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当代阿耳茨海默病研究

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ISSN (Print): 1567-2050
ISSN (Online): 1875-5828

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Systematic Review Article

BIN1、CLU 和 IDE 基因多态性与阿尔茨海默病易感性的联系：来自 Meta 分析的证据

卷 19, 期 4, 2022

发表于: 15 June, 2022

页: [302 - 316] 页: 15

弟呕挨: 10.2174/1567205019666220511140955

价格: $65

摘要

背景：阿尔茨海默病 (AD) 是最常见的神经退行性疾病。 BIN1、CLU 和 IDE 基因多态性与 AD 风险的关联已经过长时间评估，产生了相互矛盾的结果。 目的：我们进行了这项荟萃分析，以调查 BIN1（rs744373 和 rs7561528）、CLU（rs11136000 和 rs9331888）和 IDE（rs1887922）多态性对 AD 风险的贡献。 方法：从截至 2021 年 7 月 15 日的系统文献检索中，我们纳入了 25 项 rs744373 研究、16 项 rs7561528 研究、37 项 rs11136000 研究、16 项 rs9331888 研究和 4 项 rs1887922 研究。为了分析相关性，我们构建了七个使用优势比和 95% 置信区间的遗传模型。我们使用 RevMan 5.4 进行荟萃分析。 结果：我们的研究表明，BIN1 rs744373 在五种遗传模型中与显著增加的 AD 风险相关（OR>1）。同样，CLU rs11136000 在所有遗传模型中显示出减少的关联（OR<1）。 CLU rs9331888 揭示了两个模型中增加的关联（OR>1）。 IDE rs1887922 在四种模型中显示出显著增加的风险（OR>1）。根据亚组分析，在白种人和亚洲人中观察到 BIN1 rs744373 的 AD 风险显著增加。同样，BIN1 rs7561528 仅在白种人中显示出显著增加的 AD 风险。 CLU rs11136000 显示高加索人的风险显著降低，但 rs9331888 显示同一种族的风险增加。 结论：我们的荟萃分析证实了 BIN1 rs744373、CLU rs9331888 和 IDE rs1887922 多态性与 AD 风险增加的关联，尤其是在白种人中。同样，CLU rs11136000 与总体人群和高加索人的 AD 风险降低有关。

关键词: 阿尔茨海默病、桥接整合子 1、BIN1、Clusterin、CLU、胰岛素降解酶。

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[1]
Lauterborn JC, Scaduto P, Cox CD, et al. Increased excitatory to inhibitory synaptic ratio in parietal cortex samples from individuals with Alzheimer’s disease. Nat Commun 2021; 12(1): 2603.
[http://dx.doi.org/10.1038/s41467-021-22742-8] [PMID: 33972518]
[2]
Shih YH, Tu LH, Chang TY, et al. TDP-43 interacts with amyloid-β inhibits fibrillization, and worsens pathology in a model of Alzheimer’s disease. Nat Commun 2020; 11(1): 5950.
[http://dx.doi.org/10.1038/s41467-020-19786-7] [PMID: 33230138]
[3]
Barek MA, Aziz MA, Islam MS. Association of GOLPH2 gene polymorphisms (rs10868366 and rs7019241) with the risk of Alzheimer’s disease: Evidence from a meta-analysis. Meta Gene 2021; 28: 100868.
[http://dx.doi.org/10.1016/j.mgene.2021.100868]
[4]
Sumirtanurdin R, Thalib AY, Cantona K, Abdulah R. Effect of genetic polymorphisms on Alzheimer’s disease treatment outcomes: an update. Clin Interv Aging 2019; 14: 631-42.
[http://dx.doi.org/10.2147/CIA.S200109] [PMID: 30992661]
[5]
Crist AM, Hinkle KM, Wang X, et al. Transcriptomic analysis to identify genes associated with selective hippocampal vulnerability in Alzheimer’s disease. Nat Commun 2021; 12(1): 2311.
