• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

补体受体 1 基因多态性与散发性阿尔茨海默病易感性在白种人群中的相关性:一项荟萃分析。

Complement receptor 1 genetic polymorphism contributes to sporadic Alzheimer's disease susceptibility in Caucasians: a meta-analysis.

机构信息

Department of Rehabilitation Medicine, The Second People's Hospital of Hefei City, Hefei, China.

出版信息

Biosci Rep. 2020 Jun 26;40(6). doi: 10.1042/BSR20200321.

DOI:10.1042/BSR20200321
PMID:32432316
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7268259/
Abstract

Complement receptor 1 (CR1) plays an important role in the development of sporadic Alzheimer's disease (SAD) in Caucasians. However, the influence of CR1 (rs6656401A/G and rs3818361T/C) genetic polymorphisms on the risk of SAD remains controversial. A meta-analysis of 18 case-control studies was performed to derive a more precise association of CR1 (rs6656401A/G or rs3818361T/C) genetic polymorphism with the risk of SAD in Caucasians. A statistical difference was found in the dominant model (odds ratio (OR): 1.23, 95% confidence interval (CI): 1.16-1.30, P=0.00), recessive model (OR: 1.28, 95% CI: 1.05-1.56, P=0.02), homozygote comparison (OR: 1.36, 95% CI: 1.12-1.66, P=0.002) or heterozygote comparison (AG versus GG) (OR: 1.21, 95% CI: 1.15-1.29, P=0.00) of CR1 rs6656401A/G. For CR1 rs3818361T/C, a statistical difference was observed in the dominant model (OR: 1.21, 95% CI: 1.13-1.31, P=0.00), recessive model (OR: 1.28, 95% CI: 1.07-1.53, P=0.006), homozygote comparison (OR: 1.35, 95% CI: 1.13-1.62, P=0.001) or heterozygote comparison (TC versus CC) (OR: 1.20, 95% CI: 1.11-1.29, P=0.00). In summary, despite some limitations, the present meta-analysis indicated that rs6656401A/G or rs3818361T/C polymorphism was related to SAD risk. Moreover, a carrier of rs6656401A/G or T carrier of rs3818361T/C in CR1 genetic polymorphism might be an increased factor for SAD in Caucasians.

摘要

补体受体 1(CR1)在白种人散发型阿尔茨海默病(SAD)的发病机制中发挥重要作用。然而,CR1(rs6656401A/G 和 rs3818361T/C)遗传多态性对 SAD 风险的影响仍存在争议。对 18 项病例对照研究进行了荟萃分析,以更精确地评估 CR1(rs6656401A/G 或 rs3818361T/C)遗传多态性与白种人 SAD 风险的相关性。在显性模型(比值比(OR):1.23,95%置信区间(CI):1.16-1.30,P=0.00)、隐性模型(OR:1.28,95%CI:1.05-1.56,P=0.02)、纯合子比较(OR:1.36,95%CI:1.12-1.66,P=0.002)或杂合子比较(AG 与 GG)(OR:1.21,95%CI:1.15-1.29,P=0.00)中,CR1 rs6656401A/G 存在统计学差异。对于 CR1 rs3818361T/C,在显性模型(OR:1.21,95%CI:1.13-1.31,P=0.00)、隐性模型(OR:1.28,95%CI:1.07-1.53,P=0.006)、纯合子比较(OR:1.35,95%CI:1.13-1.62,P=0.001)或杂合子比较(TC 与 CC)(OR:1.20,95%CI:1.11-1.29,P=0.00)中存在统计学差异。综上所述,尽管存在一定局限性,但本荟萃分析表明 rs6656401A/G 或 rs3818361T/C 多态性与 SAD 风险相关。此外,CR1 基因多态性中 rs6656401A/G 的携带者或 rs3818361T/C 的携带者可能是白种人 SAD 的一个危险因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac6/7268259/6bdbf1be98ea/bsr-40-bsr20200321-g9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac6/7268259/dfe7e23c44d7/bsr-40-bsr20200321-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac6/7268259/7ca83bcc119e/bsr-40-bsr20200321-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac6/7268259/df6cc489c423/bsr-40-bsr20200321-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac6/7268259/75c698c6537c/bsr-40-bsr20200321-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac6/7268259/c086f8e050d2/bsr-40-bsr20200321-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac6/7268259/afc5db666177/bsr-40-bsr20200321-g7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac6/7268259/c7f6580da096/bsr-40-bsr20200321-g8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac6/7268259/6bdbf1be98ea/bsr-40-bsr20200321-g9.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac6/7268259/dfe7e23c44d7/bsr-40-bsr20200321-g1.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac6/7268259/7ca83bcc119e/bsr-40-bsr20200321-g2.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac6/7268259/df6cc489c423/bsr-40-bsr20200321-g3.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac6/7268259/75c698c6537c/bsr-40-bsr20200321-g4.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac6/7268259/c086f8e050d2/bsr-40-bsr20200321-g5.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac6/7268259/afc5db666177/bsr-40-bsr20200321-g7.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac6/7268259/c7f6580da096/bsr-40-bsr20200321-g8.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8ac6/7268259/6bdbf1be98ea/bsr-40-bsr20200321-g9.jpg

