Human epilepsies: interaction of genetic and acquired factors

被引:147
作者
Berkovic, Samuel F. [1 ]
Mulley, John C.
Scheffer, Ingrid E.
Petrou, Steven
机构
[1] Univ Melbourne, Dept Med, Heidelberg West, Vic 3081, Australia
[2] Univ Melbourne, Epilepsy Res Ctr, Austin Hlth, Heidelberg West, Vic 3081, Australia
[3] Womens & Childrens Hosp, Dept Med Genet, Adelaide, SA 5006, Australia
[4] Univ Adelaide, Sch Mol & Biomed Sci, Adelaide, SA 5006, Australia
[5] Univ Melbourne, Howard Florey Inst Expt Physiol & Med, Parkville, Vic 3010, Australia
关键词
D O I
10.1016/j.tins.2006.05.009
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Epilepsies, once regarded as due to demoniacal possession, can have both genetic and acquired causes, with interaction of these factors in many cases. To date, nearly all the genes discovered to be involved in human epilepsies encode subunits of ion channels, both voltage-gated and ligand-gated. Established acquired causes include serious brain trauma, stroke, tumours and infective lesions. Thus, in terms of exploring the neurobiology of 'nature and nurture' in disease, the epilepsies are an excellent paradigm. Here, we review the evidence and discuss the possibility that ion channels are a common biological substrate for both genetic and acquired epilepsies. This review is part of the INMED/TINS special issue Nature and nurture in brain development and neurological disorders, based on presentations at the annual INMEDITINS symposium (http://inmednet.com/).
引用
收藏
页码:391 / 397
页数:7
相关论文
共 47 条
  • [1] ANDERMANN E, 1982, GENETIC BASIS EPILEP, P355
  • [2] PROPOSAL FOR REVISED CLASSIFICATION OF EPILEPSIES AND EPILEPTIC SYNDROMES
    不详
    [J]. EPILEPSIA, 1989, 30 (04) : 389 - 399
  • [3] THE NEUROPATHOLOGY OF TEMPORAL-LOBE EPILEPSY
    ARMSTRONG, DD
    [J]. JOURNAL OF NEUROPATHOLOGY AND EXPERIMENTAL NEUROLOGY, 1993, 52 (05) : 433 - 443
  • [4] Enhanced expression of a specific hyperpolarization-activated cyclic nucleotide-gated cation channel (HCN) in surviving dentate gyrus granule cells of human and experimental epileptic hippocampus
    Bender, RA
    Soleymani, SV
    Brewster, AL
    Nguyen, ST
    Beck, H
    Mathern, GW
    Baram, TZ
    [J]. JOURNAL OF NEUROSCIENCE, 2003, 23 (17) : 6826 - 6836
  • [5] Benign familial neonatal-infantile seizures: Characterization of a new sodium channelopathy
    Berkovic, SF
    Heron, SE
    Giordano, L
    Marini, C
    Guerrini, R
    Kaplan, RE
    Gambardella, A
    Steinlein, OK
    Grinton, BE
    Dean, JT
    Bordo, L
    Hodgson, BL
    Yamamoto, T
    Mulley, JC
    Zara, F
    Scheffer, IE
    [J]. ANNALS OF NEUROLOGY, 2004, 55 (04) : 550 - 557
  • [6] Epilepsies in twins: Genetics of the major epilepsy syndromes
    Berkovic, SF
    Howell, RA
    Hay, DA
    Hopper, JL
    [J]. ANNALS OF NEUROLOGY, 1998, 43 (04) : 435 - 445
  • [7] CONCEPTS OF ABSENCE EPILEPSIES - DISCRETE SYNDROMES OR BIOLOGICAL CONTINUUM
    BERKOVIC, SF
    ANDERMANN, F
    ANDERMANN, E
    GLOOR, P
    [J]. NEUROLOGY, 1987, 37 (06) : 993 - 1000
  • [8] Genetics of the epilepsies
    Berkovic, SF
    Scheffer, IE
    [J]. EPILEPSIA, 2001, 42 : 16 - 23
  • [9] Acquired dendritic channelopathy in temporal lobe epilepsy
    Bernard, C
    Anderson, A
    Becker, A
    Poolos, NP
    Beck, H
    Johnston, D
    [J]. SCIENCE, 2004, 305 (5683) : 532 - 535
  • [10] Formation of heteromeric hyperpolarization-activated cyclic nucleotide-gated (HCN) channels in the hippocampus is regulated by developmental seizures
    Brewster, AL
    Bernard, JA
    Gall, CM
    Baram, TZ
    [J]. NEUROBIOLOGY OF DISEASE, 2005, 19 (1-2) : 200 - 207