Altered expression of ZnT10 in Alzheimer's disease brain.

Altered expression of ZnT10 in Alzheimer's disease brain.
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DOI:
10.1371/journal.pone.0065475
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发表时间:
2013
期刊:
影响因子:
3.7
通讯作者:
Valentine RA
Valentine RA
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Bosomworth HJ;Adlard PA;Ford D;Valentine RA

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越来越多的证据表明,在阿尔茨海默病(AD)的病理过程中,金属动态平衡受到失调。虽然已经研究了几个属于SLC30家族的转运蛋白在AD脑中的表达水平,但SLC30A10(ZnT10)还没有被研究过。为了确定可能同时转运锌和锰的ZnT10基因的表达异常是否可能是AD的一个因素,我们调查了AD患者和对照组的额叶皮质组织中是否存在差异,以及APP/PS1转基因(TG)小鼠模型的脑组织中是否显示出异常水平的ZnT10基因表达。我们的结果表明,AD患者额叶皮质中的ZnT10显著降低(P<0.01)。此外,我们观察到,与野生型对照组相比,APP/PS1-TG组小鼠的ZnT10mRNA水平显著降低(P&lt;0.01)。我们的结果表明,这种锌转运蛋白10的失调可能会进一步促进疾病的发展。
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.
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