Epilepsy is a common neurological disorder and around one-third of epilepsy patients do not respond well to anti-seizure drugs. New findings from the University of Kentucky published in the Journal of Neuroscience show that there may be new ways to address blood-brain barrier dysfunction in epilepsy.
Until now, it was believed that the cause and effect of epilepsy were merely based on a dysfunction in the brain's neurons.
However, recent findings suggest that epilepsy can be caused by many other factors, including a dysfunctional blood-brain barrier. Essentially, seizures erode the lining of capillaries in the brain which plays a role in letting nutrients in and keeping toxins out. This can result in a "leaky" blood-brain barrier, which leads to more seizures, resulting in epilepsy progression.
Through their research, they found that the neurotransmitter glutamate, released during seizures, increased the activity of two types of enzymes, which increased barrier leakage. They also found that blocking the enzyme cPLA2 and genetically deleting cPLA2 may prevent the changes mentioned and the associated leakage. This suggests that cPLA2 is responsible for barrier leakage.
Since 30 percent of people with epilepsy do not respond well to current anti-seizure medications, these findings demonstrate there could be new ways to treat and manage seizures that currently do not respond well to medication.
The data gathered implies that cPLA2 could be a pharmaceutical target to repair and normalize barrier dysfunction and improve the treatment of epilepsy and potentially other neurological disorders that are accompanied by blood-brain barrier leakage These strategies to repair barrier dysfunction could be valuable add-on treatments to existing pharmacotherapy.