Memory Deficits Following TBI

Memory Deficits Following TBITraumatic brain injury (TBI) is known to cause the death/dysfunction of the neurovascular unit (composed of neurons, astroglia, and brain vasculature). Strategies to improve one component may therefore not be sufficient to offer substantial cognitive improvement.  Most cells possess endogenous protective mechanism(s) as a defense against environmental insults and injury.  These cellular defenses often involve induction of cytoprotective genes whose protein products scavenge and/or neutralize toxic molecules.  Currently, we are focused on endogenous cytoprotective cascades that, when activated, can protect the function of multiple components of the neurovascular unit.  Naturally occurring compounds such as sulforaphane, which is found in cruciferous vegetables, can be used to activate cytoprotective cascades and limit cellular injury.  We are exploring the therapeutic potential of sulforaphane to improve memory function following TBI.