CLINICAL NEUROSCIENCE AND NEUROPATHOLOGYIncreased immunoreactivity of cdk5 activators in hippocampal sclerosisSen, Arjunea; Thom, Mariaa b; Martinian, Lilliana b; Yogarajah, Mahindaa; Nikolic, Margaretac; Sisodiya, Sanjay M.aAuthor Information aDepartment of Clinical and Experimental Epilepsy bDivision of Neuropathology, Institute of Neurology, University College London, Queen Square cDepartment of Cellular and Molecular Neuroscience, Faculty of Medicine, Imperial College London, Charing Cross Campus, Fulham Palace Road, London Correspondence to Dr Sanjay M. Sisodiya, PhD, FRCP, Department of Clinical and Experimental Epilepsy, Box 29, The National Hospital for Neurology and Neurosurgery, Queen Square, London, WC1N 3BG, UK Tel: +44 207 391 8983; fax: +44 207 391 8984; e-mail: email@example.com Received 18 August 2006; accepted 13 December 2006 NeuroReport: March 26th, 2007 - Volume 18 - Issue 5 - p 511-516 doi: 10.1097/WNR.0b013e3280586879 Buy Metrics Abstract Cyclin-dependent kinase 5 is important in several in-vitro neurodegeneration paradigms. Whether cyclin-dependent kinase 5 contributes to cell death in human neurodegenerative diseases remains uncertain, particularly because post-mortem delay and other extrinsic factors might influence cyclin-dependent kinase 5 activity. Here we demonstrate increased immunoreactivity for the activators of cyclin-dependent kinase 5 in post-mortem human hippocampi affected by the neurodegenerative condition hippocampal sclerosis, but not in histologically normal hippocampi. Moreover, in post-mortem brain tissue from patients with unilateral hippocampal sclerosis, increased immunoreactivity for cyclin-dependent kinase 5 activators was detected in the hippocampus with sclerosis, but not in the contralateral hippocampus, suggesting that extrinsic factors are unlikely to account for the differential staining observed. Our findings suggest that deregulation of cyclin-dependent kinase 5 might contribute to the pathogenesis of hippocampal sclerosis. © 2007 Lippincott Williams & Wilkins, Inc.