Joseph Wider, PhD

Dr. Wider’s lab studies the role of mitochondria in the brain. Mitochondria are central to normal brain function but are recognized as a common component in acute brain injuries, such as traumatic brain injury, ischemic stroke, cardiac arrest and neonatal hypoxic ischemic encephalopathy. Dr. Wider studies the molecular mechanisms of mitochondrial dysfunction and the causal relationship with the pathogenesis of injury. Using in vitro, preclinical and translational models, the Wider lab is focused on expanding our understanding of brain injury and developing therapies that improve neurological outcomes.

My lab studies the role of mitochondria in the brain. Specifically we are interested in how dysfunction of mitochondria contribute to progressive and delayed cell death after acute injuries, like stroke, cardiac arrest and neurotrauma.

My research is focused on exploring how mitochondria become dysfunctional. Energy production in the brain relies almost exclusively on oxidative phosphorylation, making mitochondria critically important for cell function. Regulating mitochondrial function and maintenance are critical to maintaining the ability to efficiently produce enough energy for all the cells in the brain to function. Mitochondrial dynamics, mitophagy and biogenesis are the primary mechanisms that regulate mitochondrial maintenance. We are studying how dysfunction of these systems contribute to cellular dysfunction and tissue damage in brain injury.

Based on our mechanistic research, we are developing mitochondrial targeted therapeutics in preclinical and translational models of acute brain injury. These technologies include non-invasive mitochondrial modulation, intranasal drug administration, intranasal cooling and gene therapy.