Evidence map›Paper›PMID 28197553›Full record

ArticleeNeuro

The Role of Sirt1 in Epileptogenesis.

Alicia M Hall, Gary P Brennan, Tiffany M Nguyen, Akanksha Singh-Taylor, Hyun-Seung Mun, Mary J Sargious, Tallie Z Baram

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

Article in eNeuro. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.

0numbers the graph read from it
0cells of the map it votes in
17citing papers in PubMed
2.8field-weighted citation impact, top 11% 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

17 citing papers in PubMed, 44 citations in OpenAlex.

  1. Article
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  9. Article
  10. Neuronal SIRT3 Deletion Predisposes to Female-Specific Alterations in Cellular Metabolism, Memory, and Network Excitability.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2023
    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

7 authors at 1 institution in 1 country.

Alicia M HallDepartment of Pediatrics, University of California, Irvine , Irvine, California 92697.ORCID 0000-0002-2746-4804
Gary P BrennanDepartment of Pediatrics, University of California, Irvine, Irvine, California 92697; Department of Anatomy and Neurobiology, University of California, Irvine, Irvine, California 92697.
Tiffany M NguyenDepartment of Pediatrics, University of California, Irvine , Irvine, California 92697.
Akanksha Singh-TaylorDepartment of Pediatrics, University of California, Irvine , Irvine, California 92697.
Hyun-Seung MunDepartment of Pediatrics, University of California, Irvine , Irvine, California 92697.
Mary J SargiousDepartment of Pediatrics, University of California, Irvine , Irvine, California 92697.
Tallie Z BaramDepartment of Pediatrics, University of California, Irvine, Irvine, California 92697; Department of Anatomy and Neurobiology, University of California, Irvine, Irvine, California 92697.
University of California, Irvine · US

Funding

Epilepsy Research Training ProgramT32NS045540 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI Tallie Z. Baram, Robert F Hunt · 2003 to 2026
$4.9M
FEBRILE SEIZURE MODEL--NEURONAL INJURY AND MECHANISMSR01NS035439 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI BARAM, TALLIE Z. · 1997 to 2018
$3.2M
Febrile Seizure Model - Neuronal Injury and MechanismsR37NS035439 · NINDS · UNIVERSITY OF CALIFORNIA-IRVINE · PI BARAM, TALLIE Z. · 2006 to 2012
$2.6M
Cognitive Deficits After Experimental Febrile Seizures: Neurobiology & BiomarkersR01NS078279 · NINDS · UNIVERSITY OF VERMONT & ST AGRIC COLLEGE · PI BARAM, TALLIE Z., HOLMES, GREGORY L. · 2011 to 2015
$1.7M
NINDS NIH HHS R01 NS035439NINDS NIH HHS R01 NS078279NINDS NIH HHS R37 NS035439NINDS NIH HHS T32 NS045540
6 · The paper itself

Abstract

The mechanisms by which brain insults lead to subsequent epilepsy remain unclear. Insults, including trauma, stroke, tumors, infections, and long seizures [status epilepticus (SE)], create a neuronal state of increased metabolic demand or decreased energy supply. Neurons express molecules that monitor their metabolic state, including sirtuins (Sirts). Sirtuins deacetylate cytoplasmic proteins and nuclear histones, and their epigenetic modulation of the chromatin governs the expression of many genes, influencing neuronal properties. Thus, sirtuins are poised to enduringly modulate neuronal properties following SE, potentially contributing to epileptogenesis, a hypothesis supported by the epilepsy-attenuating effects of blocking a downstream target of Sirt1, Neuron-Restrictive Silencer Factor (NRSF) also know as REST (RE1-Silencing Transcription factor). Here we used an adult male rat model of epileptogenesis provoked by kainic acid-induced SE (KA-SE). We assessed KA-SE-provoked Sirt1 activity, infused a Sirt1 inhibitor (EX-527) after KA-SE, and examined for epileptogenesis using continuous digital video-EEG. Sirt1 activity, measured using chromatin immunoprecipitation for Sirt1 binding at a target gene, increased rapidly after SE.

Indexed as

AnimalsBrainCarbazolesCell CountCentral Nervous System AgentsChromatin ImmunoprecipitationDisease Models, AnimalElectroencephalographyImmunohistochemistryInflammationKainic AcidMaleNeuronsRats, Sprague-DawleyReverse Transcriptase Polymerase Chain ReactionSeizures6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamideCarbazolesCentral Nervous System AgentsKainic AcidSirt1 protein, ratSirtuin 1epigeneticsepilepsyepileptogenesisinterventionmetabolic stresssirtuins

Identifiers

PMID28197553
PMCPMC5301079
OpenAlexW2581507635

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.