Early intervention, in response to rising biomarker levels, could delay the onset of epilepsy, block the progression of the disease, and eliminate impairments in memory
(Chicago - February 6, 2018) New research, funded by Citizens United for Research in Epilepsy (CURE), has discovered a ‘smoking gun’ biomarker that could result in treatments that stop some epilepsies before they even start.
“Being able to identify that a person is likely to develop epilepsy following a brain injury is one of the most important focus areas in modern-day epilepsy research,” says Dr. Laura Lubbers, CURE’s Chief Scientific Officer. “With 3.4 million Americans suffering from epilepsy and seizures in the U.S., this discovery of a predictive biomarker for a certain form of epilepsy could prevent unpredictable seizures from taking over the lives of millions of Americans and their families.”
Using a rat model of brain injury and epilepsy, CURE-funded researcher Dr. Annamaria Vezzani and her team at the Mario Negri Institute for Pharmacological Research in Milan, Italy have identified that, prior to the development of epilepsy, high levels of the protein high-mobility group box 1 – also known as HMGB1 – have been found in both the brain and blood of rats. This means that high levels of the biomarker HMGB1 may predict the impending onset of epilepsy.
The CURE-funded research team also discovered that a combination of existing medications not only prevent an increase in HMGB1 levels, but delay the onset of epilepsy, halt the disease’s progression, and eliminate memory impairments associated with epilepsy.
“This discovery suggests that early intervention could slow, or potentially stop, the development of epilepsy in those at risk,” says Dr. Lubbers. “Epilepsy costs the United States approximately $15.5 billion each year, and prevention could result in ripple effects that go far beyond the millions who may receive early treatment.”
HMGB1 is normally released in the brain in response to neuroinflammation, the brain’s response to injury. Targeting the neuroinflammation that leads to increased HMGB1 with drugs that are already in clinical use could create an entirely new therapeutic area to prevent epilepsy from developing or improve its outcomes.
“With this research, Dr. Vezzani and her team have provided hope that a treatment for preventing acquired epilepsy before it occurs is on the horizon,” says CURE CEO Kate Carr. “We thank both Dr. Vezzani as well as our supporters who have made such research possible through their generous donations.”