Evidence map›Paper›PMID 28665013›Full record

ArticleAging cell2017

Epigenetic regulation by G9a/GLP complex ameliorates amyloid-beta 1-42 induced deficits in long-term plasticity and synaptic tagging/capture in hippocampal pyramidal neurons.

Mahima Sharma, Tobias Dierkes, Sreedharan Sajikumar

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Aging cell, 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
2.2field-weighted citation impact, top 13% 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

32 citing papers in PubMed, 52 citations in OpenAlex.

  1. Simvastatin rescues cognitive impairment in an AβNeuropsychopharmacology : official publication of the American College of Neuropsychopharmacology · 2026
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  10. 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
  11. Review
  12. Article
  13. Review
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  15. Article
  16. Anti-Amyloid Immunotherapies for Alzheimer's Disease: A 2023 Clinical Update.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023
    Review
  17. Review
  18. Article
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

3 authors at 1 institution in 2 countries.

Mahima SharmaDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Block MD9, 2 Medical Drive, Singapore, 117 597, Singapore.
Tobias DierkesDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Block MD9, 2 Medical Drive, Singapore, 117 597, Singapore.
Sreedharan SajikumarDepartment of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Block MD9, 2 Medical Drive, Singapore, 117 597, Singapore.
National University of Singapore · SG

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Altered epigenetic mechanisms are implicated in the cognitive decline associated with neurodegenerative diseases such as in Alzheimer's disease (AD). AD is the most prevalent form of dementia worldwide; amyloid plaques and neurofibrillary tangles are the histopathological hallmarks of AD. We have recently reported that the inhibition of G9a/GLP complex promotes long-term potentiation (LTP) and its associative mechanisms such as synaptic tagging and capture (STC). However, the role of this complex in plasticity impairments remains elusive. Here, we investigated the involvement of G9a/GLP complex in alleviating the effects of soluble Amyloid-β 1-42 oligomers (oAβ) on neuronal plasticity and associativity in the CA1 region of acute hippocampal slices from 5- to 7-week-old male Wistar rats. Our findings demonstrate that the regulation of G9a/GLP complex by inhibiting its catalytic activity reverses the amyloid-β oligomer-induced deficits in late-LTP and STC. This is achieved by releasing the transcription repression of the brain-derived neurotrophic factor (Bdnf) gene. The catalytic inhibition of G9a/GLP complex leads to the upregulation of Bdnf expression in the slices treated with oAβ. This further ensures the availability of BDNF that subsequently binds its receptor tyrosine kinase B (TrkB) and maintains the late-LTP. Furthermore, the capture of BDNF by weakly activated synapses re-establishes STC. Our findings regarding the reinstatement of functional plasticity and associativity in AD-like conditions provide the first evidence for the role of G9a/GLP complex in AD. We propose G9a/GLP complex as the possible target for preventing oAβ-induced plasticity deficits in hippocampal neurons.

Indexed as

Epigenesis, GeneticAmyloid beta-PeptidesAnimalsAzepinesBrain-Derived Neurotrophic FactorCA1 Region, HippocampalCognitive DysfunctionHistone-Lysine N-MethyltransferaseLong-Term PotentiationMaleMicrotomyPeptide FragmentsPyramidal CellsQuinazolinesRatsRats, WistarAmyloid beta-Peptidesamyloid beta-protein (1-42)AzepinesBIX 01294Brain-Derived Neurotrophic FactorEhmt2 protein, ratHistone-Lysine N-MethyltransferaseNtrk2 protein, ratPeptide FragmentsQuinazolinesReceptor, trkBUNC 0638amyloid β oligomerBDNFepigeneticshistone lysine-methyltransferaselong-term potentiationsynaptic tagging/capture

Identifiers

PMID28665013
PMCPMC5595698
OpenAlexW2732247207

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.