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Research Article

Association of Alzheimer’s Disease with Genetic Variants of Apolipoprotein E, Clusterin, TNF-α, and IL-6 Among Elderly Saudis

Author(s): Saba Abdi*, Amani Ahmed Alghamdi, Nouf Nasser Abduallah AlGhunaim, Reem Muteb Almutairi, Farid Shokry Ataya, Mohammed Ghouse Ahmed Ansari, Syed Danish Hussain, Mohammad Masoud, Abir Alamro, Othman T. Almutairi, Nasser M. Al-Daghri and Taim Abdullah Muayqil

Volume 23, Issue 15, 2022

Published on: 20 May, 2022

Page: [1893 - 1902] Pages: 10

DOI: 10.2174/1389201023666220208093919

Price: $65

Abstract

Background: In the wake of the warning by WHO that the prevalence of dementia may have a rise of 125% in the Middle East by 2050, identification of the genetic risk factors in Arab populations is urgent.

Objectives: To investigate the association of Single Nucleotide Polymorphisms (SNPs) in apolipoprotein E (ApoE), clusterin (CLU), tumor necrotic factor- α (TNF-α) and interleukin-6 (IL-6) genes, with risk of Alzheimer’s disease (AD) in Saudi Arabian participants.

Methods: A total of 42 Saudi AD patients and 23 age-matched control participants were genotyped for eight SNPs: rs429358, rs7412 (ApoE); rs11136000, rs1532278 (CLU); rs1800629, rs1799724 (TNF-α) and rs1800796, rs1800795(IL-6), by RT-PCR using the TaqMan assay. Serum concentrations of amyloid beta peptide 1–40(Aβ1-40), amyloid beta peptide 1–42(Aβ1- 42), CLU and some other biochemical markers were measured.

Results: A significant increase (p=0.004) in the serum CLU level was detected in the AD group (340.4 ± 74.6) compared with control group (265.0 ± 80.9). For rs1532278 (CLU), genotype GA was significantly higher in AD patients (57.1%) than in the control participants (26.1%), [p=0.024, OR = 4.00, 95% CI (1.20-13.28)]. For the ApoE SNP rs7412, 40.4% of patients carried a TT genotype, whereas it was completely absent in the controls [p = 0.020, OR = 30.53, 95% CI (1.73 – 540.05)].For rs429358 (ApoE), patients showed a significantly increased frequency of the TC genotype [p = 0.006, OR = 9.33, 95% CI (1.89–46.19)] and TT [p = 0.045, OR = 19.76, 95% CI (1.07–366.0)] genotype than controls. AD patients with CC genotype for ApoE rs429358 had significantly lower levels of Aβ1-40 (p=0.04) in AD patients than controls. Carriers of genotype GG for rs1800629 (TNF-α) showed significantly higher levels of serum IL-6 (p = 0.04) in AD patients.

Conclusion: Genetic variants in ApoE and CLU may influence susceptibility to AD among Saudi Arabian participants.

Keywords: Single nucleotide polymorphism, apolipoprotein E, IL-6, TNF-α, clusterin, Alzheimer's disease, dementia, Saudi Arabia.

