Abca7基因缺失不影响小鼠的成体神经发生。

Abca7 deletion does not affect adult neurogenesis in the mouse.

作者信息

Li Hongyun, Karl Tim, Garner Brett

机构信息

Illawarra Health and Medical Research Institute, University of Wollongong, Wollongong, NSW 2522, Australia School of Biological Sciences, University of Wollongong, Wollongong, NSW 2522, Australia.

Neuroscience Research Australia, Randwick, NSW 2031, Australia School of Medical Sciences, University of New South Wales, Sydney, NSW 2052, Australia Schizophrenia Research Institute, Randwick, NSW 2031, Australia.

出版信息

Biosci Rep. 2016 Jan 20;36(2):e00308. doi: 10.1042/BSR20150308.

DOI:10.1042/BSR20150308

PMID:26792809

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4793298/

Abstract

ATP-binding cassette transporter A7 (ABCA7) is highly expressed in the brain. Recent genome-wide association studies (GWAS) have identified ABCA7 single nucleotide polymorphisms (SNPs) that increase Alzheimer's disease (AD) risk, however, the mechanisms by which ABCA7 may control AD risk remain to be fully elucidated. Based on previous research suggesting that certain ABC transporters may play a role in the regulation of neurogenesis, we conducted a study of cell proliferation and neurogenic potential using cellular bromodeoxyuridine (BrdU) incorporation and doublecortin (DCX) immunostaining in adult Abca7 deficient mice and wild-type-like (WT) littermates. In the present study counting of BrdU-positive and DCX-positive cells in an established adult neurogenesis site in the dentate gyrus (DG) indicated there were no significant differences when WT and Abca7 deficient mice were compared. We also measured the area occupied by immunohistochemical staining for BrdU and DCX in the DG and the subventricular zone (SVZ) of the same mice and this confirmed that ABCA7 does not play a significant role in the regulation of cell proliferation or neurogenesis in the adult mouse.

摘要

ATP结合盒转运蛋白A7（ABCA7）在大脑中高度表达。最近的全基因组关联研究（GWAS）已经确定了ABCA7单核苷酸多态性（SNP）会增加阿尔茨海默病（AD）风险，然而，ABCA7控制AD风险的机制仍有待充分阐明。基于先前的研究表明某些ABC转运蛋白可能在神经发生的调节中起作用，我们使用细胞溴脱氧尿苷（BrdU）掺入和双皮质素（DCX）免疫染色对成年Abca7基因缺陷小鼠和野生型同窝小鼠进行了细胞增殖和神经发生潜能的研究。在本研究中，对齿状回（DG）中已确定的成年神经发生位点的BrdU阳性和DCX阳性细胞进行计数，结果表明，比较野生型和Abca7基因缺陷小鼠时没有显著差异。我们还测量了同一小鼠DG和脑室下区（SVZ）中BrdU和DCX免疫组化染色所占的面积，这证实了ABCA7在成年小鼠的细胞增殖或神经发生调节中不发挥重要作用。