Issue 1, 2015

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.

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

Article information

Article type
Communication
Submitted
01 Oct 2014
Accepted
14 Nov 2014
First published
14 Nov 2014
This article is Open Access
Creative Commons BY-NC license

Metallomics, 2015,7, 66-70

Author version available

Spotlight

Advertisements