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Int. J. Mol. Sci. 2017, 18(12), 2506;

Zinc Signal in Brain Diseases

The Florey Institute of Neuroscience and Mental Health, The University of Melbourne, Melbourne, Victoria 3052, Australia
Author to whom correspondence should be addressed.
Received: 27 October 2017 / Revised: 15 November 2017 / Accepted: 16 November 2017 / Published: 23 November 2017
(This article belongs to the Special Issue Zinc Signaling in Physiology and Pathogenesis)
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The divalent cation zinc is an integral requirement for optimal cellular processes, whereby it contributes to the function of over 300 enzymes, regulates intracellular signal transduction, and contributes to efficient synaptic transmission in the central nervous system. Given the critical role of zinc in a breadth of cellular processes, its cellular distribution and local tissue level concentrations remain tightly regulated via a series of proteins, primarily including zinc transporter and zinc import proteins. A loss of function of these regulatory pathways, or dietary alterations that result in a change in zinc homeostasis in the brain, can all lead to a myriad of pathological conditions with both acute and chronic effects on function. This review aims to highlight the role of zinc signaling in the central nervous system, where it may precipitate or potentiate diverse issues such as age-related cognitive decline, depression, Alzheimer’s disease or negative outcomes following brain injury. View Full-Text
Keywords: zinc; brain; neurodegeneration; cognition zinc; brain; neurodegeneration; cognition

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This is an open access article distributed under the Creative Commons Attribution License which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited (CC BY 4.0).
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Portbury, S.D.; Adlard, P.A. Zinc Signal in Brain Diseases. Int. J. Mol. Sci. 2017, 18, 2506.

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