Thomas Sanderson, PhD
Associate Professor, Emergency Medicine
Associate Professor, Molecular & Integrative Physiology
(734) 764-4493
Research in the Sanderson lab is focused on understanding brain damage caused by ischemic insults during cardiac arrest, ischemic stroke, and neonatal hypoxia/ischemia. Two primary avenues of investigation are (1) the role mitochondrial dysfunction in death of neurons during post-ischemic reperfusion and (2) the development and clinical translation of a neuroprotective therapies that modulate the activity of mitochondria to reduce ischemia-reperfusion injury.
Ongoing mitochondrial mechanistic studies are focused on uncovering novel mechanisms of mitochondrial dysfunction and subsequent cell death during neuronal reperfusion. These studies center around key inner mitochondrial membrane proteins and their role in mitochondrial dynamics, quality control, cristae maintenance, and apoptosis induction. Our studies utilize novel cell and animal models of cardiac arrest/resuscitation, stroke, and neonatal hypoxic/ischemic encephalopathy and transgenic mice to evaluate mitochondrial dysfunction.
The Sanderson lab is conducting pre-clinical large animal studies with a novel therapeutic strategy to manipulate mitochondrial activity. We have shown that limiting mitochondrial hyperactivity following brain ischemia can prevent ROS production and minimize injury. Our lab has invested substantial investigative effort uncovering the molecular mechanisms by which mitochondrial modulation initiates neuroprotection. This research has resulted in two awarded US patents, which form the foundation of our startup company, Mitovation, Inc. We are now at a critical pre-clinical phase in developing this therapeutic approach. Ongoing studies supported by the NIH and DoD are focused on investigating the mechanisms of this therapy and testing it in large animals. A human prototype has been developed and is undergoing regulatory testing to bring this therapeutic device to the clinic.