Journal
FREE RADICAL BIOLOGY AND MEDICINE
Volume 69, Issue -, Pages 331-337Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.freeradbiomed.2014.01.041
Keywords
Traumatic brain injury; Iron; Mouse models; Amyloid precursor protein; Ceruloplasmin; Free radicals
Funding
- Australian Research Council
- Australian National Health AMP
- Medical Research Council
- University of Melbourne
- Florey Institute of Neuroscience and Mental Health
- Alfred Hospital
- Victorian Forensic Institute of Medicine
- Alzheimers Research UK [ART-SRF2011-1] Funding Source: researchfish
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Traumatic brain injury (TBI) is in part complicated by pro-oxidant iron elevation independent of brain hemorrhage. Ceruloplasmin (CP) and beta-amyloid protein precursor (APP) are known neuroprotective proteins that reduce oxidative damage through iron regulation. We surveyed iron, CP, and APP in brain tissue from control and TBI-affected patients who were stratified according to time of death following injury. We observed CP and APP induction after TBI accompanying iron accumulation. Elevated APP and CP expression was also observed in a mouse model of focal cortical contusion injury concomitant with iron elevation. To determine if changes in APP or CP were neuroprotective we employed the same TBI model on APP(-/-) and CP-/- mice and found that both exhibited exaggerated infarct volume and iron accumulation postinjury. Evidence supports a regulatory role of both proteins in defence against iron-induced oxidative damage after TBI, which presents as a tractable therapeutic target. (C) 2014 Elsevier Inc. All rights reserved.
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