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.
机构:
Harvard Univ, Sch Med, Howard Hughes Med Inst, Dept Pathol, Boston, MA 02115 USAHarvard Univ, Sch Med, Howard Hughes Med Inst, Dept Pathol, Boston, MA 02115 USA
Dhavan, R
Tsai, LH
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机构:
Harvard Univ, Sch Med, Howard Hughes Med Inst, Dept Pathol, Boston, MA 02115 USAHarvard Univ, Sch Med, Howard Hughes Med Inst, Dept Pathol, Boston, MA 02115 USA
机构:
Harvard Univ, Sch Med, Howard Hughes Med Inst, Dept Pathol, Boston, MA 02115 USAHarvard Univ, Sch Med, Howard Hughes Med Inst, Dept Pathol, Boston, MA 02115 USA
Dhavan, R
Tsai, LH
论文数: 0引用数: 0
h-index: 0
机构:
Harvard Univ, Sch Med, Howard Hughes Med Inst, Dept Pathol, Boston, MA 02115 USAHarvard Univ, Sch Med, Howard Hughes Med Inst, Dept Pathol, Boston, MA 02115 USA