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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Main Author: Cathy W. Levenson
Format: Article
Language:English
Published: MDPI AG 2020-08-01
Series:Medical Sciences
Subjects:
Online Access:https://www.mdpi.com/2076-3271/8/3/36
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spelling 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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