Evidence map›Paper›PMID 23516302›Full record

ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2013

Centaurin-α1-Ras-Elk-1 signaling at mitochondria mediates β-amyloid-induced synaptic dysfunction.

Erzsebet M Szatmari, Ana F Oliveira, Elizabeth J Sumner, Ryohei Yasuda

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.

0numbers the graph read from it
0cells of the map it votes in
21citing papers in PubMed
1.8field-weighted citation impact, top 16% 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

21 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Loss of ADAP1/CentA1 Protects Against Autoimmune Demyelination.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025
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  8. Length Polymorphism and Methylation Status of UPS29 Minisatellite of theInternational journal of molecular sciences · 2020
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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

4 authors at 4 institutions in 3 countries.

Erzsebet M SzatmariDepartment of Neurobiology and Howard Hughes Medical Institute, Duke University Medical Center, Durham, NC 27710, USA.
Ana F Oliveira
Elizabeth J Sumner
Ryohei Yasuda
Duke University Hospital · USInstitute of Neurobiology · BGMax Planck Florida Institute for Neuroscience · USUniversity of Coimbra · PT

Funding

Mechanisms of Ras Signaling in Single SynapsesR01MH080047 · NIMH · MAX PLANCK FLORIDA CORPORATION · PI YASUDA, RYOHEI · 2007 to 2023
$6.8M
Imaging signal transduction in single dendritic spinesR01NS068410 · NINDS · MAX PLANCK FLORIDA CORPORATION · PI YASUDA, RYOHEI · 2009 to 2013
$2.0M
Large Scale Development of Sensors for Imaging Small GTPase Signals in SynapsesR01MH095090 · NIMH · MAX PLANCK FLORIDA CORPORATION · PI YASUDA, RYOHEI · 2011 to 2014
$1.7M
Howard Hughes Medical InstituteNIMH NIH HHS R01 MH080047NIMH NIH HHS R01 MH095090NINDS NIH HHS R01 NS068410
6 · The paper itself

Abstract

Alzheimer's disease is thought to be caused by β-amyloid peptide (Aβ)-dependent synaptic dysfunction. However, the signaling pathways connecting Aβ and synaptic dysfunction remain elusive. Here we report that Aβ transiently increases the expression level of centaurin-α1 (CentA1) in neurons, which induces a Ras-dependent association of Elk-1 with mitochondria, leading to mitochondrial and synaptic dysfunction in organotypic hippocampal slices of rats. Downregulation of the CentA1-Ras-Elk-1 pathway restored normal mitochondrial activity, spine structural plasticity, spine density, and the amplitude and frequency of miniature EPSCs in Aβ-treated neurons, whereas upregulation of the pathway was sufficient to decrease spine density. Elevations of CentA1 and association of Elk-1 with mitochondria were also observed in transgenic mice overexpressing a human mutant form of amyloid precursor protein. Therefore, the CentA1-Ras-Elk-1 signaling pathway acts on mitochondria to regulate dendritic spine density and synaptic plasticity in response to Aβ in hippocampal neurons, providing new pharmacological targets for Alzheimer's disease.

Indexed as

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsCells, CulturedDendritic Spinesets-Domain Protein Elk-1Excitatory Postsynaptic PotentialsGTPase-Activating ProteinsHippocampusHumansMaleMAP Kinase Signaling SystemMiceMice, Inbred StrainsMice, TransgenicMitochondriaAdap1 protein, ratAmyloid beta-PeptidesElk1 protein, mouseElk1 protein, ratets-Domain Protein Elk-1GTPase-Activating ProteinsNerve Tissue Proteinsras Proteins

Identifiers

PMID23516302
PMCPMC3866502
OpenAlexW2035331545

What OpenQuestion holds

Textmetadata
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.