[http://dx.doi.org/10.1038/s41467-021-22399-3] [PMID: 33875655]
[6]
Shin JY, Choi EY, Kim M, Lee HK, Byeon SH. Changes in retinal microvasculature and retinal layer thickness in association with apolipoprotein E genotype in Alzheimer’s disease. Sci Rep 2021; 11(1): 1847.
[http://dx.doi.org/10.1038/s41598-020-80892-z] [PMID: 33469106]
[7]
Guerini FR, Farina E, Costa AS, et al. APOE and SNAP-25 polymorphisms predict the outcome of multidimensional stimulation therapy rehabilitation in Alzheimer’s disease. Neurorehabil Neural Repair 2016; 30(9): 883-93.
[http://dx.doi.org/10.1177/1545968316642523] [PMID: 27075583]
[8]
Knopman DS, Amieva H, Petersen RC, et al. Alzheimer disease. Nat Rev Dis Primers 2021; 7(1): 33.
[http://dx.doi.org/10.1038/s41572-021-00269-y] [PMID: 33986301]
[9]
Jansen IE, Savage JE, Watanabe K, et al. Author Correction: Genome-wide meta-analysis identifies new loci and functional pathways influencing Alzheimer’s disease risk. Nat Genet 2020; 52(3): 354.
[http://dx.doi.org/10.1038/s41588-019-0573-x] [PMID: 32029921]
[10]
Scheltens P, Blennow K, Breteler MMB, et al. Alzheimer’s disease. Lancet 2016; 388(10043): 505-17.
[http://dx.doi.org/10.1016/S0140-6736(15)01124-1] [PMID: 26921134]
[11]
Spillantini MG, Goedert M. Tau pathology and neurodegeneration. Lancet Neurol 2013; 12(6): 609-22.
[http://dx.doi.org/10.1016/S1474-4422(13)70090-5] [PMID: 23684085]
[12]
Moustafa AA, Hassan M, Hewedi DH, et al. Genetic underpinnings in Alzheimer’s disease - a review. Rev Neurosci 2018; 29(1): 21-38.
[http://dx.doi.org/10.1515/revneuro-2017-0036] [PMID: 28949931]
[13]
Harold D, Abraham R, Hollingworth P, et al. Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer’s disease. Nat Genet 2009; 41(10): 1088-93.
[http://dx.doi.org/10.1038/ng.440] [PMID: 19734902]
[14]
Lambert JC, Heath S, Even G, et al. Genome-wide association study identifies variants at CLU and CR1 associated with Alzheimer’s disease. Nat Genet 2009; 41(10): 1094-9.
[http://dx.doi.org/10.1038/ng.439] [PMID: 19734903]
[15]
Hu H, Tan L, Bi YL, et al. Association between methylation of BIN1 promoter in peripheral blood and preclinical Alzheimer’s disease. Transl Psychiatry 2021; 11(1): 89.
[http://dx.doi.org/10.1038/s41398-021-01218-9] [PMID: 33531457]
[16]
Prokic I, Cowling BS, Laporte J. Amphiphysin 2 (BIN1) in physiology and diseases. J Mol Med (Berl) 2014; 92(5): 453-63.
[http://dx.doi.org/10.1007/s00109-014-1138-1] [PMID: 24590001]
[17]
Tan L, Yu JT, Zhang W, et al. Association of GWAS-linked loci with late-onset Alzheimer’s disease in a northern Han Chinese population. Alzheimers Dement 2013; 9(5): 546-53.
[http://dx.doi.org/10.1016/j.jalz.2012.08.007] [PMID: 23232270]
[18]
Franzmeier N, Rubinski A, Neitzel J, Ewers M. The BIN1 rs744373 SNP is associated with increased tau-PET levels and impaired memory. Nat Commun 2019; 10(1): 1766.
[http://dx.doi.org/10.1038/s41467-019-09564-5] [PMID: 30992433]
[19]
Bungenberg J, Surano N, Grote A, et al. Gene expression variance in hippocampal tissue of temporal lobe epilepsy patients corresponds to differential memory performance. Neurobiol Dis 2016; 86: 121-30.
