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Review

Impaired regulation of immune responses in cognitive decline and Alzheimer’s disease: lessons from genetic association studies

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Pages 1327-1336 | Published online: 10 Jan 2014

References

  • Aronson MK, Ooi WL, Geva DL, Masur D, Blau A, Frishman W. Dementia. Age-dependent incidence, prevalence, and mortality in the old old. Arch. Intern. Med.151(5), 989–992 (1991).
  • Terry RD. Neuropathological changes in Alzheimer’s disease. Prog. Brain Res.101, 383–390 (1994).
  • Trojanowski JQ, Clark CM, Schmidt ML, Arnold SE, Lee VM. Strategies for improving the postmortem neuropathological diagnosis of Alzheimer's disease. Neurobiol. Aging18(Suppl. 4), S75–S79 (1997).
  • McKhann G, Drachman D, Folstein M, Katzman R, Price D, Stadlan EM. Clinical diagnosis of Alzheimer's disease: report of the NINCDS-ADRDA Work Group under the auspices of Department of Health and Human Services Task Force on Alzheimer's Disease. Neurology34(7), 939–944 (1984).
  • Breteler MMB, Claus JJ, van Duijn CM et al. Epidemiology of Alzheimer’s disease. Epidemiol. Rev.14, 59–82 (1992).
  • Dickson DW, Farlo J, Davies P, Crystal H, Fuld P, Yen SH. Alzheimer’s disease. A double-labeling immunohistochemical study of senile plaques.Am. J. Pathol.132, 86–101 (1988).
  • Rogers J, Luber-Narod J, Styren SD, Civin WH. Expression of immune system-associated antigens by cells of the human central nervous system: relationship to the pathology of Alzheimer’s disease. Neurobiol. Aging9, 339–349 (1988).
  • McGeer PL, Schulzer M, McGeer EG. Arthritis and anti-inflammatory agents as possible protective factors for Alzheimer's disease: a review of 17 epidemiologic studies. Neurology47(2), 425–432 (1996).
  • Breitner JC, Gau BA, Welsh KA et al. Inverse association of anti-inflammatory treatments and Alzheimer’s disease: initial results of a co-twin control study. Neurology44, 227–232 (1994).
  • Landi F, Cesari M, Onder G, Russo A, Torre S, Bernabei R. Non steroidal anti-inflammatory drug (NSAID) use and Alzheiemer’s disease in community-dwelling elderly patients. Am. J. Geriatr. Psychiatry11(2), 179–185 (2003)
  • Lindsay J, Laurin D, Verreault R et al. Risk factor for Alzheimer’s disease: a prospective analysis from the Canadian Study of Health and Aging. Am. J. Epidemiol.156(5), 445–453 (2002).
  • In t’ Veld BA, Ruitenberg A, Hofman A et al. Nonsteroidal anti-inflammatory drugs and the risk of Alzheimer’s disease. N. Engl. J. Med.345(21), 1515–1521 (2001).
  • Licastro F, Pedrini S, Caputo L et al. Increased plasma levels of interleukin-1, interleukin-6 and α-1-antichymotrypsin in patients with Alzheimer's disease: peripheral inflammation or signals from the brain? J. Neuroimmunol.103(1), 97–102 (2000).
  • Mancardi GL, Liwnicz BH, Mandybur TI. Fibrous astrocytes in Alzheimer’s disease and senile dementia of Alzheimer’s type. Acta. Neurophathol. (Berl.)61, 76–80 (1983).
  • Griffin WS, Stanley LC, Ling C et al. Brain interleukin-1 and S-100 immunoreactivity are elevated in Down’s syndrome and Alzheimer’s disease. Proc. Natl Acad. Sci. USA86, 7611–7615 (1989).
  • Bauer J, Ganter U, Strauss S et al. The participation of interleukin-6 in the pathogenesis of Alzheimer’s disease. Res. Immunol.143, 650–657 (1992).