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[1]
Weller, J.; Budson, A. Current understanding of Alzheimer’s disease diagnosis and treatment. F1000 Res., 2018, 7, 7.
[http://dx.doi.org/10.12688/f1000research.14506.1] [PMID: 30135715]
[2]
Sumirtanurdin, R.; Thalib, A.Y.; Cantona, K.; Abdulah, R. Effect of genetic polymorphisms on Alzheimer’s disease treatment outcomes: an update. Clin. Interv. Aging, 2019, 14, 631-642.
[http://dx.doi.org/10.2147/CIA.S200109] [PMID: 30992661]
[3]
Alkhunizan, M.; Alkhenizan, A.; Basudan, L. Prevalence of mild cognitive impairment and dementia in Saudi Arabia: a community-based study. Dement. Geriatr. Cogn. Disord. Extra, 2018, 8(1), 98-103.
[http://dx.doi.org/10.1159/000487231] [PMID: 29706986]
[4]
Algahtani, H.; Shirah, B.; Alhazmi, A.; Alshareef, A.; Bajunaid, M.; Samman, A. Perception and attitude of the general population towards Alzheimer’s disease in Jeddah, Saudi Arabia. Acta Neurol. Belg., 2020, 120(2), 313-320.
[http://dx.doi.org/10.1007/s13760-018-1040-7] [PMID: 30421351]
[5]
Karch, C.M.; Cruchaga, C.; Goate, A.M. Alzheimer’s disease genetics: from the bench to the clinic. Neuron, 2014, 83(1), 11-26.
[http://dx.doi.org/10.1016/j.neuron.2014.05.041] [PMID: 24991952]
[6]
Fan, L.; Mao, C.; Hu, X.; Zhang, S.; Yang, Z.; Hu, Z.; Sun, H.; Fan, Y.; Dong, Y.; Yang, J.; Shi, C.; Xu, Y. New insights into the pathogenesis of Alzheimer’s disease. Front. Neurol., 2020, 10, 1312.
[http://dx.doi.org/10.3389/fneur.2019.01312] [PMID: 31998208]
[7]
Richardson, J.R.; German, D.; Levey, A. Alzheimer disease risk factors. JAMA Neurol., 2014, 71(8), 1051-1051.
[http://dx.doi.org/10.1001/jamaneurol.2014.1525] [PMID: 25111206]
[8]
Gatz, M.; Reynolds, C.A.; Fratiglioni, L.; Johansson, B.; Mortimer, J.A.; Berg, S.; Fiske, A.; Pedersen, N.L. Role of genes and environments for explaining Alzheimer disease. Arch. Gen. Psychiatry, 2006, 63(2), 168-174.
[http://dx.doi.org/10.1001/archpsyc.63.2.168] [PMID: 16461860]
[9]
Wingo, T.S.; Lah, J.J.; Levey, A.I.; Cutler, D.J. Autosomal recessive causes likely in early-onset alzheimer disease. Arch. Neurol., 2012, 69(1), 59-64.
[http://dx.doi.org/10.1001/archneurol.2011.221] [PMID: 21911656]
[10]
Fan, J.; Tao, W.; Li, X.; Li, H.; Zhang, J.; Wei, D.; Chen, Y.; Zhang, Z. The contribution of genetic factors to cognitive impairment and dementia: apolipoprotein E gene, gene interactions, and polygenic risk. Int. J. Mol. Sci., 2019, 20(5), 1177.
[http://dx.doi.org/10.3390/ijms20051177] [PMID: 30866553]
[11]
Sims, R.; Hill, M.; Williams, J. The multiplex model of the genetics of Alzheimer’s disease. Nat. Neurosci., 2020, 23(3), 311-322.
[http://dx.doi.org/10.1038/s41593-020-0599-5] [PMID: 32112059]
[12]
Bellenguez, C.; Grenier-Boley, B.; Lambert, J-C. Genetics of Alzheimer’s disease: where we are, and where we are going. Curr. Opin. Neurobiol., 2020, 61, 40-48.
[http://dx.doi.org/10.1016/j.conb.2019.11.024] [PMID: 31863938]
[13]
