Altered Expression of ZnT10 in Alzheimer's Disease Brain

There is an increasing body of evidence suggesting that metal homeostasis is dysregulated in the pathology of Alzheimer's disease (AD). Although expression levels of several transporters belonging the SLC30 family, which comprises predominantly zinc transporters, have been studied in the AD bra...

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Main Authors:	Bosomworth, Helen J., Adlard, Paul A., Ford, Dianne, Valentine, Ruth A.
Format:	Online
Language:	English
Published:	Public Library of Science 2013
Online Access:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3669266/

id	pubmed-3669266
recordtype	oai_dc
spelling	pubmed-36692662013-06-05 Altered Expression of ZnT10 in Alzheimer's Disease Brain Bosomworth, Helen J. Adlard, Paul A. Ford, Dianne Valentine, Ruth A. Research Article There is an increasing body of evidence suggesting that metal homeostasis is dysregulated in the pathology of Alzheimer's disease (AD). Although expression levels of several transporters belonging the SLC30 family, which comprises predominantly zinc transporters, have been studied in the AD brain, SLC30A10 (ZnT10) has not been studied in this context. To determine if dysregulated expression of ZnT10, which may transport both Zn and Mn, could be a factor that contributes to AD, we investigated if there were differences in ZnT10 mRNA levels in specimens of frontal cortex from AD patients and controls and also if brain tissue from the APP/PS1 transgenic (Tg) mouse model showed abnormal levels of ZnT10 mRNA expression. Our results show that ZnT10 is significantly (P<0.01) decreased in the frontal cortex in AD. Furthermore, we observed a significant decrease in ZnT10 mRNA levels in the APP/PS1-Tg mice compared with wild-type controls (P<0.01). Our results suggest that this dysregulation in ZnT10 could further contribute to disease progression. Public Library of Science 2013-05-31 /pmc/articles/PMC3669266/ /pubmed/23741496 http://dx.doi.org/10.1371/journal.pone.0065475 Text en © 2013 Bosomworth et al http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are properly credited.
repository_type	Open Access Journal
institution_category	Foreign Institution
institution	US National Center for Biotechnology Information
building	NCBI PubMed
collection	Online Access
language	English
format	Online
author	Bosomworth, Helen J. Adlard, Paul A. Ford, Dianne Valentine, Ruth A.
spellingShingle	Bosomworth, Helen J. Adlard, Paul A. Ford, Dianne Valentine, Ruth A. Altered Expression of ZnT10 in Alzheimer's Disease Brain
author_facet	Bosomworth, Helen J. Adlard, Paul A. Ford, Dianne Valentine, Ruth A.
author_sort	Bosomworth, Helen J.
title	Altered Expression of ZnT10 in Alzheimer's Disease Brain
title_short	Altered Expression of ZnT10 in Alzheimer's Disease Brain
title_full	Altered Expression of ZnT10 in Alzheimer's Disease Brain
title_fullStr	Altered Expression of ZnT10 in Alzheimer's Disease Brain
title_full_unstemmed	Altered Expression of ZnT10 in Alzheimer's Disease Brain
title_sort	altered expression of znt10 in alzheimer's disease brain
description	There is an increasing body of evidence suggesting that metal homeostasis is dysregulated in the pathology of Alzheimer's disease (AD). Although expression levels of several transporters belonging the SLC30 family, which comprises predominantly zinc transporters, have been studied in the AD brain, SLC30A10 (ZnT10) has not been studied in this context. To determine if dysregulated expression of ZnT10, which may transport both Zn and Mn, could be a factor that contributes to AD, we investigated if there were differences in ZnT10 mRNA levels in specimens of frontal cortex from AD patients and controls and also if brain tissue from the APP/PS1 transgenic (Tg) mouse model showed abnormal levels of ZnT10 mRNA expression. Our results show that ZnT10 is significantly (P<0.01) decreased in the frontal cortex in AD. Furthermore, we observed a significant decrease in ZnT10 mRNA levels in the APP/PS1-Tg mice compared with wild-type controls (P<0.01). Our results suggest that this dysregulation in ZnT10 could further contribute to disease progression.
publisher	Public Library of Science
publishDate	2013
url	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3669266/
_version_	1611982679054483456

Altered Expression of ZnT10 in Alzheimer's Disease Brain

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