Evidence map›Paper›PMID 22001434›Full record

ReviewEpilepsy research2011

The relevance of individual genetic background and its role in animal models of epilepsy.

P Elyse Schauwecker

Open access · greenAbstract readReview
In one paragraph

Review in Epilepsy research, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 46 papers.

0numbers the graph read from it
0cells of the map it votes in
46citing papers in PubMed
2.6field-weighted citation impact, top 10% 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

46 citing papers in PubMed, 81 citations in OpenAlex.

  1. ACMG/AMP variant classification specifications from the ClinGen Epilepsy Sodium Channel Variant Curation Expert Panel.Genetics in medicine : official journal of the American College of Medical Genetics · 2026
    Article
  2. Article
  3. Article
  4. Article
  5. Review
  6. Article
  7. Article
  8. Review
  9. Article
  10. Analyzing the Role of the P2X7 Receptor in Epilepsy.Methods in molecular biology (Clifton, N.J.) · 2022
    Article
  11. Review
  12. Article
  13. Article
  14. Article
  15. Investigating Developmental and Epileptic Encephalopathy UsingInternational journal of molecular sciences · 2020
    Review
  16. Article
  17. Article
  18. A Transient Developmental Window of Fast-Spiking Interneuron Dysfunction in a Mouse Model of Dravet Syndrome.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018
    Article
  19. Article
  20. Article
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.

P Elyse SchauweckerDepartment of Cell and Neurobiology, USC Keck School of Medicine, 1333 San Pablo Street, BMT 403, Los Angeles, CA 90089-9112, United States. schauwec@usc.edu
Keck Hospital of USC · US

Funding

MECHANISMS OF RESISTANCE TO EXCITOTOXIC CELL DEATHR01NS038696 · NINDS · UNIVERSITY OF SOUTHERN CALIFORNIA · PI SCHAUWECKER, PAULA E · 1999 to 2014
$3.6M
NINDS NIH HHS NS38696NINDS NIH HHS R01 NS038696
6 · The paper itself

Abstract

Growing evidence has indicated that genetic factors contribute to the etiology of seizure disorders. Most epilepsies are multifactorial, involving a combination of additive and epistatic genetic variables. However, the genetic factors underlying epilepsy have remained unclear, partially due to epilepsy being a clinically and genetically heterogeneous syndrome. Similar to the human situation, genetic background also plays an important role in modulating both seizure susceptibility and its neuropathological consequences in animal models of epilepsy, which has too often been ignored or not been paid enough attention to in published studies. Genetic homogeneity within inbred strains and their general amenability to genetic manipulation have made them an ideal resource for dissecting the physiological function(s) of individual genes. However, the inbreeding that makes inbred mice so useful also results in genetic divergence between them. This genetic divergence is often unaccounted for but may be a confounding factor when comparing studies that have utilized distinct inbred strains. The purpose of this review is to discuss the effects of genetic background strain on epilepsy phenotypes of mice, to remind researchers that the background genetics of a knockout strain can have a profound influence on any observed phenotype, and outline the means by which to overcome potential genetic background effects in experimental models of epilepsy.

Indexed as

Disease Models, AnimalAnimalsEpilepsyFemaleGenetic Association StudiesGenetic HeterogeneityHumansMaleMiceMice, Inbred Strains

Identifiers

PMID22001434
PMCPMC3215836
OpenAlexW2143511568

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.