[http://dx.doi.org/10.1016/j.nbd.2015.11.011] [PMID: 26631617]
[20]
Li HL, Yang P, Liu ZJ, et al. Common variants at Bin1 are associated with sporadic Alzheimer’s disease in the Han Chinese population. Psychiatr Genet 2015; 25(1): 21-5.
[http://dx.doi.org/10.1097/YPG.0000000000000071] [PMID: 25461955]
[21]
Xiao Q, Liu ZJ, Tao S, et al. Risk prediction for sporadic Alzheimer’s disease using genetic risk score in the Han Chinese population. Oncotarget 2015; 6(35): 36955-64.
[http://dx.doi.org/10.18632/oncotarget.6271] [PMID: 26543236]
[22]
Antúnez C, Boada M, González-Pérez A, et al. The membrane-spanning 4-domains, subfamily A (MS4A) gene cluster contains a common variant associated with Alzheimer’s disease. Genome Med 2011; 3(5): 33.
[http://dx.doi.org/10.1186/gm249] [PMID: 21627779]
[23]
Hu X, Pickering E, Liu YC, et al. Meta-analysis for genome-wide association study identifies multiple variants at the BIN1 locus associated with late-onset Alzheimer’s disease. PLoS One 2011; 6(2): e16616.
[http://dx.doi.org/10.1371/journal.pone.0016616] [PMID: 21390209]
[24]
Tan L, Wang HF, Tan MS, et al. Effect of CLU genetic variants on cerebrospinal fluid and neuroimaging markers in healthy, mild cognitive impairment and Alzheimer’s disease cohorts. Sci Rep 2016; 6(1): 26027.
[http://dx.doi.org/10.1038/srep26027] [PMID: 27229352]
[25]
Rajagopalan P, Hibar DP, Thompson PM. TREM2 and neurodegenerative disease. N Engl J Med 2013; 369(16): 1565-7.
[PMID: 24131186]
[26]
Chen LH, Heng Mak TS, Fan Y, et al. Associations between CLU polymorphisms and memory performance: The role of serum lipids in Alzheimer’s disease. J Psychiatr Res 2020; 129: 281-8.
[http://dx.doi.org/10.1016/j.jpsychires.2020.07.015] [PMID: 32882505]
[27]
Matukumalli SR, Tangirala R, Rao CM. Clusterin: full-length protein and one of its chains show opposing effects on cellular lipid accumulation. Sci Rep 2017; 7(1): 41235.
[http://dx.doi.org/10.1038/srep41235] [PMID: 28120874]
[28]
Zhou Y, Hayashi I, Wong J, Tugusheva K, Renger JJ, Zerbinatti C. Intracellular clusterin interacts with brain isoforms of the bridging integrator 1 and with the microtubule-associated protein Tau in Alzheimer’s disease. PLoS One 2014; 9(7): e103187.
[http://dx.doi.org/10.1371/journal.pone.0103187] [PMID: 25051234]
[29]
Xing YY, Yu JT, Cui WZ, et al. Blood clusterin levels, rs9331888 polymorphism, and the risk of Alzheimer’s disease. J Alzheimers Dis 2012; 29(3): 515-9.
[http://dx.doi.org/10.3233/JAD-2011-111844] [PMID: 22258514]
[30]
González-Casimiro CM, Merino B, Casanueva-Álvarez E, et al. Modulation of insulin sensitivity by insulin-degrading enzyme. Biomedicines 2021; 9(1): 86.
[http://dx.doi.org/10.3390/biomedicines9010086] [PMID: 33477364]
[31]
Minchenko DO, Khita OO, Tsymbal DO, et al. Expression of IDE and PITRM1 genes in ERN1 knockdown U87 glioma cells: effect of hypoxia and glucose deprivation. Endocr Regul 2020; 54(3): 183-95.
[http://dx.doi.org/10.2478/enr-2020-0021] [PMID: 32857715]
[32]
Stefanidis L, Fusco ND, Cooper SE, Smith-Carpenter JE, Alper BJ. Molecular determinants of substrate specificity in human insulin-degrading enzyme. Biochemistry 2018; 57(32): 4903-14.
