Abnormal expression of cdk5 in focal cortical dysplasia in humans

被引:19
作者
Sisodiya, SM
Thom, M
Lin, WR
Bajaj, NPS
Cross, JH
Harding, BN
机构
[1] UCL, Neurol Inst, Dept Clin & Exptl Epilepsy, London WC1N 3BG, England
[2] GKT Sch Med, Inst Psychiat, Dept Neurosci, London, England
[3] UCL, Inst Child Hlth, London WC1N 3BG, England
[4] Great Ormond St Hosp Sick Children, GKT Sch Med, London, England
关键词
cdk5; focal cortical dysplasia; refractory epilepsy;
D O I
10.1016/S0304-3940(02)00520-7
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
Focal cortical dysplasia (FCD) is an important cause of refractory epilepsy in humans. The origin of its pathognomonic abnormal cell types and the links between abnormal cell morphology and epileptogenicity remain unknown. The developmentally-regulated kinase cdk5 and its neuronal activator p35 are known to be central to a number of key components in neuronal development, cellular morphology, cytoskeletal function, synaptic plasticity and neurodegeneration. Here we examine eight cases of human FCD for expression of cdk5. We show abnormal cdk5 immunoreactivity and aggregation of protein suggesting alterations in cdk5 may also be involved in this important epileptogenic human pathology. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.
引用
收藏
页码:217 / 220
页数:4
相关论文
共 11 条
  • [1] Mice lacking p35, a neuronal specific activator of Cdk5, display cortical lamination defects, seizures, and adult lethality
    Chae, T
    Kwon, YT
    Bronson, R
    Dikkes, P
    Li, E
    Tsai, LH
    [J]. NEURON, 1997, 18 (01) : 29 - 42
  • [2] Chen JS, 2000, J NEUROSCI, V20, P8965
  • [3] A decade of CDK5
    Dhavan, R
    Tsai, LH
    [J]. NATURE REVIEWS MOLECULAR CELL BIOLOGY, 2001, 2 (10) : 749 - 759
  • [4] NEURONAL CYTOSKELETAL ABNORMALITIES IN HUMAN CEREBRAL CORTICAL DYSPLASIA
    DUONG, T
    DEROSA, MJ
    POUKENS, V
    VINTERS, HV
    FISHER, RS
    [J]. ACTA NEUROPATHOLOGICA, 1994, 87 (05) : 493 - 503
  • [5] Regulation of NMDA receptors by cyclin-dependent kinase-5
    Li, BS
    Sun, MK
    Zhang, L
    Takahashi, S
    Ma, W
    Vinade, L
    Kulkarni, AB
    Brady, RO
    Pant, HC
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 2001, 98 (22) : 12742 - 12747
  • [6] Epileptogenicity correlated with increased N-methyl-D-aspartate receptor subunit NR2A/B in human focal cortical dysplasia
    Najm, IM
    Ying, Z
    Babb, T
    Mohamed, A
    Hadam, J
    LaPresto, E
    Wyllie, E
    Kotagal, P
    Bingaman, W
    Foldvary, N
    Morris, H
    Lüders, HO
    [J]. EPILEPSIA, 2000, 41 (08) : 971 - 976
  • [7] Migration defects of cdk5-/- neurons in the developing cerebellum is cell autonomous
    Ohshima, T
    Gilmore, EC
    Longenecker, G
    Jacobowitz, DM
    Brady, RO
    Herrup, K
    Kulkarni, AB
    [J]. JOURNAL OF NEUROSCIENCE, 1999, 19 (14) : 6017 - 6026
  • [8] Targeted disruption of the cyclin-dependent kinase 5 gene results in abnormal corticogenesis, neuronal pathology and perinatal death
    Ohshima, T
    Ward, JM
    Huh, CG
    Longenecker, G
    Veeranna
    Pant, HC
    Brady, RO
    Martin, LJ
    Kulkarni, AB
    [J]. PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1996, 93 (20) : 11173 - 11178
  • [9] Conversion of p35 to p25 deregulates Cdk5 activity and promotes neurodegeneration
    Patrick, GN
    Zukerberg, L
    Nikolic, M
    de la Monte, S
    Dikkes, P
    Tsai, LH
    [J]. NATURE, 1999, 402 (6762) : 615 - 622
  • [10] Surgery for malformations of cortical development causing epilepsy
    Sisodiya, SM
    [J]. BRAIN, 2000, 123 : 1075 - 1091