Metabolic Brain Vulnerability: The (In)Visible Risk Following Concussion
Giuseppe Lazzarino (University of Catania)
“Metabolic Brain Vulnerability: The (In)Visible Risk Following Concussion,” Giuseppe Lazzarino, Ph.D., Professor of Biochemistry, School of Biology, University of Catania, Catania, Sicily, Italy, 3:05 pm to 4:20 pm, 127 Noll Laboratory, host: Department of Kinesiology (865-7575).
Abstract: Concussion is a peculiar type of mild traumatic brain injury (mTBI) occurring when a sudden acceleration-deceleration phenomenon involves the brain tissue causing a variety of symptoms and neurocognitive deficits. About the 30% of all concussions are sports-related and it is still under debate when concussed athletes should be allowed to return to play.
In rats, we demonstrated that concussive mTBI causes a transient mitochondrial dysfunction with imbalance in glucose metabolism, amino acid metabolism, N-acetylaspartate (NAA) homeostasis. These changes are measurable by quantifying either energy-related metabolites (ATP, high-energy phosphates, NAA), or expressions of selected genes of main metabolic pathways, or activities of enzymes of glucose metabolism, or expressions of proteins controlling the Mitochondrial Quality Control (MQC). Hence, concussion opens a window of metabolic brain vulnerability. We showed that a second impact during this period may have dramatic consequences. Our animal studies also demonstrated that changes in NAA mirror those occurring to ATP.
In clinics, using 1H-MRS, we found that NAA is decreased in athletes following concussion, for a period of time much longer than that of symptom disappearance. This metabolic biomarker is tremendously useful to monitor the closure of the window of metabolic brain vulnerability, representing the (in)visible risk following concussion.