[http://dx.doi.org/10.1021/acs.biochem.8b00474] [PMID: 30004674]
[33]
Mittal K, Mani RJ, Katare DP. Type 3 diabetes: Cross talk between differentially regulated proteins of type 2 diabetes mellitus and Alzheimer’s disease. Sci Rep 2016; 6(1): 25589.
[http://dx.doi.org/10.1038/srep25589] [PMID: 27151376]
[34]
Giri M, Shah A, Upreti B, Rai JC. Unraveling the genes implicated in Alzheimer’s disease. Biomed Rep 2017; 7(2): 105-14.
[http://dx.doi.org/10.3892/br.2017.927] [PMID: 28781776]
[35]
McFall GP, Wiebe SA, Vergote D, Westaway D, Jhamandas J, Dixon RA. IDE (rs6583817) polymorphism and type 2 diabetes differentially modify executive function in older adults. Neurobiol Aging 2013; 34(9): 2208-16.
[http://dx.doi.org/10.1016/j.neurobiolaging.2013.03.010] [PMID: 23597493]
[36]
Bartl J, Scholz CJ, Hinterberger M, et al. Disorder-specific effects of polymorphisms at opposing ends of the Insulin Degrading Enzyme gene. BMC Med Genet 2011; 12(1): 151.
[http://dx.doi.org/10.1186/1471-2350-12-151] [PMID: 22107728]
[37]
Ozturk A, DeKosky Kamboh MI. Lack of association of 5 SNPs in the vicinity of the insulin-degrading enzyme (IDE) gene with late onset Alzheimer’s disease. Neurosci let 2006; 406: 265-9.
[38]
Moher D, Liberati A, Tetzlaff J, Altman DG. Preferred reporting items for systematic reviews and meta-analyses: the PRISMA statement. Int J Surg 2010; 8(5): 336-41.
[http://dx.doi.org/10.1016/j.ijsu.2010.02.007] [PMID: 20171303]
[39]
Wells G, Shea B, O’Connell DL, et al. The Newcastle-Ottawa Scale (NOS) for assessing the quality of nonrandomised studies in meta-analyses. 2014.
[40]
Egger M, Davey Smith G, Schneider M, Minder C. Bias in meta-analysis detected by a simple, graphical test. BMJ 1997; 315(7109): 629-34.
[http://dx.doi.org/10.1136/bmj.315.7109.629] [PMID: 9310563]
[41]
Begg CB, Mazumdar M. Operating characteristics of a rank correlation test for publication bias. Biometrics 1994; 50(4): 1088-101.
[http://dx.doi.org/10.2307/2533446] [PMID: 7786990]
[42]
Carrasquillo MM, Khan Q, Murray ME, et al. Late-onset Alzheimer disease genetic variants in posterior cortical atrophy and posterior AD. Neurology 2014; 82(16): 1455-62.
[http://dx.doi.org/10.1212/WNL.0000000000000335] [PMID: 24670887]
[43]
Carrasquillo MM, Belbin O, Hunter TA, et al. Replication of BIN1 association with Alzheimer’s disease and evaluation of genetic interactions. J Alzheimers Dis 2011; 24(4): 751-8.
[http://dx.doi.org/10.3233/JAD-2011-101932] [PMID: 21321396]
[44]
Chen W, Zhou X, Duan Y, et al. Association of OGG1 and DLST promoter methylation with Alzheimer’s disease in Xinjiang population. Exp Ther Med 2018; 16(4): 3135-42.
[http://dx.doi.org/10.3892/etm.2018.6524] [PMID: 30214536]
[45]
Hohman TJ, Koran ME, Thornton-Wells T. Alzheimer’s neuroimaging initiative. Epistatic genetic effects among Alzheimer’s candidate genes. PLoS One 2013; 8(11): e80839.
[http://dx.doi.org/10.1371/journal.pone.0080839] [PMID: 24260488]
[46]
Hou M, Xu G, Ran M, Luo W, Wang H. APOE-ε4 carrier status and gut microbiota dysbiosis in patients with Alzheimer disease. Front Neurosci 2021; 15: 1-11.
