Evidence map›Paper›PMID 26926225›Full record

ArticleScientific reports2016

Epigenetic modification of PKMζ rescues aging-related cognitive impairment.

Chen Chen, Shi-Qiu Meng, Yan-Xue Xue, Ying Han, Cheng-Yu Sun, Jia-Hui Deng, Na Chen, Yan-Ping Bao, Fei-Long Zhang, Lin-Lin Cao and 4 more

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing 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

11 citing papers in PubMed, 19 citations in OpenAlex.

  1. Article
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  8. Review
  9. Increased GSNOR Expression during Aging Impairs Cognitive Function and Decreases S-Nitrosation of CaMKIIα.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2017
    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

14 authors at 5 institutions in 2 countries.

Chen ChenInstitute of Mental Health, Peking University Sixth Hospital, and Key Laboratory of Mental Health, Beijing 100191, China.
Shi-Qiu MengInstitute of Mental Health, Peking University Sixth Hospital, and Key Laboratory of Mental Health, Beijing 100191, China.
Yan-Xue XueNational Institute on Drug Dependence and Beijing Key Laboratory of Drug Dependence Research, Peking University, Beijing 100191, China.
Ying HanNational Institute on Drug Dependence and Beijing Key Laboratory of Drug Dependence Research, Peking University, Beijing 100191, China.
Cheng-Yu SunInstitute of Mental Health, Peking University Sixth Hospital, and Key Laboratory of Mental Health, Beijing 100191, China.
Jia-Hui DengInstitute of Mental Health, Peking University Sixth Hospital, and Key Laboratory of Mental Health, Beijing 100191, China.
Na ChenNational Institute on Drug Dependence and Beijing Key Laboratory of Drug Dependence Research, Peking University, Beijing 100191, China.
Yan-Ping BaoNational Institute on Drug Dependence and Beijing Key Laboratory of Drug Dependence Research, Peking University, Beijing 100191, China.
Fei-Long ZhangNational Institute on Drug Dependence and Beijing Key Laboratory of Drug Dependence Research, Peking University, Beijing 100191, China.
Lin-Lin CaoDepartment of Biochemistry and Molecular Biology, Peking University Health Science Center, Beijing 100191, China.
Wei-Guo ZhuDepartment of Biochemistry and Molecular Biology, Peking University Health Science Center, Beijing 100191, China.
Jie ShiNational Institute on Drug Dependence and Beijing Key Laboratory of Drug Dependence Research, Peking University, Beijing 100191, China.
Wei-Hong SongBrain Research Centre, Departments of Medicine and Psychiatry, University of British Columbia, Vancouver, British Columbia, V6T 1Z3, Canada.
Lin LuInstitute of Mental Health, Peking University Sixth Hospital, and Key Laboratory of Mental Health, Beijing 100191, China.
Peking University · CNNational Institutes for Food and Drug Control · CNCenter for Life Sciences · CNPeking University Sixth Hospital · CNUniversity of British Columbia · CA

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Cognition is impacted by aging. However, the mechanisms that underlie aging-associated cognitive impairment are unclear. Here we showed that cognitive decline in aged rats was associated with changes in DNA methylation of protein kinase Mζ (PKMζ) in the prelimbic cortex (PrL). PKMζ is a crucial molecule involved in the maintenance of long-term memory. Using different behavioral models, we confirmed that aged rats exhibited cognitive impairment in memory retention test 24 h after training, and overexpression of PKMζ in the PrL rescued cognitive impairment in aged rats. After fear conditioning, the protein levels of PKMζ and the membrane expression of GluR2 increased in the PrL in young and adult rats but not in aged rats, and the levels of methylated PKMζ DNA in the PrL decreased in all age groups, whereas the levels of unmethylated PKMζ DNA increased only in young and adult rats. We also found that environmentally enriched housing reversed the hypermethylation of PKMζ and restored cognitive performance in aged rats. Inactivation of PKMζ prevented the potentiating effects of environmental enrichment on memory retention in aged rats. These results indicated that PKMζ might be a potential target for the treatment of aging-related cognitive impairment, suggesting a potential therapeutic avenue.

Indexed as

Epigenesis, GeneticAgingAnimalsCognitive DysfunctionDNA MethylationLearningMaleMemory, Long-TermPrefrontal CortexProtein Kinase CRatsRats, Sprague-DawleyProtein Kinase Cprotein kinase M zeta, rat

Identifiers

PMID26926225
PMCPMC4772003
OpenAlexW2312199390

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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.