Research is on the neurobiology of aging. The central hypothesis of my aging research program proposes that aged related impairments in cognition and synaptic plasticity share similar underlying cellular and molecular mechanisms. According to our model, oxidative stress causes impairment in neuronal excitability and maintenance of long-term potentiation (LTP), a form of synaptic plasticity believed to mediate learning and memory processes. The impairment in these physiological processes ultimately impairs spatial learning and memory in aged animals.