[http://dx.doi.org/10.3389/fnins.2021.619051]
[47]
Huang F, Shang Y, Luo Y, et al. Lower prevalence of Alzheimer’s disease among tibetans: Association with religious and genetic factors. J Alzheimers Dis 2016; 50(3): 659-67.
[http://dx.doi.org/10.3233/JAD-150697] [PMID: 26757186]
[48]
Jiao B, Liu X, Zhou L, et al. Polygenic analysis of late-onset Alzheimer’s disease from mainland China. PLoS One 2015; 10(12): e0144898.
[http://dx.doi.org/10.1371/journal.pone.0144898] [PMID: 26680604]
[49]
Kaya G, Gündüz E, Acar M, et al. Potential genetic biomarkers in the early diagnosis of Alzheimer disease: APOE and BIN1. Turk J Med Sci 2015; 45(5): 1058-72.
[http://dx.doi.org/10.3906/sag-1405-96] [PMID: 26738348]
[50]
Lambert JC, Zelenika D, Hiltunen M, et al. Evidence of the association of BIN1 and PICALM with the AD risk in contrasting European populations. Neurobiol Aging 2011; 32: 756.e11-e7.56E15.
[http://dx.doi.org/10.1016/j.neurobiolaging.2010.11.022]
[51]
Li WW, Wang Z, Fan DY, et al. Association of polygenic risk score with age at onset and cerebrospinal fluid biomarkers of Alzheimer’s disease in a chinese cohort. Neurosci Bull 2020; 36(7): 696-704.
[http://dx.doi.org/10.1007/s12264-020-00469-8] [PMID: 32072450]
[52]
Liao YC, Lee WJ, Hwang JP, et al. ABCA7 gene and the risk of Alzheimer’s disease in Han Chinese in Taiwan. Neurobiol Aging 2014; 35(10): 2423.e7-2423.e13.
[http://dx.doi.org/10.1016/j.neurobiolaging.2014.05.009] [PMID: 24908168]
[53]
Ohara T, Ninomiya T, Hirakawa Y, et al. Association study of susceptibility genes for late-onset Alzheimer’s disease in the Japanese population. Psychiatr Genet 2012; 22(6): 290-3.
[http://dx.doi.org/10.1097/YPG.0b013e3283586215] [PMID: 22935915]
[54]
Ramos Dos Santos L, Belcavello L, Camporez D, et al. Association study of the BIN1 and IL-6 genes on Alzheimer’s disease. Neurosci Lett 2016; 614: 65-9.
[http://dx.doi.org/10.1016/j.neulet.2015.12.046] [PMID: 26733302]
[55]
Rezazadeh M, Khorrami A, Yeghaneh T, et al. Genetic factors affecting late-onset Alzheimer’s disease susceptibility. neuromolecular med 2016; 18(1): 37-49.
[http://dx.doi.org/10.1007/s12017-015-8376-4] [PMID: 26553058]
[56]
Sleegers K, Bettens K, De Roeck A, et al. A 22-single nucleotide polymorphism Alzheimer’s disease risk score correlates with family history, onset age, and cerebrospinal fluid Aβ42. Alzheimers Dement 2015; 11(12): 1452-60.
[http://dx.doi.org/10.1016/j.jalz.2015.02.013] [PMID: 26086184]
[57]
Wang HZ, Bi R, Hu QX, et al. Validating GWAS-identified risk loci for Alzheimer’s disease in Han Chinese populations. Mol Neurobiol 2016; 53(1): 379-90.
[http://dx.doi.org/10.1007/s12035-014-9015-z] [PMID: 25452228]
[58]
Zou T, Chen W, Zhou X, et al. Association of multiple candidate genes with mild cognitive impairment in an elderly Chinese Uygur population in Xinjiang. Psychogeriatrics 2019; 19(6): 574-83.
