Epilepsy is a common serious neurological disorder. Unfortunately, the treatment of epilepsy has severe shortcomings. Many epilepsy patients become refractory to the drugs available. In more than 40 % of cases, the disorder cannot be controlled by medicat ion, and surgically removal of the hippocampus is needed for seizure control. The mechanisms underlying the pathogenesis of epilepsy remain unclear. Studies have shown a reduction in the metabolic rate in epileptic areas of the brain, this can potentially damage neurons. This is the case in patients with mesial temporal lobe epilepsy (MTLE), whose distinctive characteristic is neuron cell loss in parts of the hippocampus, known as sclerosis. In MTLE, studies indicate that the seizures originate from the s clerotic hippocampus. It is unknown whether hippocampal neuron cell loss is related to a reduced supply of energy substrates in these areas.
A low carbohydrate diet (ketogenic) have long been used an alternative treatment for epilepsy and is remarkably e ffective against multiple seizure types. One possible explanation is that the diet increases the amount of MCT1 in the brain, a protein that transport brain fuels such as ketone bodies from the blood into the brain. It is unknown whether the MCT expressio n is altered in epileptic versus in normal brains.
We will study the MCT expression in hippocampus surgically removed from patients with epilepsy. Further, we will study MCT expression in rats using an animal model, which replicates key features of human MTLE. By using rats, we can study whether a ketogenic diet increases MCT expression, and if it reduces seizure frequency. These studies may contribute to the understanding of the cellular changes occurring in epileptic tissue, which in the future can be used to develop new, more effective epileptic drugs.