Clinical and Genetic Aspects of Epilepsy by Z. Afawi

By Z. Afawi

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This includes altered expression of transporters and metabolic enzymes as well as barrier leakage that have been linked to antiepileptic drug resistance and seizure genesis, respectively. Here we highlight current understanding of these pathological changes. Three critical components of barrier function 1) tight junctions, 2) metabolising enzymes and 3) transporter proteins - are introduced and we describe how they are changed in epilepsy and affected by epilepsy treatment. Recent efforts in blood-brain barrier research to overcome drug-resistant epilepsy are also discussed.

1993). , 1994). Dauchy et al. , 2008). Immunohistological studies by Rieder et al. , 2000). In a follow up study, Dauchy et al. , 2009). CYPs with low mRNA expression included CYP2R1, 2B6, 2E1, 1A1, 2D6, 2C18, 1B1, 2J2, 1A2 and 2C8. Except for CYP2C18, all CYP genes found in hCMEC/D3 cells were also detected in isolated human brain microvessels. A novel CYP P450, Cyp4x1, was identified in 2006 by Al-Aznizy et al. , 2006). Immunohistochemical staining showed strong Cyp4x1 protein expression in neurons, choroid plexus epithelial cells, and brain microvessel endothelial cells.

Thus, since potent and specific inhibitors that can be safely given to patients are currently not available, transporter inhibition does not seem to be a viable treatment option in drug-resistant epilepsy at this point in time. 2 Modulation of transporter regulation Targeting signalling pathways that regulate drug efflux transporters is another strategy to overcome transporter-mediated AED resistance. The advantages of this approach are threefold. First, modulating transporter regulation to increase AED brain delivery may allow fine tuning of the transporter.

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