Evidence map›Paper›PMID 19332325›Full record

ReviewNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2009

Alteration of epileptogenesis genes.

Amy R Brooks-Kayal, Yogendra H Raol, Shelley J Russek

Open access · bronzeAbstract readReview
In one paragraph

Review in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2009. 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
3.4field-weighted citation impact, top 7% 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, 59 citations in OpenAlex.

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  8. Role of GABAMolecular brain · 2017
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  20. The role of gap junction channels during physiologic and pathologic conditions of the human central nervous system.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2012
    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.

Amy R Brooks-KayalDivision of Neurology, Department of Pediatrics, University of Colorado Denver School of Medicine, Aurora, Colorado 80045, USA. brooks-kayal.amy@tchden.org
Yogendra H Raol
Shelley J Russek
University of Colorado Denver · USBoston University · US

Funding

GABA(A) Receptor Subunit Regulation in EpileptogenesisR01NS051710 · NINDS · UNIVERSITY OF COLORADO DENVER · PI BROOKS-KAYAL, AMY R., RUSSEK, SHELLEY J · 2006 to 2018
$5.5M
Molecular Determinants of GABAA Receptor Gene RegulationR01NS050393 · NINDS · BOSTON UNIVERSITY MEDICAL CAMPUS · PI RUSSEK, SHELLEY J · 2006 to 2010
$1.8M
NINDS NIH HHS R01 NS050393NINDS NIH HHS R01 NS051710
6 · The paper itself

Abstract

Retrospective studies suggest that precipitating events such as prolonged seizures, stroke, or head trauma increase the risk of developing epilepsy later in life. The process of epilepsy development, known as epileptogenesis, is associated with changes in the expression of a myriad of genes. One of the major challenges for the epilepsy research community has been to determine which of these changes contributes to epileptogenesis, which may be compensatory, and which may be noncontributory. Establishing this for any given gene is essential if it is to be considered a therapeutic target for the prevention or treatment of epilepsy. Our laboratories have examined alterations in gene expression related to inhibitory neurotransmission that have been proposed as contributing factors in epileptogenesis. The GABA(A) receptor mediates most fast synaptic inhibition, and changes in GABA(A) receptor subunit expression and function have been reported in adult animals beginning immediately after prolonged seizures (status epilepticus [SE]) and continue as animals become chronically epileptic. Prevention of GABA(A) receptor subunit changes after SE using viral gene transfer inhibits development of epilepsy in an animal model, suggesting that these changes directly contribute to epileptogenesis. The mechanisms that regulate differential expression of GABA(A) receptor subunits in hippocampus after SE have recently been identified, and include the CREB-ICER, JAK-STAT, BDNF, and Egr3 signaling pathways. Targeting signaling pathways that alter the expression of genes involved in epileptogenesis may provide novel therapeutic approaches for preventing or inhibiting the development of epilepsy after a precipitating insult.

Indexed as

Gene Expression RegulationAnimalsEpilepsyHippocampusHumansReceptors, GABA-ASignal TransductionReceptors, GABA-A

Identifiers

PMID19332325
PMCPMC2700027
OpenAlexW2023656585

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.