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Issue 1, 2015
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Traumatic brain injury induces elevation of Co in the human brain

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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.

Graphical abstract: Traumatic brain injury induces elevation of Co in the human brain

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Publication details

The article was received on 01 Oct 2014, accepted on 14 Nov 2014 and first published on 14 Nov 2014


Article type: Communication
DOI: 10.1039/C4MT00258J
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Metallomics, 2015,7, 66-70
  • Open access: Creative Commons BY-NC license
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    Traumatic brain injury induces elevation of Co in the human brain

    B. R. Roberts, D. J. Hare, C. A. McLean, A. Conquest, M. Lind, Q. Li, A. I. Bush, C. L. Masters, M. Morganti-Kossmann and T. Frugier, Metallomics, 2015, 7, 66
    DOI: 10.1039/C4MT00258J

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