[http://dx.doi.org/10.1111/psyg.12440] [PMID: 30983028]
[59]
Biffi A, Anderson CD, Desikan RS, et al. Genetic variation and neuroimaging measures in Alzheimer disease. Arch Neurol 2010; 67(6): 677-85.
[http://dx.doi.org/10.1001/archneurol.2010.108] [PMID: 20558387]
[60]
Chung SJ, Lee JH, Kim SY, et al. Association of GWAS top hits with late-onset Alzheimer disease in Korean population. Alzheimer Dis Assoc Disord 2013; 27(3): 250-7.
[http://dx.doi.org/10.1097/WAD.0b013e31826d7281] [PMID: 22975751]
[61]
Liu G, Wang T, Tian R, et al. Alzheimer’s disease risk variant rs2373115 regulates GAB2 and NARS2 expression in human brain tissues. J Mol Neurosci 2018; 66(1): 37-43.
[http://dx.doi.org/10.1007/s12031-018-1144-9] [PMID: 30088171]
[62]
Omoumi A, Fok A, Greenwood T, Sadovnick AD, Feldman HH, Hsiung GY. Evaluation of late-onset Alzheimer disease genetic susceptibility risks in a Canadian population. Neurobiol Aging 2014; 35(4): 936.e5-936.e12.
[http://dx.doi.org/10.1016/j.neurobiolaging.2013.09.025] [PMID: 24176626]
[63]
Wijsman EM, Pankratz ND, Choi Y, et al. Genome-wide association of familial late-onset Alzheimer’s disease replicates BIN1 and CLU and nominates CUGBP2 in interaction with APOE. PLoS Genet 2011; 7(2): e1001308.
[http://dx.doi.org/10.1371/journal.pgen.1001308] [PMID: 21379329]
[64]
Alaylıoğlu M, Gezen-Ak D, Dursun E, et al. The association between clusterin and APOE polymorphisms and late-onset Alzheimer disease in a Turkish cohort. J Geriatr Psychiatry Neurol 2016; 29(4): 221-6.
[http://dx.doi.org/10.1177/0891988716640373] [PMID: 27076484]
[65]
Balcar VJ, Zeman T, Janout V, Janoutová J, Lochman J, Šerý O. Single nucleotide polymorphism rs11136000 of CLU gene (Clusterin, ApoJ) and the risk of late-onset Alzheimer’s disease in a central european population. Neurochem Res 2021; 46(2): 411-22.
[http://dx.doi.org/10.1007/s11064-020-03176-y] [PMID: 33206315]
[66]
Belcavello L, Camporez D, Almeida LD, Morelato RL, Batitucci MC, de Paula F. Association of MTHFR and PICALM polymorphisms with Alzheimer’s disease. Mol Biol Rep 2015; 42(3): 611-6.
[http://dx.doi.org/10.1007/s11033-014-3806-1] [PMID: 25359311]
[67]
Carrasquillo MM, Belbin O, Hunter TA, et al. Replication of CLU, CR1, and PICALM associations with alzheimer disease. Arch Neurol 2010; 67(8): 961-4.
[http://dx.doi.org/10.1001/archneurol.2010.147] [PMID: 20554627]
[68]
Chen LH, Kao PYP, Fan YH, et al. Polymorphisms of CR1, CLU and PICALM confer susceptibility of Alzheimer’s disease in a southern Chinese population. Neurobiol Aging 2012; 33(1): 210.e1-7.
[http://dx.doi.org/10.1016/j.neurobiolaging.2011.09.016] [PMID: 22015308]
[69]
Giedraitis V, Kilander L, Degerman-Gunnarsson M, et al. Genetic analysis of Alzheimer’s disease in the Uppsala Longitudinal Study of Adult Men. Dement Geriatr Cogn Disord 2009; 27(1): 59-68.
[http://dx.doi.org/10.1159/000191203] [PMID: 19141999]
[70]
Golenkina SA, Gol’tsov AIu, Kuznetsova IL, et al. [Analysis of clusterin gene (CLU/APOJ) polymorphism in Alzheimer’s disease patients and in normal cohorts from Russian populations]. Mol Biol (Mosk) 2010; 44(4): 620-6.
