Janna L. Harris1, Henry Yeh2, Nancy E. Berman3, William M. Brooks1
1Hoglund Brain Imaging Center, University of Kansas Medical Center, Kansas City, KS, United States; 2Department of Biostatistics, University of Kansas Medical Center, Kansas City, KS, United States; 3Department of Anatomy & Cell Biology, University of Kansas Medical Center, Kansas City, KS, United States
N-acetylaspartate (NAA), a metabolite synthesized in neuronal mitochondria and detected by proton magnetic resonance spectroscopy (MRS), might serve as a non-invasive biomarker of mitochondrial integrity after traumatic brain injury (TBI). Previous studies in human survivors of TBI have linked NAA with cognitive recovery, although the specific mechanism has not been elucidated. We have examined a time course of changes in NAA and behavioral impairment after TBI in a well-characterized animal model. We then investigated whether these NAA changes are sensitive to manipulation of mitochondrial status by cyclosporine A (CsA), an experimental neuroprotective agent that inhibits mitochondrial permeability transition after TBI.