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ABCA7基因分型改变了无痴呆的阿尔茨海默病患者脑脊液中的β-淀粉样蛋白水平。

ABCA7 genotype altered Aβ levels in cerebrospinal fluid in Alzheimer's disease without dementia.

作者信息

Ma Fang-Chen, Zong Yu, Wang Hui-Fu, Li Jie-Qiong, Cao Xi-Peng, Tan Lan

机构信息

Department of Neurology, Weifang Medical University, Weifang 261042, China.

Department of Neurology, Qingdao Municipal Hospital, Qingdao University, Qingdao 266071, China.

出版信息

Ann Transl Med. 2018 Nov;6(22):437. doi: 10.21037/atm.2018.07.04.

Abstract

BACKGROUND

ATP-binding cassette transporter A7 (ABCA7) rs3764650 has been identified to be a susceptibility locus for Alzheimer's disease (AD), but its role in cerebrospinal fluid (CSF) proteins was still unclear.

METHODS

The associations of rs3764650 with CSF Aβ, t-tau and p-tau were analyzed in non-dementia AD, including preclinical and prodromal AD from the Alzheimer's Disease Neuroimaging Initiative (ADNI) cohort.

RESULTS

Finally, GG + GT genotypes significantly decreased CSF Aβ level, but did not alter CSF t-tau and p-tau levels in non-dementia AD at baseline, which was further confirmed in longitudinal studies.

CONCLUSIONS

Our findings supported that ABCA7 modified AD risk by altering Aβ deposition rather than tau pathology.

摘要

背景

ATP结合盒转运蛋白A7(ABCA7)基因rs3764650已被确定为阿尔茨海默病(AD)的一个易感位点,但其在脑脊液(CSF)蛋白质中的作用仍不清楚。

方法

在非痴呆型AD中,包括来自阿尔茨海默病神经影像倡议(ADNI)队列的临床前期和前驱期AD,分析rs3764650与脑脊液Aβ、总tau蛋白(t-tau)和磷酸化tau蛋白(p-tau)的相关性。

结果

最终,GG + GT基因型在基线时显著降低了非痴呆型AD患者脑脊液Aβ水平,但未改变脑脊液t-tau和p-tau水平,这在纵向研究中得到了进一步证实。

结论

我们的研究结果支持ABCA7通过改变Aβ沉积而非tau病理来改变AD风险。

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