membrane promotes RhoA activation, leading to growth cone collapse and neurite retraction, which might be responsible for hampered neuronal pathfinding and migration in Alzheimer's disease (AD). The inhibition of HDAC6 by Aβ increases the level of heterodimeric acetylated tubulin and acetylated tau, both of which have been found altered in AD. We also find that the loss of HDAC6 activity perturbs the integrity of axon initial segment (AIS), resulting in mislocalization of ankyrin G and increased MT instability in the AIS concomitant with loss of polarized localization of tau and impairment of action potential firing.

Indexed as

AcetylationActinsAmyloid beta-PeptidesAnimalsGrowth ConesHistone Deacetylase 6Histone DeacetylasesMice, Inbred C57BLrhoA GTP-Binding Proteintau ProteinsTubulinActinsAmyloid beta-PeptidesHdac6 protein, mouseHistone Deacetylase 6Histone DeacetylasesrhoA GTP-Binding Proteintau ProteinsTubulin

Identifiers

PMID26198811
OpenAlexW1001294977

What OpenQuestion holds

Texttitle and abstract
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.