Neuroscientists prevented the development of epileptic activity in mice after TBI by using a drug that mimics the metabolic effects of the ketogenic diet, as published in JCI Insight. Post-traumatic epilepsy develops within three years of a TBI in about 1 out of 10 people. TBIs lead to the dysfunction of the brain’s inhibitory network, including the cells that normally quiet down brain activity. Without inhibition, brain activity increases, causing the behavioral and cognitive challenges seen after injury. Researcher inhibited glycolysis with a drug called 2-deoxyglucose (2-DG) to mimic the metabolic effects of the ketogenic diet. By recording brain activity from cells in the injured area, researchers determined that excitatory cells were more active in injured tissue, compared to control brain tissue from mice.
Comparatively, the cells which usually inhibit others were dying after injury, leaving the brain without a brake on activity. Application of 2-DG directly on the brain tissue was able to reduce cell excitation and epileptic activity from TBI. In a follow-up experiment, the research team gave mice 2-DG or saline, as a control, in injection form for one week after injury to assess its effect. They found that 2-DG treatment reduced cell excitation, lessened cell loss, and prevented the development of epileptic brain activity.