Evidence map›Paper›PMID 32810756›Full record

ArticleNeurobiology of aging2020

Repression of eEF2 kinase improves deficits in novel object recognition memory in aged mice.

Saahj P Gosrani, Hannah M Jester, Xueyan Zhou, Alexey G Ryazanov, Tao Ma

Open access · greenAbstract read
In one paragraph

Article in Neurobiology of aging, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
1.1field-weighted citation impact, top 24% 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

17 citing papers in PubMed, 62 citations in OpenAlex.

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  5. ACS medicinal chemistry letters · 2025
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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

5 authors at 2 institutions in 1 country.

Saahj P GosraniDepartment of Internal Medicine-Gerontology and Geriatric Medicine, Wake Forest University School of Medicine, Winston-Salem, NC, USA.
Hannah M JesterDepartment of Internal Medicine-Gerontology and Geriatric Medicine, Wake Forest University School of Medicine, Winston-Salem, NC, USA.
Xueyan ZhouDepartment of Internal Medicine-Gerontology and Geriatric Medicine, Wake Forest University School of Medicine, Winston-Salem, NC, USA.
Alexey G RyazanovDepartment of Pharmacology, Robert Wood Johnson Medical School, Rutgers University, Piscataway, NJ, USA.
Tao MaDepartment of Internal Medicine-Gerontology and Geriatric Medicine, Wake Forest University School of Medicine, Winston-Salem, NC, USA; Department of Physiology and Pharmacology, Wake Forest University School of Medicine, Winston-Salem, NC, USA; Department of Neurobiology and Anatomy, Wake Forest University School of Medicine, Winston-Salem, NC, USA. Electronic address: tma@wakehealth.edu.
Wake Forest University · USRutgers, The State University of New Jersey · US

Funding

Isoform-specific roles of AMPK in synaptic failure and memory deficit in Alzheimer's DiseaseR01AG055581 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI MA, TAO · 2017 to 2021
$2.9M
Role of protein synthesis in Alzheimers disease-associated impairments of synaptic plasticity and memoryR01AG056622 · NIA · WAKE FOREST UNIVERSITY HEALTH SCIENCES · PI MA, TAO · 2017 to 2021
$2.4M
NIA NIH HHS R01 AG055581NIA NIH HHS R01 AG056622
6 · The paper itself

Abstract

The normal aging process is commonly associated with mild cognitive deficits including memory decline. Previous studies indicate a role of dysregulated messenger ribonucleic acid translation capacity in cognitive defects associated with aging and aging-related diseases, including hyperphosphorylation of eukaryotic elongation factor 2 (eEF2). Phosphorylation of eEF2 by the kinase eEF2K inhibits its activity, hindering general protein synthesis. Here, we sought to determine whether cognitive deficits in aged mice can be improved by genetically deleting eEF2K (eEF2K KO) and consequently reduction of eEF2 phosphorylation. We found that suppression of eEF2K prevented aging-related deficits in novel object recognition memory. Interestingly, deletion of eEF2K did not alter overall protein synthesis in the hippocampus. Ultrastructural analysis revealed increase size and larger active zone lengths of postsynaptic densities in the hippocampus of aged eEF2K KO mice. Biochemical assays showed hippocampal eIF2α hyperphosphorylation in aged eEF2K KO mice, indicating inhibition of translation initiation. Our findings may provide insight into mechanistic understanding and thus development of novel therapeutic strategies for aging-related cognitive decline.

Indexed as

Cognitive AgingMemoryRecognition, PsychologyAgingAnimalsCognitive DysfunctionDisease Models, AnimalElongation Factor 2 KinaseFemaleHippocampusMaleMice, KnockoutPhosphorylationEef2k protein, mouseElongation Factor 2 KinaseAgingElongation factor 2MemoryProtein synthesisSignalingSynapse

Identifiers

PMID32810756
PMCPMC7948257
OpenAlexW3043961008

What OpenQuestion holds

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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.