Zinc and Traumatic Brain Injury: From Chelation to Supplementation
With a worldwide incidence rate of almost 70 million annually, traumatic brain injury (TBI) is a frequent cause of both disability and death. Our modern understanding of the zinc-regulated neurochemical, cellular, and molecular mechanisms associated with TBI is the result of a continuum of research...
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doaj-96f931b3952844f482456e52023a7baa2020-11-25T03:30:56ZengMDPI AGMedical Sciences2076-32712020-08-018363610.3390/medsci8030036Zinc and Traumatic Brain Injury: From Chelation to SupplementationCathy W. Levenson0Department of Biomedical Sciences and Program in Neuroscience, College of Medicine, Florida State University, Tallahassee, FL 32306, USAWith a worldwide incidence rate of almost 70 million annually, traumatic brain injury (TBI) is a frequent cause of both disability and death. Our modern understanding of the zinc-regulated neurochemical, cellular, and molecular mechanisms associated with TBI is the result of a continuum of research spanning more than three decades. This review describes the evolution of the field beginning with the initial landmark work on the toxicity of excess neuronal zinc accumulation after injury. It further shows how the field has expanded and shifted to include examination of the cellular pools of zinc after TBI, identification of the role of zinc in TBI-regulated gene expression and neurogenesis, and the use of zinc to prevent cognitive and behavioral deficits associated with brain injury.https://www.mdpi.com/2076-3271/8/3/36brain injurytraumazincexcitotoxicityneuroprotectionchelation |
collection |
DOAJ |
language |
English |
format |
Article |
sources |
DOAJ |
author |
Cathy W. Levenson |
spellingShingle |
Cathy W. Levenson Zinc and Traumatic Brain Injury: From Chelation to Supplementation Medical Sciences brain injury trauma zinc excitotoxicity neuroprotection chelation |
author_facet |
Cathy W. Levenson |
author_sort |
Cathy W. Levenson |
title |
Zinc and Traumatic Brain Injury: From Chelation to Supplementation |
title_short |
Zinc and Traumatic Brain Injury: From Chelation to Supplementation |
title_full |
Zinc and Traumatic Brain Injury: From Chelation to Supplementation |
title_fullStr |
Zinc and Traumatic Brain Injury: From Chelation to Supplementation |
title_full_unstemmed |
Zinc and Traumatic Brain Injury: From Chelation to Supplementation |
title_sort |
zinc and traumatic brain injury: from chelation to supplementation |
publisher |
MDPI AG |
series |
Medical Sciences |
issn |
2076-3271 |
publishDate |
2020-08-01 |
description |
With a worldwide incidence rate of almost 70 million annually, traumatic brain injury (TBI) is a frequent cause of both disability and death. Our modern understanding of the zinc-regulated neurochemical, cellular, and molecular mechanisms associated with TBI is the result of a continuum of research spanning more than three decades. This review describes the evolution of the field beginning with the initial landmark work on the toxicity of excess neuronal zinc accumulation after injury. It further shows how the field has expanded and shifted to include examination of the cellular pools of zinc after TBI, identification of the role of zinc in TBI-regulated gene expression and neurogenesis, and the use of zinc to prevent cognitive and behavioral deficits associated with brain injury. |
topic |
brain injury trauma zinc excitotoxicity neuroprotection chelation |
url |
https://www.mdpi.com/2076-3271/8/3/36 |
work_keys_str_mv |
AT cathywlevenson zincandtraumaticbraininjuryfromchelationtosupplementation |
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1724574605459324928 |