The main focus of Dr. Friedlander’s research has been the study of the basic mechanisms of neuronal cell death, with a particular interest in translational neurosciences. On the basic side, the work has focused on the study of a family of cell death proteases called caspases. Caspases play a key role in the execution of program cell death pathways, also known as apoptosis. Work from Dr. Friedlander, initially as a post-doctoral fellow in Dr. Juying Yuan’s laboratory, was the first to demonstrate that caspases are activated in an experimental model of a neurologic disease (stroke). They demonstrated that inhibiting the activity of caspases resulted in reduction of lesion size and significant improvement in neurologic outcome. Dr. Friedlander demonstrated the specific activation of caspases in CNS neurons in animal models and in humans with Huntington’s disease (HD) and amyotrophic lateral sclerosis (ALS). Furthermore, his work was the first to experimentally extend survival in HD and ALS mice by genetic and by pharmacologic manipulations. Based on the mechanistic knowledge gained by his studies, he demonstrated that the antibiotic minocycline is protective in models of HD and ALS. He demonstrated that minocycline is concentrated in the mitochondria, where it protects mitochondrial normal function, and inhibits release of mitochondrial cell death factors into the cytosol. Release of these factors into the cytosol is a key trigger of terminal cell death pathways. Based on these results, human clinical trials of minocycline are currently underway for HD, ALS, Parkinson’s disease, Multiple Sclerosis, and spinal cord injury.