Lutz, M.W.; Sprague, D.; Barrera, J.; Chiba-Falek, O. Shared genetic etiology underlying Alzheimer’s disease and major depressive disorder. Transl. Psychiatry, 2020, 10(1), 88.
[http://dx.doi.org/10.1038/s41398-020-0769-y] [PMID: 32152295]
[14]
Rosenthal, S.L.; Kamboh, M.I. Late-onset alzheimer’s disease genes and the potentially implicated pathways. Curr. Genet. Med. Rep., 2014, 2(2), 85-101.
[http://dx.doi.org/10.1007/s40142-014-0034-x] [PMID: 24829845]
[15]
Guerreiro, R.J.; Gustafson, D.R.; Hardy, J. The genetic architecture of Alzheimer’s disease: beyond APP, PSENs and APOE. Neurobiol. Aging, 2012, 33(3), 437-456.
[http://dx.doi.org/10.1016/j.neurobiolaging.2010.03.025] [PMID: 20594621]
[16]
Bhatt, S.; Puli, L.; Patil, C.R. Role of reactive oxygen species in the progression of Alzheimer’s disease. Drug Discov. Today, 2021, 26(3), 794-803.
[http://dx.doi.org/10.1016/j.drudis.2020.12.004] [PMID: 33306995]
[17]
Cheignon, C.; Tomas, M.; Bonnefont-Rousselot, D.; Faller, P.; Hureau, C.; Collin, F. Oxidative stress and the amyloid beta peptide in Alzheimer’s disease. Redox Biol., 2018, 14, 450-464.
[http://dx.doi.org/10.1016/j.redox.2017.10.014] [PMID: 29080524]
[18]
Llibre Rodriguez, J.J.; Ferri, C.P.; Acosta, D.; Guerra, M.; Huang, Y.; Jacob, K.S.; Krishnamoorthy, E.S.; Salas, A.; Sosa, A.L.; Acosta, I.; Dewey, M.E.; Gaona, C.; Jotheeswaran, A.T.; Li, S.; Rodriguez, D.; Rodriguez, G.; Kumar, P.S.; Valhuerdi, A.; Prince, M. 10/66 Dementia Research Group. Prevalence of dementia in Latin America, India, and China: a population-based cross-sectional survey. Lancet, 2008, 372(9637), 464-474.
[http://dx.doi.org/10.1016/S0140-6736(08)61002-8] [PMID: 18657855]
[19]
Association, A.P. Diagnostic and statistical manual of mental disorders (DSM-5®); American Psychiatric Pub, 2013.
[http://dx.doi.org/10.1176/appi.books.9780890425596]
[20]
McKhann, G.M.; Knopman, D.S.; Chertkow, H.; Hyman, B.T.; Jack, C.R., Jr; Kawas, C.H.; Klunk, W.E.; Koroshetz, W.J.; Manly, J.J.; Mayeux, R.; Mohs, R.C.; Morris, J.C.; Rossor, M.N.; Scheltens, P.; Carrillo, M.C.; Thies, B.; Weintraub, S.; Phelps, C.H. The diagnosis of dementia due to Alzheimer’s disease: recommendations from the National Institute on Aging-Alzheimer’s Association workgroups on diagnostic guidelines for Alzheimer’s disease. Alzheimers Dement., 2011, 7(3), 263-269.
[http://dx.doi.org/10.1016/j.jalz.2011.03.005] [PMID: 21514250]
[21]
Storandt, M.; Head, D.; Fagan, A.M.; Holtzman, D.M.; Morris, J.C. Toward a multifactorial model of Alzheimer disease. Neurobiol. Aging, 2012, 33(10), 2262-2271.
[http://dx.doi.org/10.1016/j.neurobiolaging.2011.11.029] [PMID: 22261556]
[22]
Delikkaya, B.; Moriel, N.; Tong, M.; Gallucci, G.; de la Monte, S.M. Altered expression of insulin-degrading enzyme and regulator of calcineurin in the rat intracerebral streptozotocin model and human apolipoprotein E-ε4-associated Alzheimer’s disease. Alzheimers Dement. (Amst.), 2019, 11, 392-404.
