Temporal Lobe Epilepsy: Genetic Determinants of Temporal Lobe Epilepsy

Philip A Schwartzkroin, H. Jurgen Wenzel

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

Temporal lobe epilepsy (TLE) has long been the focus of both clinical and basic laboratory investigations. Most studies have approached this common and often medically refractory form of epilepsy as a unitary disorder. TLE has been identified as perhaps the prototypical 'acquired' epilepsy, thought to arise as a result of a brain injury or insult. However, recent studies suggest that TLE may include a number of distinct disorders, some of which arise because of genetic mutations in genes that normally control patterns of brain development and/or excitability. Animal models can help to explore these possibilities. Two specific mouse models - the Kv1.1 knockout mouse and the p35 knockout mouse - show typical TLE-like seizure phenotypes and present with histopathological features also seen in human TLE. They arise, however, from very different processes; seizures in Kv1.1-/- mice reflect a 'channelopathy'-like disorder, while seizures in p35-/- mice arise from a disruption of normal brain development.

Original languageEnglish (US)
Title of host publicationEncyclopedia of Basic Epilepsy Research
PublisherElsevier Inc.
Pages1361-1365
Number of pages5
ISBN (Print)9780123739612
DOIs
StatePublished - Jan 1 2009

Fingerprint

Temporal Lobe Epilepsy
Epilepsy
Knockout Mice
Seizures
Channelopathies
Brain
Brain Injuries
Animal Models
Phenotype
Mutation
Genes

Keywords

  • 1
  • Acquired epilepsy
  • Granule cell dispersion
  • Hippocampus
  • Kv1
  • LGI1
  • P35
  • Reelin
  • Temporal lobe epilepsy

ASJC Scopus subject areas

  • Medicine(all)
  • Neuroscience(all)

Cite this

Schwartzkroin, P. A., & Wenzel, H. J. (2009). Temporal Lobe Epilepsy: Genetic Determinants of Temporal Lobe Epilepsy. In Encyclopedia of Basic Epilepsy Research (pp. 1361-1365). Elsevier Inc.. https://doi.org/10.1016/B978-012373961-2.00370-2

Temporal Lobe Epilepsy : Genetic Determinants of Temporal Lobe Epilepsy. / Schwartzkroin, Philip A; Wenzel, H. Jurgen.

Encyclopedia of Basic Epilepsy Research. Elsevier Inc., 2009. p. 1361-1365.

Research output: Chapter in Book/Report/Conference proceedingChapter

Schwartzkroin, PA & Wenzel, HJ 2009, Temporal Lobe Epilepsy: Genetic Determinants of Temporal Lobe Epilepsy. in Encyclopedia of Basic Epilepsy Research. Elsevier Inc., pp. 1361-1365. https://doi.org/10.1016/B978-012373961-2.00370-2
Schwartzkroin PA, Wenzel HJ. Temporal Lobe Epilepsy: Genetic Determinants of Temporal Lobe Epilepsy. In Encyclopedia of Basic Epilepsy Research. Elsevier Inc. 2009. p. 1361-1365 https://doi.org/10.1016/B978-012373961-2.00370-2
Schwartzkroin, Philip A ; Wenzel, H. Jurgen. / Temporal Lobe Epilepsy : Genetic Determinants of Temporal Lobe Epilepsy. Encyclopedia of Basic Epilepsy Research. Elsevier Inc., 2009. pp. 1361-1365
@inbook{2153cd4b71b94010a288c831a0cbb74f,
title = "Temporal Lobe Epilepsy: Genetic Determinants of Temporal Lobe Epilepsy",
abstract = "Temporal lobe epilepsy (TLE) has long been the focus of both clinical and basic laboratory investigations. Most studies have approached this common and often medically refractory form of epilepsy as a unitary disorder. TLE has been identified as perhaps the prototypical 'acquired' epilepsy, thought to arise as a result of a brain injury or insult. However, recent studies suggest that TLE may include a number of distinct disorders, some of which arise because of genetic mutations in genes that normally control patterns of brain development and/or excitability. Animal models can help to explore these possibilities. Two specific mouse models - the Kv1.1 knockout mouse and the p35 knockout mouse - show typical TLE-like seizure phenotypes and present with histopathological features also seen in human TLE. They arise, however, from very different processes; seizures in Kv1.1-/- mice reflect a 'channelopathy'-like disorder, while seizures in p35-/- mice arise from a disruption of normal brain development.",
keywords = "1, Acquired epilepsy, Granule cell dispersion, Hippocampus, Kv1, LGI1, P35, Reelin, Temporal lobe epilepsy",
author = "Schwartzkroin, {Philip A} and Wenzel, {H. Jurgen}",
year = "2009",
month = "1",
day = "1",
doi = "10.1016/B978-012373961-2.00370-2",
language = "English (US)",
isbn = "9780123739612",
pages = "1361--1365",
booktitle = "Encyclopedia of Basic Epilepsy Research",
publisher = "Elsevier Inc.",

}

TY - CHAP

T1 - Temporal Lobe Epilepsy

T2 - Genetic Determinants of Temporal Lobe Epilepsy

AU - Schwartzkroin, Philip A

AU - Wenzel, H. Jurgen

PY - 2009/1/1

Y1 - 2009/1/1

N2 - Temporal lobe epilepsy (TLE) has long been the focus of both clinical and basic laboratory investigations. Most studies have approached this common and often medically refractory form of epilepsy as a unitary disorder. TLE has been identified as perhaps the prototypical 'acquired' epilepsy, thought to arise as a result of a brain injury or insult. However, recent studies suggest that TLE may include a number of distinct disorders, some of which arise because of genetic mutations in genes that normally control patterns of brain development and/or excitability. Animal models can help to explore these possibilities. Two specific mouse models - the Kv1.1 knockout mouse and the p35 knockout mouse - show typical TLE-like seizure phenotypes and present with histopathological features also seen in human TLE. They arise, however, from very different processes; seizures in Kv1.1-/- mice reflect a 'channelopathy'-like disorder, while seizures in p35-/- mice arise from a disruption of normal brain development.

AB - Temporal lobe epilepsy (TLE) has long been the focus of both clinical and basic laboratory investigations. Most studies have approached this common and often medically refractory form of epilepsy as a unitary disorder. TLE has been identified as perhaps the prototypical 'acquired' epilepsy, thought to arise as a result of a brain injury or insult. However, recent studies suggest that TLE may include a number of distinct disorders, some of which arise because of genetic mutations in genes that normally control patterns of brain development and/or excitability. Animal models can help to explore these possibilities. Two specific mouse models - the Kv1.1 knockout mouse and the p35 knockout mouse - show typical TLE-like seizure phenotypes and present with histopathological features also seen in human TLE. They arise, however, from very different processes; seizures in Kv1.1-/- mice reflect a 'channelopathy'-like disorder, while seizures in p35-/- mice arise from a disruption of normal brain development.

KW - 1

KW - Acquired epilepsy

KW - Granule cell dispersion

KW - Hippocampus

KW - Kv1

KW - LGI1

KW - P35

KW - Reelin

KW - Temporal lobe epilepsy

UR - http://www.scopus.com/inward/record.url?scp=85069291570&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=85069291570&partnerID=8YFLogxK

U2 - 10.1016/B978-012373961-2.00370-2

DO - 10.1016/B978-012373961-2.00370-2

M3 - Chapter

AN - SCOPUS:85069291570

SN - 9780123739612

SP - 1361

EP - 1365

BT - Encyclopedia of Basic Epilepsy Research

PB - Elsevier Inc.

ER -