Evidence map›Paper›PMID 29233183›Full record

ArticleMolecular brain2017

Restoring synaptic plasticity and memory in mouse models of Alzheimer's disease by PKR inhibition.

Kyoung-Doo Hwang, Myeong Seong Bak, Sang Jeong Kim, Sangmyung Rhee, Yong-Seok Lee

Open access · goldAbstract read
In one paragraph

Article in Molecular brain, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 45 papers.

0numbers the graph read from it
0cells of the map it votes in
45citing papers in PubMed
1.9field-weighted citation impact, top 14% 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

45 citing papers in PubMed, 60 citations in OpenAlex.

  1. Distinct cell type-specific mechanisms underlie cognitive dysfunction during persistent integrated stress response activation.Proceedings of the National Academy of Sciences of the United States of America · 2026
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  4. Molecular Signatures of Id2- and Ascl4-Induced Wiring of Adult Hippocampal Neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2026
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  5. Review
  6. ComplexFrontiers in pediatrics · 2026
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  16. Luteolin protects DYT-Frontiers in pharmacology · 2023
    Article
  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

5 authors at 2 institutions in 1 country.

Kyoung-Doo HwangDepartment of Life Science, College of Natural Science, Chung-Ang University, Seoul, 06974, Republic of Korea.
Myeong Seong BakDepartment of Physiology, Seoul National University College of Medicine, Seoul, 03080, Republic of Korea.
Sang Jeong KimDepartment of Physiology, Seoul National University College of Medicine, Seoul, 03080, Republic of Korea.
Sangmyung RheeDepartment of Life Science, College of Natural Science, Chung-Ang University, Seoul, 06974, Republic of Korea. sangmyung.rhee@cau.ac.kr.
Yong-Seok LeeDepartment of Physiology, Seoul National University College of Medicine, Seoul, 03080, Republic of Korea. yongseok7@snu.ac.kr.
Seoul National University · KRChung-Ang University · KR

Funding

Korea National Institute of Health HI14C-1922-010014
6 · The paper itself

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder associated with deficits in cognition and synaptic plasticity. While accumulation of amyloid β (Aβ) and hyper-phosphorylation of tau are parts of the etiology, AD can be caused by a large number of different genetic mutations and other unknown factors. Considering such a heterogeneous nature of AD, it would be desirable to develop treatment strategies that can improve memory irrespective of the individual causes. Reducing the phosphorylation of eukaryotic translation initiation factor 2α (eIF2α) was shown to enhance long-term memory and synaptic plasticity in naïve mice. Moreover, hyper-phosphorylation of eIF2α is observed in the brains of postmortem AD patients. Therefore, regulating eIF2α phosphorylation can be a plausible candidate for restoring memory in AD by targeting memory-enhancing mechanism. In this study, we examined whether PKR inhibition can rescue synaptic and learning deficits in two different AD mouse models; 5XFAD transgenic and Aβ

Indexed as

MemoryAlzheimer DiseaseAmyloid beta-PeptidesAnimalsDisease Models, AnimaleIF-2 KinaseHippocampusLong-Term PotentiationMaleMice, Inbred ICRMice, TransgenicNeuronal PlasticitySignal TransductionAmyloid beta-PeptideseIF-2 KinaseAlzheimer’s disease (AD)Amyloid β (Aβ)Contextual fear conditioningLong-term potentiation (LTP)Object recognition memoryPKR inhibitor (PKRi)

Identifiers

PMID29233183
PMCPMC5727890
OpenAlexW2774783630

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.