相似文献

1
Complement receptor 1 genetic polymorphism contributes to sporadic Alzheimer's disease susceptibility in Caucasians: a meta-analysis.补体受体 1 基因多态性与散发性阿尔茨海默病易感性在白种人群中的相关性:一项荟萃分析。
Biosci Rep. 2020 Jun 26;40(6). doi: 10.1042/BSR20200321.
2
GAB2 polymorphism rs2373115 confers susceptibility to sporadic Alzheimer's disease.GAB2 基因多态性 rs2373115 与散发型阿尔茨海默病易感性相关。
Neurosci Lett. 2013 Nov 27;556:216-20. doi: 10.1016/j.neulet.2013.10.036. Epub 2013 Oct 22.
3
Meta-analysis of the association between CR1 polymorphisms and risk of late-onset Alzheimer's disease.CR1基因多态性与晚发型阿尔茨海默病风险关联的荟萃分析。
Neurosci Lett. 2014 Aug 22;578:165-70. doi: 10.1016/j.neulet.2014.06.055. Epub 2014 Jul 1.
4
Association of the CR1 polymorphism with late-onset Alzheimer's disease in Chinese Han populations: a meta-analysis.CR1 多态性与中国汉族人群晚发性阿尔茨海默病的关联:荟萃分析。
Neurosci Lett. 2012 Oct 3;527(1):46-9. doi: 10.1016/j.neulet.2012.08.032. Epub 2012 Aug 27.
5
CR1 in Alzheimer's disease.阿尔茨海默病中的补体受体1(CR1)
Mol Neurobiol. 2015 Apr;51(2):753-65. doi: 10.1007/s12035-014-8723-8. Epub 2014 May 4.
6
Explore the role of CR1 genetic variants in late-onset Alzheimer's disease susceptibility.探索补体受体1(CR1)基因变异在晚发型阿尔茨海默病易感性中的作用。
Psychiatr Genet. 2021 Dec 1;31(6):216-229. doi: 10.1097/YPG.0000000000000291.
7
Alzheimer's disease is associated with low density of the long CR1 isoform.阿尔茨海默病与长链CR1同工型的低密度有关。
Neurobiol Aging. 2015 Apr;36(4):1766.e5-1766.e12. doi: 10.1016/j.neurobiolaging.2015.01.006. Epub 2015 Jan 9.
8
CR1 rs3818361 Polymorphism Contributes to Alzheimer's Disease Susceptibility in Chinese Population.CR1 rs3818361 多态性与中国人群阿尔茨海默病易感性相关。
Mol Neurobiol. 2016 Aug;53(6):4054-4059. doi: 10.1007/s12035-015-9343-7. Epub 2015 Jul 21.
9
An Updated Analysis with 85,939 Samples Confirms the Association Between CR1 rs6656401 Polymorphism and Alzheimer's Disease.一项更新的分析,包含 85939 个样本,证实了 CR1 rs6656401 多态性与阿尔茨海默病之间的关联。
Mol Neurobiol. 2015;51(3):1017-23. doi: 10.1007/s12035-014-8761-2. Epub 2014 May 31.
10
Evaluation of memory endophenotypes for association with CLU, CR1, and PICALM variants in black and white subjects.评估黑人和白人受试者中与CLU、CR1和PICALM基因变异相关的记忆内表型。
Alzheimers Dement. 2014 Mar;10(2):205-13. doi: 10.1016/j.jalz.2013.01.016. Epub 2013 May 2.