[PMID: 20873220]
[71]
Gu H, Wei X, Chen S, et al. Association of clusterin gene polymorphisms with late-onset Alzheimer’s disease. Dement Geriatr Cogn Disord 2011; 32(3): 198-201.
[http://dx.doi.org/10.1159/000331276] [PMID: 22122982]
[72]
Kamboh MI, Minster RL, Demirci FY, et al. Association of CLU and PICALM variants with Alzheimer’s disease. Neurobiol Aging 2012; 33(3): 518-21.
[http://dx.doi.org/10.1016/j.neurobiolaging.2010.04.015] [PMID: 20570404]
[73]
Lin YL, Chen SY, Lai LC, et al. Genetic polymorphisms of clusterin gene are associated with a decreased risk of Alzheimer’s disease. Eur J Epidemiol 2012; 27(1): 73-5.
[http://dx.doi.org/10.1007/s10654-012-9650-5] [PMID: 22286716]
[74]
Lu SJ, Li HL, Sun YM, Liu ZJ, Yang P, Wu ZY. Clusterin variants are not associated with southern Chinese patients with Alzheimer’s disease. Neurobiol Aging 2014; 35(11): 2656.e9-2656.e11.
[http://dx.doi.org/10.1016/j.neurobiolaging.2014.05.015] [PMID: 24958191]
[75]
Luo HY. Association study of clusterin polymorphism rs11136000 with late-onset Alzheimer’s disease in Bai population. Chinese J Behav Med Brain Sci 2016; 25: 240-3.
[76]
Ma JF, Liu LH, Zhang Y, et al. Association study of clusterin polymorphism rs11136000 with late onset Alzheimer’s disease in Chinese Han population. Am J Alzheimers Dis Other Demen 2011; 26(8): 627-30.
[http://dx.doi.org/10.1177/1533317511432735] [PMID: 22296908]
[77]
Roussotte FF, Gutman BA, Madsen SK, Colby JB, Thompson PM. Combined effects of Alzheimer risk variants in the CLU and ApoE genes on ventricular expansion patterns in the elderly. J Neurosci 2014; 34(19): 6537-45.
[http://dx.doi.org/10.1523/JNEUROSCI.5236-13.2014] [PMID: 24806679]
[78]
Santos-Rebouças CB, Gonçalves AP, Dos Santos JM, et al. rs3851179 Polymorphism at 5′ to the PICALM Gene is Associated with Alzheimer and Parkinson Diseases in Brazilian Population. Neuromolecular Med 2017; 19(2-3): 293-9.
[http://dx.doi.org/10.1007/s12017-017-8444-z] [PMID: 28567584]
[79]
Sen A, Arslan M, Erdal ME, et al. Lack of associations between CLU and PICALM gene polymorphisms and Alzheimer’s disease in a Turkish population. Ideggyogy Sz 2015; 68(3-4): 113-20.
[PMID: 26434199]
[80]
Seripa D, Panza F, Paroni G, et al. Role of CLU, PICALM, and TNK1 Genotypes in Aging With and Without Alzheimer’s Disease. Mol Neurobiol 2018; 55(5): 4333-44.
[PMID: 28631188]
[81]
Seshadri S, Fitzpatrick AL, Ikram MA, et al. Genome-wide analysis of genetic loci associated with Alzheimer disease. JAMA 2010; 303(18): 1832-40.
[http://dx.doi.org/10.1001/jama.2010.574] [PMID: 20460622]
[82]
Shankarappa BM, Kota LN, Purushottam M, et al. Effect of CLU and PICALM polymorphisms on AD risk: A study from south India. Asian J Psychiatr 2017; 27: 7-11.
[http://dx.doi.org/10.1016/j.ajp.2016.12.017] [PMID: 28558900]
[83]
Yu JT, Li L, Zhu QX, et al. Implication of CLU gene polymorphisms in Chinese patients with Alzheimer’s disease. Clin Chim Acta 2010; 411(19-20): 1516-9.
