John Carib Gensel, PhD

Endogenous microglia and blood-borne monocytes (collectively referred to as CNS macrophages) are activated by CNS trauma and home to the site of injury. Once these cells occupy the CNS, they persist there indefinitely. This phenomenon has been documented extensively in different models of mammalian brain and spinal cord injury and is also a feature of human neurotrauma. I am interested in understanding the biological mechanisms that regulate this ubiquitous response to injury with the goal of manipulating CNS macrophages to promote repair. Ongoing studies are focused on answering these questions:

1) Can a pro-reparative macrophage phenotype be induced after injury using therapeutic interventions?

2) What receptors pathways drive reparative macrophage phenotypes and can those pathways be manipulated after spinal cord injury?

3) What is the function and phenotype of macrophages responding to traumatic brain injury?

4) How does age affect the inflammatory response to neurotrauma? The goal of these studies is to develop therapies that will translate to the human population.