Evidence map›Paper›PMID 26551858›Full record

ArticleNeuro-degenerative diseases2016

Impaired Eukaryotic Elongation Factor 1A Expression in Alzheimer's Disease.

Brenna C Beckelman, Xueyan Zhou, C Dirk Keene, Tao Ma

Abstract read
In one paragraph

Article in Neuro-degenerative diseases, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
20citing papers in PubMed, 1 pooled it
–field-weighted citation impact
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

20 citing papers in PubMed, 1 synthesis or guideline pooled it.

  1. Pooled it
  2. Article
  3. Review
  4. Article
  5. Article
  6. Article
  7. Article
  8. Article
  9. Translational control in aging and neurodegeneration.Wiley interdisciplinary reviews. RNA · 2021
    Review
  10. Functions and Regulation of Translation Elongation Factors.Frontiers in molecular biosciences · 2021
    Review
  11. Article
  12. Article
  13. Article
  14. Review
  15. Review
  16. Review
  17. Article
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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.

Brenna C BeckelmanDepartments of Internal Medicine-Gerontology and Geriatric Medicine, Wake Forest University School of Medicine, Winston-Salem, N.C., USA.
Xueyan Zhou
C Dirk Keene
Tao Ma

Funding

THERAPEUTIC EFFECTS OF INTRA-NASAL INSULIN DETEMIRP50AG005136 · NIA · UNIVERSITY OF WASHINGTON · PI WIJSMAN, ELLEN M · 1985 to 2019
$57.2M
AMPK in Alzheimer's Disease-Associated Synaptic Failure and Memory DeficitsR00AG044469 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI MA, TAO · 2015 to 2017
$739k
AMPK in Alzheimer's Disease-Associated Synaptic Failure and Memory DeficitsK99AG044469 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI MA, TAO · 2013 to 2014
$171k
NIA NIH HHS K99 AG044469NIA NIH HHS P50 AG005136NIA NIH HHS P50 AG05136NIA NIH HHS R00 AG044469
6 · The paper itself

Abstract

BACKGROUND/

aimsRecent studies have indicated a link between the impaired capacity of de novo protein synthesis and neurodegenerative diseases including Alzheimer's disease (AD). Moreover, it has been established that eukaryotic elongation factor 1A (eEF1A) plays a critical role in maintaining long-term synaptic plasticity, a cellular model for learning and memory. The aim of the present study is to determine whether brain eEF1A protein levels are dysregulated in brain tissue from AD patients compared with controls.

methodsPostmortem human brain samples collected from patients clinically diagnosed as AD, and from age-matched healthy controls, were utilized for this study. Both Western blot and immunohistochemistry approaches were utilized to investigate the potential alteration of eEF1A protein levels by using a specific antibody.

resultsOur data demonstrate that eEF1A expression is reduced in AD patients in the hippocampus, but not in the cerebellum or midfrontal gyrus. Furthermore, immunohistochemical experiments reveal that neuronal eEF1A reduction in the AD hippocampus is localized to the CA1 and dentate gyrus, but not to the CA3.

conclusionDysregulation of eEF1A and its associated signaling pathways might represent novel molecular mechanisms underlying AD pathogenesis. Further investigation is necessary to determine whether eEF1A is a viable therapeutic target for AD and other cognitive syndromes.

Indexed as

AgedAged, 80 and overAlzheimer DiseaseBlotting, WesternFemaleHippocampusHumansImmunohistochemistryMaleNeuronsPeptide Elongation Factor 1EEF1A1 protein, humanPeptide Elongation Factor 1

Identifiers

PMID26551858
PMCPMC4674306

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Registered trials

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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.