AMPK and Cardiac Dysfunction in Chronic Epilepsy: A Prognostic Indicator of SUDEP Risk
Dr. Grabenstatter’s experiments will address, in the pilocarpine rat model of TLE and a mouse model of tuberous sclerosis, whether impaired activation of AMP-activated protein kinase (AMPK), a molecule that is critical for maintaining energy balance in cells results in cardiac dysfunction, higher seizure burden, and higher SUDEP risk. Using chronic video/electroencephalography (EEG)/electrocardiography (EKG) and cutting-edge signal processing, the team will determine whether AMPK can be used as both an indicator of SUDEP risk and a therapeutic target aimed at both reducing seizure burden and any associated cardiac dysfunction.
Dr. Grabenstatter’s research is funded by the National Institute of Neurological Disorders and Stroke. The CURE Epilepsy Research Continuity Fund will allow Dr. Grabenstatter’s team to purchase required hardware and software to enable remote work and data analysis in order to successfully complete these studies.