Abnormal expression of cdk5 in focal cortical dysplasia in humans

• Published in: Neuroscience letters Vol. 328; no. 3; pp. 217 - 220
• Main Authors: Sisodiya, Sanjay M, Thom, Maria, Lin, Woan-Ru, Bajaj, Narinder P.S, Cross, J.Helen, Harding, Brian N
• Format: Journal Article
• Language: English
• Published: Shannon Elsevier Ireland Ltd 16.08.2002; Elsevier
• Subjects: Biological and medical sciences; Cdk5; Cerebral Cortex - abnormalities; Cerebral Cortex - enzymology; Congenital Abnormalities - enzymology; Cyclin-Dependent Kinase 5; Cyclin-Dependent Kinases - metabolism; Focal cortical dysplasia; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy; Humans; Medical sciences; Nervous system (semeiology, syndromes); Neurology; Neurons - enzymology; Refractory epilepsy; Cdk5; Refractory epilepsy; Focal cortical dysplasia; Human; Nervous system diseases; Cerebral cortex; Dysplasia; Enzyme; Transferases; Epilepsy; Central nervous system; Gene expression; Cerebral disorder; Refractory; Kinase; Central nervous system disease; Brain (vertebrata)
• ISSN: 0304-3940; 1872-7972
• DOI: 10.1016/S0304-3940(02)00520-7

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.