Peripheral complement interactions with amyloid β peptide in Alzheimer's disease: Polymorphisms, structure, and function of complement receptor 1.
Peripheral complement interactions with amyloid β peptide in Alzheimer's disease: Polymorphisms, structure, and function of complement receptor 1.
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DOI：
10.1016/j.jalz.2018.04.003
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发表时间：
2018-11
期刊：
影响因子：
--
通讯作者：
Rogers J
中科院分区：
文献类型：
--
作者：
Johansson JU;Brubaker WD;Javitz H;Bergen AW;Nishita D;Trigunaite A;Crane A;Ceballos J;Mastroeni D;Tenner AJ;Sabbagh M;Rogers J
全基因组关联研究一致表明，补体受体1（CR1）基因中的单核苷酸多态性（SNP）适度但显著地改变阿尔茨海默病（AD）的风险。后续研究假设CR1在人类大脑中表达，尽管缺乏证据证明其功能。或者，红细胞含有>80%的身体的CR1，其中，在灵长类动物中，已知结合循环病原体。采用了多学科方法。常规的Western印迹和qPCR未能检测到人脑中的CR1。脑免疫组化显示，只有血管CR1。相比之下，红细胞CR1免疫反应性很容易观察到，并且在AD中显著缺乏，CR1介导的红细胞捕获循环Aβ也是如此。与红细胞CR1减少相关的CR1 SNP增加AD风险，而与红细胞CR1增加相关的CR1 SNP降低AD风险。SNP对红细胞CR1的影响可能是CR1多态性与AD风险相关的基础。
Genome-wide association studies consistently show that single nucleotide polymorphisms (SNPs) in the complement receptor 1 (CR1) gene modestly but significantly alter Alzheimer’s disease (AD) risk. Follow-up research has assumed that CR1 is expressed in human brain, despite a paucity of evidence for its function there. Alternatively, erythrocytes contain >80% of the body’s CR1, where, in primates, it is known to bind circulating pathogens. Multidisciplinary methods were employed. Conventional Western blots and qPCR failed to detect CR1 in human brain. Brain immunohistochemistry revealed only vascular CR1. By contrast, erythrocyte CR1 immunoreactivity was readily observed and was significantly deficient in AD, as was CR1-mediated erythrocyte capture of circulating Aβ. CR1 SNPs associated with decreased erythrocyte CR1 increased AD risk, whereas a CR1 SNP associated with increased erythrocyte CR1 decreased AD risk. SNP effects on erythrocyte CR1 likely underlie the association of CR1 polymorphisms with AD risk.
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影响因子：
11.2
作者：
Chibnik, Lori B.;Shulman, Joshua M.;Leurgans, Sue E.;Schneider, Julie A.;Wilson, Robert S.;Tran, Dong;Aubin, Cristin;Buchman, Aron S.;Heward, Christopher B.;Myers, Amanda J.;Hardy, John A.;Huentelman, Matthew J.;Corneveaux, Jason J.;Reiman, Eric M.;Evans, Denis A.;Bennett, David A.;De Jager, Philip L.
通讯作者：
De Jager, Philip L.
影响因子：
4.2
作者：
Hazrati, Lili-Naz;Van Cauwenberghe, Caroline;Rogaeva, Ekaterina
通讯作者：
Rogaeva, Ekaterina
针对适当的淀粉样β神经元毒素：阿尔茨海默病免疫治疗的前进之路。
DOI：
10.1186/alzrt272
发表时间：
2014
期刊：
Alzheimer's research & therapy
影响因子：
--
作者：
Goure WF;Krafft GA;Jerecic J;Hefti F
通讯作者：
Hefti F
影响因子：
30.8
作者：
Harold, Denise;Abraham, Richard;Hollingworth, Paul;Sims, Rebecca;Gerrish, Amy;Hamshere, Marian L.;Pahwa, Jaspreet Singh;Moskvina, Valentina;Dowzell, Kimberley;Williams, Amy;Jones, Nicola;Thomas, Charlene;Stretton, Alexandra;Morgan, Angharad R.;Lovestone, Simon;Powell, John;Proitsi, Petroula;Lupton, Michelle K.;Brayne, Carol;Rubinsztein, David C.;Gill, Michael;Lawlor, Brian;Lynch, Aoibhinn;Morgan, Kevin;Brown, Kristelle S.;Passmore, Peter A.;Craig, David;McGuinness, Bernadette;Todd, Stephen;Holmes, Clive;Mann, David;Smith, A. David;Love, Seth;Kehoe, Patrick G.;Hardy, John;Mead, Simon;Fox, Nick;Rossor, Martin;Collinge, John;Maier, Wolfgang;Jessen, Frank;Schuermann, Britta;van den Bussche, Hendrik;Heuser, Isabella;Kornhuber, Johannes;Wiltfang, Jens;Dichgans, Martin;Froelich, Lutz;Hampel, Harald;Huell, Michael;Rujescu, Dan;Goate, Alison M.;Kauwe, John S. K.;Cruchaga, Carlos;Nowotny, Petra;Morris, John C.;Mayo, Kevin;Sleegers, Kristel;Bettens, Karolien;Engelborghs, Sebastiaan;De Deyn, Peter P.;Van Broeckhoven, Christine;Livingston, Gill;Bass, Nicholas J.;Gurling, Hugh;McQuillin, Andrew;Gwilliam, Rhian;Deloukas, Panagiotis;Al-Chalabi, Ammar;Shaw, Christopher E.;Tsolaki, Magda;Singleton, Andrew B.;Guerreiro, Rita;Muehleisen, Thomas W.;Noethen, Markus M.;Moebus, Susanne;Joeckel, Karl-Heinz;Klopp, Norman;Wichmann, H-Erich;Carrasquillo, Minerva M.;Pankratz, V. Shane;Younkin, Steven G.;Holmans, Peter A.;O'Donovan, Michael;Owen, Michael J.;Williams, Julie
通讯作者：
Williams, Julie
DOI：
10.1073/pnas.151261398
发表时间：
2001-07-17
影响因子：
11.1
作者：
DeMattos, RB;Bales, KR;Holtzman, DM
通讯作者：
Holtzman, DM