Evidence map›Paper›PMID 23216574›Full record

ReviewEpilepsia2012

Epigenetics and epilepsy.

Avtar Roopra, Raymond Dingledine, Jenny Hsieh

Open access · bronzeAbstract readReview
In one paragraph

Review in Epilepsia, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.

0numbers the graph read from it
0cells of the map it votes in
41citing papers in PubMed
6.8field-weighted citation impact, top 3% 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

41 citing papers in PubMed, 85 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Article
  5. Article
  6. Review
  7. Review
  8. Tiered analysis of whole-exome sequencing for epilepsy diagnosis.Molecular genetics and genomics : MGG · 2020
    Article
  9. Article
  10. Epigenetics and Neurological Disorders in ART.International journal of molecular sciences · 2019
    Review
  11. Article
  12. Article
  13. Article
  14. Article
  15. Drug design, development and therapy · 2018
    Article
  16. Review
  17. Review
  18. Article
  19. Article
  20. β-Hydroxybutyrate: A Signaling Metabolite.Annual review of nutrition · 2017
    Review
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

3 authors at 2 institutions in 1 country.

Avtar RoopraDepartment of Neuroscience, University of Wisconsin-Madison, Madison, Wisconsin 53706, USA. asroopra@wisc.edu
Raymond Dingledine
Jenny Hsieh
Emory University · USUniversity of Wisconsin–Madison · US

Funding

Metabolic and Epigenetic Regulation of Genes Controlling Neuronal PlasticityR01NS065067 · NINDS · UNIVERSITY OF WISCONSIN-MADISON · PI ROOPRA, AVTAR S · 2010 to 2014
$1.6M
Epigenetic regulation of adult neurogenesisR01AG032383 · NIA · UT SOUTHWESTERN MEDICAL CENTER · PI HSIEH, JENNY · 2009 to 2013
$1.5M
Regulation of epileptogenesis by the transcriptional repressor, RESTR01NS076775 · NINDS · EMORY UNIVERSITY · PI DINGLEDINE, RAYMOND J, HSIEH, JENNY · 2011 to 2014
$1.4M
Novel Mechanisms of Adult Neurogenesis in Physiological and Pathological ContextsK02AG041815 · NIA · UT SOUTHWESTERN MEDICAL CENTER · PI HSIEH, JENNY · 2012 to 2016
$646k
NIA NIH HHS AG032383NIA NIH HHS AG041815NIA NIH HHS K02 AG041815NIA NIH HHS R01 AG032383NIMH NIH HHS MH0947515NINDS NIH HHS NS065067NINDS NIH HHS NS076775NINDS NIH HHS R01 NS065067NINDS NIH HHS R01 NS076775
6 · The paper itself

Abstract

Seizures can give rise to enduring changes that reflect alterations in gene-expression patterns, intracellular and intercellular signaling, and ultimately network alterations that are a hallmark of epilepsy. A growing body of literature suggests that long-term changes in gene transcription associated with epilepsy are mediated via modulation of chromatin structure. One transcription factor in particular, repressor element 1-silencing transcription factor (REST), has received a lot of attention due to the possibility that it may control fundamental transcription patterns that drive circuit excitability, seizures, and epilepsy. REST represses a suite of genes in the nervous system by utilizing nuclear protein complexes that were originally identified as mediators of epigenetic inheritance. Epigenetics has traditionally referred to mechanisms that allow a heritable change in gene expression in the absence of DNA mutation. However a more contemporaneous definition acknowledges that many of the mechanisms used to perpetuate epigenetic traits in dividing cells are utilized by neurons to control activity-dependent gene expression. This review surveys what is currently understood about the role of epigenetic mechanisms in epilepsy. We discuss how REST controls gene expression to affect circuit excitability and neurogenesis in epilepsy. We also discuss how the repressor methyl-CpG-binding protein 2 (MeCP2) and activator cyclic AMP response element binding protein (CREB) regulate neuronal activity and are themselves controlled by activity. Finally we highlight possible future directions in the field of epigenetics and epilepsy.

Indexed as

Epigenesis, GeneticEpigenomicsAnimalsBrain-Derived Neurotrophic FactorChromatinCyclic AMP Response Element-Binding ProteinEpilepsyHistonesHumansMethyl-CpG-Binding Protein 2NeurogenesisRE1-Silencing Transcription FactorRepressor ProteinsTranscription, GeneticBrain-Derived Neurotrophic FactorChromatinCyclic AMP Response Element-Binding ProteinHistonesMECP2 protein, humanMethyl-CpG-Binding Protein 2RE1-Silencing Transcription FactorRepressor Proteins

Identifiers

PMID23216574
PMCPMC3531878
OpenAlexW1751414410

What OpenQuestion holds

Textmetadata
LicenceTDM
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.