[http://dx.doi.org/10.1016/j.dadm.2019.03.004] [PMID: 31193223]
[23]
Roda, A.R.; Montoliu-Gaya, L.; Villegas, S. The role of apolipoprotein E isoforms in Alzheimer’s disease. J. Alzheimers Dis., 2019, 68(2), 459-471.
[http://dx.doi.org/10.3233/JAD-180740] [PMID: 30775980]
[24]
Wang, Y.; Du, X.; Zhao, R.; Niu, J.; Wang, H.; Li, J. Association of APOE polymorphisms with lipid-lowering efficacy of statins in atherosclerotic cardiovascular diseases. Ann. Acad. Med. Singap., 2021, 50(6), 474-480.
[http://dx.doi.org/10.47102/annals-acadmedsg.2020505] [PMID: 34195754]
[25]
Al-Dabbagh, N.M.; Al-Dohayan, N.; Arfin, M.; Tariq, M. Apolipoprotein E polymorphisms and primary glaucoma in Saudis. Mol. Vis., 2009, 15, 912-919.
[PMID: 19421411]
[26]
Singh, P.P.; Singh, M.; Mastana, S.S. APOE distribution in world populations with new data from India and the UK. Ann. Hum. Biol., 2006, 33(3), 279-308.
[http://dx.doi.org/10.1080/03014460600594513] [PMID: 17092867]
[27]
Liu, C-C.; Liu, C.C.; Kanekiyo, T.; Xu, H.; Bu, G. Apolipoprotein E and Alzheimer disease: risk, mechanisms and therapy. Nat. Rev. Neurol., 2013, 9(2), 106-118.
[http://dx.doi.org/10.1038/nrneurol.2012.263] [PMID: 23296339]
[28]
Roses, A.D.; Saunders, A.M.; Apo, E. ApoE, Alzheimer’s disease, and recovery from brain stress. Ann. N. Y. Acad. Sci., 1997, 826(1), 200-212.
[http://dx.doi.org/10.1111/j.1749-6632.1997.tb48471.x] [PMID: 9329691]
[29]
Rebeck, G.W.; Kindy, M.; LaDu, M.J. Apolipoprotein E and Alzheimer’s disease: the protective effects of ApoE2 and E3. J. Alzheimers Dis., 2002, 4(3), 145-154.
[http://dx.doi.org/10.3233/JAD-2002-4304] [PMID: 12226533]
[30]
Liu, M.; Bian, C.; Zhang, J.; Wen, F. Apolipoprotein E gene polymorphism and Alzheimer’s disease in Chinese population: a meta-analysis. Sci. Rep., 2014, 4(1), 4383.
[http://dx.doi.org/10.1038/srep04383] [PMID: 24632849]
[31]
Kulminski, A.M.; Shu, L.; Loika, Y.; He, L.; Nazarian, A.; Arbeev, K.; Ukraintseva, S.; Yashin, A.; Culminskaya, I. Genetic and regulatory architecture of Alzheimer’s disease in the APOE region. Alzheimers Dement. (Amst.), 2020, 12(1), e12008.
[http://dx.doi.org/10.1002/dad2.12008] [PMID: 32211503]
[32]
Hampel, H.; Hardy, J.; Blennow, K.; Chen, C.; Perry, G.; Kim, S.H.; Villemagne, V.L.; Aisen, P.; Vendruscolo, M.; Iwatsubo, T.; Masters, C.L.; Cho, M.; Lannfelt, L.; Cummings, J.L.; Vergallo, A. The amyloid-β pathway in Alzheimer’s disease. Mol. Psychiatry, 2021, 26(10), 5481-5503.
[PMID: 34456336]
[33]
Mayeux, R.; Honig, L.S.; Tang, M-X.; Manly, J.; Stern, Y.; Schupf, N.; Mehta, P.D. Plasma A[β]40 and A[β]42 and Alzheimer’s disease: relation to age, mortality, and risk. Neurology, 2003, 61(9), 1185-1190.
[http://dx.doi.org/10.1212/01.WNL.0000091890.32140.8F] [PMID: 14610118]
[34]
Hilal, S.; Wolters, F.J.; Verbeek, M.M.; Vanderstichele, H.; Ikram, M.K.; Stoops, E.; Ikram, M.A.; Vernooij, M.W. Plasma amyloid-β levels, cerebral atrophy and risk of dementia: a population-based study. Alzheimers Res. Ther., 2018, 10(1), 63.
