Traumatic brain injury induces elevation of Co in the human brain
Blaine R Roberts, Dominic J Hare, Catriona A McLean, Alison Conquest, Monica Lind, Qiao-Xin Li, Ashley I Bush, Colin L Masters, Maria-Christina Morganti-Kossmann, Tony Frugier
METALLOMICS | ROYAL SOC CHEMISTRY | Published : 2015
Traumatic brain injury (TBI) is the most common cause of death and disability in young adults, yet the molecular mechanisms that follow TBI are poorly understood. We previously reported a perturbation in iron (Fe) levels following TBI. Here we report that the distribution of cobalt (Co) is modulated in post-mortem human brain following injury. We also investigated how the distribution of other biologically relevant elements changes in TBI. Cobalt is increased due to TBI while copper (Cu), magnesium (Mg), manganese (Mn), phosphorus (P), potassium (K), rubidium (Rb), selenium (Se) and zinc (Zn) remain unchanged. The elevated Co has important implications for positron emission tomography neuroi..View full abstract
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This study was supported by the Victorian Neurotrauma Initiative. Brain tissues were obtained from the Victorian Brain Bank Network, supported by The National Trauma Research Institute, The University of Melbourne, The Florey Institute of Neuroscience and Mental Health, The Victorian Institute of Forensic Medicine and funded by the Victorian Neurotrauma Initiative, Neurosciences Australia, the National Health & Medical Research Council of Australia and the Victorian Government's Operational Infrastructure Support Program.