Mike Robbins Lab

Progressive dementia occurs in 50% of adults and almost 100% of pediactric brain tumor patients who are long-term survivors after treatment with large field or whole brain irradiation (WBI). There are no successful treatments for radiation-induced brain injury, nor are there any known effective preventive strategies.

We hypothesize that the development and progression of radiation-induced late effects are driven, in part, by a chronic oxidative stress. To test this hypothesis, we are currently evaluating the ability of Peroxisomal Proliferator-Activated Receptor (PPAR) α and PPARγ agonists, to modulate the radiation response of the normal brain.

We are also investigating the role of the intrinsic brain renin-angiotensin system (RAS) in radiation-induced brain injury. We hypothesize that the intrinsic brain RAS modulates the radiation-induced changes in normal brain cell phenotype following WBI. These changes in phenotype result in the development and progression of radiation-induced brain injury, including cognitive impairment.