[http://dx.doi.org/10.1186/s13195-018-0395-6] [PMID: 29960604]
[35]
Yu, J-T.; Tan, L. The role of clusterin in Alzheimer’s disease: pathways, pathogenesis, and therapy. Mol. Neurobiol., 2012, 45(2), 314-326.
[http://dx.doi.org/10.1007/s12035-012-8237-1] [PMID: 22274961]
[36]
Yang, C.; Wang, H.; Li, C.; Niu, H.; Luo, S.; Guo, X. Association between clusterin concentration and dementia: a systematic review and meta-analysis. Metab. Brain Dis., 2019, 34(1), 129-140.
[http://dx.doi.org/10.1007/s11011-018-0325-0] [PMID: 30291488]
[37]
Thambisetty, M.; Simmons, A.; Velayudhan, L.; Hye, A.; Campbell, J.; Zhang, Y.; Wahlund, L-O.; Westman, E.; Kinsey, A.; Güntert, A.; Proitsi, P.; Powell, J.; Causevic, M.; Killick, R.; Lunnon, K.; Lynham, S.; Broadstock, M.; Choudhry, F.; Howlett, D.R.; Williams, R.J.; Sharp, S.I.; Mitchelmore, C.; Tunnard, C.; Leung, R.; Foy, C.; O’Brien, D.; Breen, G.; Furney, S.J.; Ward, M.; Kloszewska, I.; Mecocci, P.; Soininen, H.; Tsolaki, M.; Vellas, B.; Hodges, A.; Murphy, D.G.; Parkins, S.; Richardson, J.C.; Resnick, S.M.; Ferrucci, L.; Wong, D.F.; Zhou, Y.; Muehlboeck, S.; Evans, A.; Francis, P.T.; Spenger, C.; Lovestone, S. Association of plasma clusterin concentration with severity, pathology, and progression in Alzheimer disease. Arch. Gen. Psychiatry, 2010, 67(7), 739-748.
[http://dx.doi.org/10.1001/archgenpsychiatry.2010.78] [PMID: 20603455]
[38]
Gupta, V.B.; Hone, E.; Pedrini, S.; Doecke, J.; O’Bryant, S.; James, I.; Bush, A.I.; Rowe, C.C.; Villemagne, V.L.; Ames, D.; Masters, C.L.; Martins, R.N. AIBL research group. altered levels of blood proteins in alzheimer’s disease longitudinal study: results from australian imaging biomarkers lifestyle study of ageing cohort. Alzheimers Dement. (Amst.), 2017, 8, 60-72.
[http://dx.doi.org/10.1016/j.dadm.2017.04.003] [PMID: 28508031]
[39]
Harold, D.; Abraham, R.; Hollingworth, P.; Sims, R.; Gerrish, A.; Hamshere, M.L.; Pahwa, J.S.; Moskvina, V.; Dowzell, K.; Williams, A.; Jones, N.; Thomas, C.; Stretton, A.; Morgan, A.R.; Lovestone, S.; Powell, J.; Proitsi, P.; Lupton, M.K.; Brayne, C.; Rubinsztein, D.C.; Gill, M.; Lawlor, B.; Lynch, A.; Morgan, K.; Brown, K.S.; Passmore, P.A.; Craig, D.; McGuinness, B.; Todd, S.; Holmes, C.; Mann, D.; Smith, A.D.; Love, S.; Kehoe, P.G.; Hardy, J.; Mead, S.; Fox, N.; Rossor, M.; Collinge, J.; Maier, W.; Jessen, F.; Schürmann, B.; Heun, R.; van den Bussche, H.; Heuser, I.; Kornhuber, J.; Wiltfang, J.; Dichgans, M.; Frölich, L.; Hampel, H.; Hüll, M.; Rujescu, D.; Goate, A.M.; Kauwe, J.S.; Cruchaga, C.; Nowotny, P.; Morris, J.C.; Mayo, K.; Sleegers, K.; Bettens, K.; Engelborghs, S.; De Deyn, P.P.; Van Broeckhoven, C.; Livingston, G.; Bass, N.J.; Gurling, H.; McQuillin, A.; Gwilliam, R.; Deloukas, P.; Al-Chalabi, A.; Shaw, C.E.; Tsolaki, M.; Singleton, A.B.; Guerreiro, R.; Mühleisen, T.W.; Nöthen, M.M.; Moebus, S.; Jöckel, K.H.; Klopp, N.; Wichmann, H.E.; Carrasquillo, M.M.; Pankratz, V.S.; Younkin, S.G.; Holmans, P.A.; O’Donovan, M.; Owen, M.J.; Williams, J. Genome-wide association study identifies variants at CLU and PICALM associated with Alzheimer’s disease. Nat. Genet., 2009, 41(10), 1088-1093.
