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Focal cortical dysplasia (FCD) is the most common malformation of cortical development found in epilepsy surgical series. Characterised by cortical mislamination, dysplastic neurons and, in a subgroup of cases, balloon cells, FCD is potently epileptogenic. Despite decades of study, the underlying aetiology of FCD remains uncertain and research has been hampered by the lack of a good animal model in which to simulate the condition. In this article we review some of the potential molecular mechanisms that might underpin human FCD. In particular we examine the potential role of cyclin-dependent kinase 5 and its principal activator p35 in FCD and estimate the contribution that deregulation of cyclin-dependent kinase 5 might make to the pathogenesis of this condition.

Original publication




Journal article


Dev Neurosci

Publication Date





96 - 104


Adaptor Proteins, Signal Transducing, Cell Cycle Proteins, Cell Movement, Cerebral Cortex, Cyclin-Dependent Kinase 5, Enzyme Activation, Epilepsy, Gene Expression Regulation, Developmental, Humans, Malformations of Cortical Development, Signal Transduction