“The Effect of Fisetin on the Glutamate Mediated Increase in Toxic Neuronal Glycation Products”
Joseph Burdo, Bridgewater State College, Bridgewater, MA 02325

Stroke is the third most common cause of death in the United States. Excess release of the neurotransmitter glutamate is associated with the neuronal degeneration present in stroke, as well as traumatic brain injury and several neurodegenerative diseases. While much is known about how excess glutamate causes acute excitotoxic injury, less is known about the effects of oxidative glutamate toxicity (oxytosis) in the brain. Preliminary evidence has indicated the presence of toxic methylglyoxal protein adducts in neurons treated with high levels of glutamate. Methylglyoxal is a normal byproduct of glycolysis that becomes toxic when it is not metabolized properly within cells. We will investigate the mechanism of increased methylglyoxal formation and determine its relationship to oxytosis-mediated damage. Our preliminary work also indicated that antioxidants known as flavonoids, which are found commonly in fruits and vegetables, can protect against this glutamate mediated damage. My student and I will use well accepted cell culture methods to model the effects of stroke in neurons by exposing them to high levels of glutamate and assessing the damage in the presence and absence of flavonoids.