[http://dx.doi.org/10.1038/ng.440] [PMID: 19734902]
[40]
Carrasquillo, M.M.; Belbin, O.; Hunter, T.A.; Ma, L.; Bisceglio, G.D.; Zou, F.; Crook, J.E.; Pankratz, V.S.; Dickson, D.W.; Graff-Radford, N.R.; Petersen, R.C.; Morgan, K.; Younkin, S.G. Replication of CLU, CR1, and PICALM associations with alzheimer disease. Arch. Neurol., 2010, 67(8), 961-964.
[http://dx.doi.org/10.1001/archneurol.2010.147] [PMID: 20554627]
[41]
Tan, L.; Wang, H-F.; Tan, M-S.; Tan, C-C.; Zhu, X-C.; Miao, D.; Yu, W-J.; Jiang, T.; Tan, L.; Yu, J-T. Alzheimer’s Disease Neuroimaging Initiative. 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]
[42]
Kao, Y-C.; Ho, P-C.; Tu, Y-K.; Jou, I.M.; Tsai, K-J. Lipids and Alzheimer’s disease. Int. J. Mol. Sci., 2020, 21(4), 1505.
[http://dx.doi.org/10.3390/ijms21041505] [PMID: 32098382]
[43]
Reitz, C.; Tang, M-X.; Luchsinger, J.; Mayeux, R. Relation of plasma lipids to Alzheimer disease and vascular dementia. Arch. Neurol., 2004, 61(5), 705-714.
[http://dx.doi.org/10.1001/archneur.61.5.705] [PMID: 15148148]
[44]
Proitsi, P.; Kim, M.; Whiley, L.; Simmons, A.; Sattlecker, M.; Velayudhan, L.; Lupton, M.K.; Soininen, H.; Kloszewska, I.; Mecocci, P.; Tsolaki, M.; Vellas, B.; Lovestone, S.; Powell, J.F.; Dobson, R.J.; Legido-Quigley, C. Association of blood lipids with Alzheimer’s disease: A comprehensive lipidomics analysis. Alzheimers Dement., 2017, 13(2), 140-151.
[http://dx.doi.org/10.1016/j.jalz.2016.08.003] [PMID: 27693183]
[45]
Alam, Q.; Alam, M.Z.; Mushtaq, G.; Damanhouri, G.A.; Rasool, M.; Kamal, M.A.; Haque, A.G.; Rasool, M.; Amjad Kamal, M.; Haque, A. Inflammatory process in Alzheimer’s and Parkinson’s diseases: central role of cytokines. Curr. Pharm. Des., 2016, 22(5), 541-548.
[http://dx.doi.org/10.2174/1381612822666151125000300] [PMID: 26601965]
[46]
Cojocaru, I.M.; Cojocaru, M.; Miu, G.; Sapira, V. Study of interleukin-6 production in Alzheimer’s disease. Rom. J. Intern. Med., 2011, 49(1), 55-58.
[PMID: 22026253]
[47]
Khemka, V.K.; Ganguly, A.; Bagchi, D.; Ghosh, A.; Bir, A.; Biswas, A.; Chattopadhyay, S.; Chakrabarti, S. Raised serum proinflammatory cytokines in Alzheimer’s disease with depression. Aging Dis., 2014, 5(3), 170-176.
[http://dx.doi.org/10.14336/ad.2014.0500170] [PMID: 24900939]
[48]
Qi, H-P.; Qu, Z-Y.; Duan, S-R.; Wei, S-Q.; Wen, S-R.; Bi, S. IL-6-174 G/C and -572 C/G polymorphisms and risk of Alzheimer’s disease. PLoS One, 2012, 7(6), e37858.
[http://dx.doi.org/10.1371/journal.pone.0037858] [PMID: 22701584]
[49]
Baune, B.T.; Ponath, G.; Rothermundt, M.; Riess, O.; Funke, H.; Berger, K. Association between genetic variants of IL-1β, IL-6 and TNF-α cytokines and cognitive performance in the elderly general population of the MEMO-study. Psychoneuroendocrinology, 2008, 33(1), 68-76.