[http://dx.doi.org/10.1016/j.cca.2010.06.013] [PMID: 20599866]
[84]
Komatsu M, Shibata N, Kuerban B, Ohnuma T, Baba H, Arai H. Genetic association between clusterin polymorphisms and Alzheimer’s disease in a Japanese population. Psychogeriatrics 2011; 11(1): 14-8.
[http://dx.doi.org/10.1111/j.1479-8301.2010.00346.x] [PMID: 21447104]
[85]
Liu XY. Association analysis of late onset Alzheimer’s disease and Susceptibility genes in Chinese Han population. Central South University 2014.
[86]
Wang B. Association of polymorphisms in Alzheimer’S disease and CLU and clusterin in people with mild cognitive impairment. Fudan University 2014.
[87]
Cui PJ, Cao L, Wang Y, et al. The association between two single nucleotide polymorphisms within the insulin-degrading enzyme gene and Alzheimer’s disease in a Chinese Han population. J Clin Neurosci 2012; 19(5): 745-9.
[http://dx.doi.org/10.1016/j.jocn.2011.08.036] [PMID: 22502914]
[88]
Elias-Sonnenschein LS, Helisalmi S, Natunen T, et al. Genetic loci associated with Alzheimer’s disease and cerebrospinal fluid biomarkers in a Finnish case-control cohort. PLoS One 2013; 8(4): e59676.
[http://dx.doi.org/10.1371/journal.pone.0059676] [PMID: 23573206]
[89]
Wang S, He F, Wang Y. Association between polymorphisms of the insulin-degrading enzyme gene and late-onset Alzheimer disease. J Geriatr Psychiatry Neurol 2015; 28(2): 94-8.
[http://dx.doi.org/10.1177/0891988714554707] [PMID: 25414272]
[90]
Hao X, Wang A, Li C, Shao L, Li Y, Yang P. Genetic association of BIN1 and GAB2 in Alzheimer’s disease: A meta-analysis and systematic review. Geriatr Gerontol Int 2021; 21(2): 185-91.
[http://dx.doi.org/10.1111/ggi.14109] [PMID: 33331110]
[91]
Han Z, Qu J, Zhao J, Zou X. Analyzing 74,248 samples confirms the association between CLU rs11136000 polymorphism and Alzheimer’s disease in caucasian but not Chinese population. Sci Rep 2018; 8(1): 11062.
[http://dx.doi.org/10.1038/s41598-018-29450-2] [PMID: 30038359]
[92]
Zhu R, Liu X, He Z. Association between CLU gene rs11136000 polymorphism and Alzheimer’s disease: an updated meta-analysis. Neurol Sci 2018; 39(4): 679-89.
[http://dx.doi.org/10.1007/s10072-018-3259-8] [PMID: 29396813]
[93]
Dong X, Zhang L, Meng Q, Gao Q. Association Between Interleukin-1A, Interleukin-1B, and Bridging integrator 1 Polymorphisms and Alzheimer’s Disease: a standard and Cumulative Meta-analysis. Mol Neurobiol 2017; 54(1): 736-47.
[http://dx.doi.org/10.1007/s12035-015-9683-3] [PMID: 26768592]
[94]
Lambert JC, Ibrahim-Verbaas CA, Harold D, et al. Meta-analysis of 74,046 individuals identifies 11 new susceptibility loci for Alzheimer’s disease. Nat Genet 2013; 45(12): 1452-8.
[http://dx.doi.org/10.1038/ng.2802] [PMID: 24162737]
[95]
Zhang Y, Wang B, Wan H, Zhou Q, Li T. Meta-analysis of the insulin degrading enzyme polymorphisms and susceptibility to Alzheimer’s disease. Neurosci Lett 2013; 541: 132-7.
[http://dx.doi.org/10.1016/j.neulet.2013.01.051] [PMID: 23416320]
[96]
Levey AI. Progress with Treatments for Alzheimer’s Disease. N Engl J Med 2021; 384(18): 1762-3.
[http://dx.doi.org/10.1056/NEJMe2103722] [PMID: 33951366]

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