Traumatic brain injury induces elevation of Co in the human brain

Abstract

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 neuroimaging. This is the first demonstration of the accumulation of Co in injured tissue explaining the previous utility of ⁵⁵Co-PET imaging in TBI.