引用本文的文献

1
Complement Cascades and Brain Disorders.补体级联反应与脑部疾病
Biomolecules. 2025 Aug 17;15(8):1179. doi: 10.3390/biom15081179.
2
Immune cells in Alzheimer's disease: insights into pathogenesis and potential therapeutic targets.阿尔茨海默病中的免疫细胞:对发病机制和潜在治疗靶点的见解
Med Rev (2021). 2024 Dec 23;5(3):179-202. doi: 10.1515/mr-2024-0064. eCollection 2025 Jun.
3
A Review of the Knops Blood Group System.诺普斯血型系统综述

本文引用的文献

1
Understanding the Role of Systemic Inflammation in Alzheimer's Disease.了解系统性炎症在阿尔茨海默病中的作用。
ACS Chem Neurosci. 2019 Aug 21;10(8):3340-3342. doi: 10.1021/acschemneuro.9b00333. Epub 2019 Jun 26.
2
Immune Signaling in Neurodegeneration.神经退行性变中的免疫信号转导。
Immunity. 2019 Apr 16;50(4):955-974. doi: 10.1016/j.immuni.2019.03.016.
3
Contribution of Neurons and Glial Cells to Complement-Mediated Synapse Removal during Development, Aging and in Alzheimer's Disease.神经元和神经胶质细胞在发育、衰老和阿尔茨海默病过程中介导补体介导的突触消除中的作用。
Clin Appl Thromb Hemost. 2024 Jan-Dec;30:10760296241309638. doi: 10.1177/10760296241309638.
Mediators Inflamm. 2018 Nov 11;2018:2530414. doi: 10.1155/2018/2530414. eCollection 2018.
4
Peripheral complement interactions with amyloid β peptide in Alzheimer's disease: Polymorphisms, structure, and function of complement receptor 1.阿尔茨海默病中淀粉样β肽与外周补体的相互作用:补体受体 1 的多态性、结构和功能。
Alzheimers Dement. 2018 Nov;14(11):1438-1449. doi: 10.1016/j.jalz.2018.04.003. Epub 2018 May 21.
5
Peripheral complement interactions with amyloid β peptide in Alzheimer's disease: 2. Relationship to amyloid β immunotherapy.阿尔茨海默病中外周补体与淀粉样 β 肽的相互作用:2. 与淀粉样 β 免疫疗法的关系。
Alzheimers Dement. 2018 Feb;14(2):243-252. doi: 10.1016/j.jalz.2017.04.015. Epub 2017 Jul 26.
6
Biomarkers for Alzheimer Disease: Classical and Novel Candidates' Review.阿尔茨海默病的生物标志物:经典和新型候选物的综述。
Neuroscience. 2018 Feb 1;370:181-190. doi: 10.1016/j.neuroscience.2017.07.017. Epub 2017 Jul 17.
7
rs3851179 Polymorphism at 5' to the PICALM Gene is Associated with Alzheimer and Parkinson Diseases in Brazilian Population.rs3851179 位于 PICALM 基因 5'端的多态性与巴西人群的阿尔茨海默病和帕金森病相关。
Neuromolecular Med. 2017 Sep;19(2-3):293-299. doi: 10.1007/s12017-017-8444-z. Epub 2017 May 31.
8
Late onset Alzheimer's disease genetics implicates microglial pathways in disease risk.迟发性阿尔茨海默病遗传学研究表明小胶质细胞通路与疾病风险有关。
Mol Neurodegener. 2017 May 26;12(1):43. doi: 10.1186/s13024-017-0184-x.
9
Validating GWAS Variants from Microglial Genes Implicated in Alzheimer's Disease.验证与阿尔茨海默病相关的小胶质细胞基因的全基因组关联研究变异体
J Mol Neurosci. 2017 Jun;62(2):215-221. doi: 10.1007/s12031-017-0928-7. Epub 2017 May 5.
10
Peripheral complement interactions with amyloid β peptide: Erythrocyte clearance mechanisms.外周补体与淀粉样β肽的相互作用:红细胞清除机制。
Alzheimers Dement. 2017 Dec;13(12):1397-1409. doi: 10.1016/j.jalz.2017.03.010. Epub 2017 May 2.