Evidence map›Paper›PMID 28484012›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2017

Metaplasticity mechanisms restore plasticity and associativity in an animal model of Alzheimer's disease.

Qin Li, Sheeja Navakkode, Martin Rothkegel, Tuck Wah Soong, Sreedharan Sajikumar, Martin Korte

Abstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.

0numbers the graph read from it
0cells of the map it votes in
32citing papers in PubMed
–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

32 citing papers in PubMed.

  1. Article
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  6. Synapses tagged, memories kept: synaptic tagging and capture hypothesis in brain health and disease.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024
    Review
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  17. The two faces of synaptic failure in AppAlzheimer's research & therapy · 2020
    Article
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  19. Review
  20. Article
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

6 authors.

Qin LiDivision of Cellular Neurobiology, Zoological Institute, Technische Universität Braunschweig, D-38106 Braunschweig, Germany.
Sheeja NavakkodeDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, 117597 Singapore.
Martin RothkegelDivision of Cellular Neurobiology, Zoological Institute, Technische Universität Braunschweig, D-38106 Braunschweig, Germany.
Tuck Wah SoongDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, 117597 Singapore.
Sreedharan SajikumarDivision of Cellular Neurobiology, Zoological Institute, Technische Universität Braunschweig, D-38106 Braunschweig, Germany; phssks@nus.edu.sg m.korte@tu-bs.de.ORCID 0000-0002-5761-8982
Martin KorteDivision of Cellular Neurobiology, Zoological Institute, Technische Universität Braunschweig, D-38106 Braunschweig, Germany; phssks@nus.edu.sg m.korte@tu-bs.de.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Dynamic regulation of plasticity thresholds in a neuronal population is critical for the formation of long-term plasticity and memory and is achieved by mechanisms such as metaplasticity. Metaplasticity tunes the synapses to undergo changes that are necessary prerequisites for memory storage under physiological and pathological conditions. Here we discovered that, in amyloid precursor protein (APP)/presenilin-1 (PS1) mice (age 3-4 mo), a prominent mouse model of Alzheimer's disease (AD), late long-term potentiation (LTP; L-LTP) and its associative plasticity mechanisms such as synaptic tagging and capture (STC) were impaired already in presymptomatic mice. Interestingly, late long-term depression (LTD; L-LTD) was not compromised, but the positive associative interaction of LTP and LTD, cross-capture, was altered in these mice. Metaplastic activation of ryanodine receptors (RyRs) in these neurons reestablished L-LTP and STC. We propose that RyR-mediated metaplastic mechanisms can be considered as a possible therapeutic target for counteracting synaptic impairments in the neuronal networks during the early progression of AD.

Indexed as

Neuronal PlasticityAlzheimer DiseaseAmyloidogenic ProteinsAnimalsDisease Models, AnimalHumansMiceMice, TransgenicPresenilin-1Protein Kinase CProtein Kinase C zetaRyanodine Receptor Calcium Release ChannelAmyloidogenic ProteinsPresenilin-1Protein Kinase CProtein Kinase C zetaRyanodine Receptor Calcium Release ChannelAPP/PS1 micehippocampusL-LTPmetaplasticitysynaptic tagging

Identifiers

PMID28484012
PMCPMC5448214

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.