[http://dx.doi.org/10.1016/j.psyneuen.2007.10.002] [PMID: 17988804]
[50]
Rasmussen, L.; Delabio, R.; Horiguchi, L.; Mizumoto, I.; Terazaki, C-R.; Mazzotti, D.; Bertolucci, P-H.; Pinhel, M-A.; Souza, D.; Krieger, H.; Kawamata, C.; Minett, T.; Smith, M.C.; Payão, S.L. Association between interleukin 6 gene haplotype and Alzheimer’s disease: a Brazilian case-control study. J. Alzheimers Dis., 2013, 36(4), 733-738.
[http://dx.doi.org/10.3233/JAD-122407] [PMID: 23666170]
[51]
Bagli, M.; Papassotiropoulos, A.; Knapp, M.; Jessen, F.; Luise Rao, M.; Maier, W.; Heun, R. Association between an interleukin-6 promoter and 3′ flanking region haplotype and reduced Alzheimer’s disease risk in a German population. Neurosci. Lett., 2000, 283(2), 109-112.
[http://dx.doi.org/10.1016/S0304-3940(00)00917-4] [PMID: 10739887]
[52]
Ravaglia, G.; Paola, F.; Maioli, F.; Martelli, M.; Montesi, F.; Bastagli, L.; Bianchin, M.; Chiappelli, M.; Tumini, E.; Bolondi, L.; Licastro, F. Interleukin-1β and interleukin-6 gene polymorphisms as risk factors for AD: a prospective study. Exp. Gerontol., 2006, 41(1), 85-92.
[http://dx.doi.org/10.1016/j.exger.2005.10.005] [PMID: 16297587]
[53]
Yue, H.; Han, W.; Sheng, L. Association of pro-inflammatory cytokines gene polymorphisms with Alzheimer’s disease susceptibility in the Han Chinese population. Int. J. Clin. Exp. Med., 2017, 10(3), 5422.
[54]
Bales, K. Neuroinflammation and Alzheimer's disease: critical roles for cytokine/A beta-induced glial activation, NF-kappaB, and apolipo-protein E. Neurobiol. Aging, 2000, 21, 427-432.
[55]
Di Bona, D.; Candore, G.; Franceschi, C.; Licastro, F.; Colonna-Romano, G.; Cammà, C.; Lio, D.; Caruso, C. Systematic review by meta-analyses on the possible role of TNF-α polymorphisms in association with Alzheimer’s disease. Brain Res. Brain Res. Rev., 2009, 61(2), 60-68.
[http://dx.doi.org/10.1016/j.brainresrev.2009.05.001] [PMID: 19445962]
[56]
Lee, Y.H.; Choi, S.J.; Ji, J.D.; Song, G.G. Association between TNF-α promoter -308 A/G polymorphism and Alzheimer’s disease: a meta-analysis. Neurol. Sci., 2015, 36(6), 825-832.
[http://dx.doi.org/10.1007/s10072-015-2102-8] [PMID: 25647294]
[57]
Ng, A.; Tam, W.W.; Zhang, M.W.; Ho, C.S.; Husain, S.F.; McIntyre, R.S.; Ho, R.C. IL-1β, IL-6, TNF-α and CRP in elderly patients with depression or Alzheimer’s disease: systematic review and meta-analysis. Sci. Rep., 2018, 8(1), 1-12.
[http://dx.doi.org/10.1038/s41598-018-30487-6] [PMID: 29311619]
[58]
Jiao, Z.; Wang, W.; Ma, J.; Wang, S.; Su, Z.; Xu, H. Notch signaling mediates TNF-α-induced IL-6 production in cultured fibroblastlike synoviocytes from rheumatoid arthritis. Clinical and Developmental Immunology, 2012, 2012, 350209.
[PMID: 22190977] [http://dx.doi.org/10.1155/2012/350209]

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