Evidence map›Paper›PMID 19665252›Full record

ReviewTrends in genetics : TIG2009

Genetics of complex neurological disease: challenges and opportunities for modeling epilepsy in mice and rats.

Wayne N Frankel

Abstract readReview
In one paragraph

Review in Trends in genetics : TIG, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 40 papers.

0numbers the graph read from it
0cells of the map it votes in
40citing papers in PubMed
4.6field-weighted citation impact, top 5% 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

40 citing papers in PubMed, 80 citations in OpenAlex.

  1. Article
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  6. Review
  7. Fly seizure EEG: field potential activity in theJournal of neurogenetics · 2021
    Article
  8. Cycles in epilepsy.Nature reviews. Neurology · 2021
    Review
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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

1 author at 1 institution in 1 country.

Wayne N FrankelThe Jackson Laboratory, 600 Main Street, Bar Harbor, ME 04609, USA. wayne.frankel@jax.org
Jackson Laboratory · US

Funding

GENETIC DETERMINANTS OF EPILEPSY IN MURINE SYSTEMSR01NS031348 · NINDS · JACKSON LABORATORY · PI SANDS, TRISTAN T · 1993 to 2025
$11.5M
NINDS NIH HHS R01 NS031348
6 · The paper itself

Abstract

Currently, approximately 20 genetic variants are known to cause Mendelian forms of human epilepsy, leaving a vast heritability undefined. Rodent models for genetically complex epilepsy have been studied for many years, but only recently have strong candidate genes emerged, including Cacna1 g in the GAERS rat model of absence epilepsy and Kcnj10 in the low seizure threshold of DBA/2 mice. In parallel, a growing number of mouse mutations studied on multiple strain backgrounds reveal the impact of genetic modifiers on seizure severity, incidence or form--perhaps mimicking the complexity seen in humans. The field of experimental genetics in rodents is poised to study discrete epilepsy mutations on a diverse choice of strain backgrounds to develop better models and identify modifiers. But, it must find the right balance between embracing the strain diversity available, with the ability to detect and characterize genetic effects. Using alternative strain backgrounds when studying epilepsy mutations will enhance the modeling of epilepsy as a complex genetic disease.

Indexed as

Disease Models, AnimalAnimalsCrosses, GeneticEpilepsyHumansMiceMice, Inbred StrainsMutationPhenotypeRats

Identifiers

PMID19665252
PMCPMC2736783
OpenAlexW2164753853

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.