  • Sawada M, Kondo N, Suzumura A, Marunouchi T. Production of tumor necrosis factor-α by microglia and astrocytes in culture. Brain Res.491, 394–397 (1989).
  • Abraham CR, Selkoe DJ, Potter H. Immunochemical identification of the serine protease inhibitor, α-1-antichymotrypsin in the brain amyloid deposits. Cell52, 487–501 (1988).
  • Goldgaber D, Harris HW, Hla T et al. Interleukin-1 regulates syntesis of amyloid β-protein precursor mRNA in human endothelial cells. Proc. Natl Acad. Sci. USA86, 7606 (1989).
  • Selkoe DJ. Amyloid beta protein precursor and the pathogenesis of Alzheimer’s disease. Cell58, 611 (1989).
  • McGeer PL, Kawamata T, Walker DG, Akiyama H, Tooyama I, McGeer EG. Microglia in degenerative neurological disease. Glia7, 84–92 (1993).
  • Rozemuller JM, Eikelenboom P, Pals ST, Stam FC. Microglial cells around amyloid plaques in Alzheimer’s disease express leukocyte adhesion molecules of the LFA-1 family. Neurosci. Lett.101, 288–292 (1989).
  • Canning DR, McKeon RJ, DeWitt DA et al. Beta-amyloid of Alzheimer’s disease induces reactive gliosis that inhibits axonal outgrowth. Exp. Neurol.124, 289–298 (1993).
  • Hoke A, Canning DR, Malemud CJ, Silver J. Regional difference in reactive gliosis induced by substrate-bound β-amyloid. Exp. Neurol.130, 56–66 (1994).
  • Griffin WS, Sheng JG, Royston MC et al. Glial-neuronal interactions in Alzheimer's disease: the potential role of a ‘cytokine cycle’ in disease progression. Brain Pathol.8(1), 65–72 (1998).
  • Mrak RE, Sheng JG, Griffin WS. Glial cytokines in Alzheimer’s disease: review and pathogenic implications. Hum. Pathol.26(8), 816–823 (1995).
  • Kelso A. Cytokines: principles and prospect. Immunol. Cell Biol.76, 300–317 (1998).
  • Frei K, Malipiero UV, Leist TP, Zinkernagel RM, Schwab ME, Fontana A. On the cellular source and function of interleukin 6 produced in the central nervous system in viral diseases. Eur. J. Immunol.19(4), 689–694 (1989).
  • Griffin WS, Sheng JG, Roberts GW, Mrak RE. Interleukin-1 expression in different plaque types in Alzheimer's disease: significance in plaque evolution. J. Neuropathol. Exp. Neurol.54(2), 276–281 (1995).
  • Tarkowski E, Blennow K, Wallin A, Tarkowski A. Intracerebral production of tumor necrosis factor-alpha, a local neuroprotective agent, in Alzheimer disease and vascular dementia. J. Clin. Immunol.19(4), 223–230 (1999).
  • Rubinsztein DC. The genetics of Alzheimer’s disease. Prog. Neurobiol.52, 447–454 (1997).
  • Corder EH, Saunders AM, Strittmatter WJ et al. Gene dose of apolipoprotein E type 4 allele and the risk of Alzheimer’s disease in late onset families. Science261, 921–923 (1993).
  • Poirier J, Davignon J, Bouthillier D, Kogan S, Bertrand P, Gauthier S. Apolipoprotein E polymorphism and Alzheimer’s disease. Lancet342, 697–699 (1993).
  • McGeer PL, Rogers J, McGeer EG. Neuroimmune mechanisms in Alzheimer’s disease pathogenesis. Alzheimer Dis. Assoc. Disord.8, 149–158 (1994).
  • Dinarello CA. The interleukin-1 family: 10 years of discovery. FASEB J.8, 1314–1325 (1994).
  • Mrak RE, Griffin WST. Interleukin-1 and the immunogenetics of Alzheimer’s disease. J. Neurophatol. Exp. Neurol.59, 471–476 (2000).
  • Buxbaum JD, Liu KN, Luo Y et al. Evidence that tumor necrosis factor alpha converting enzyme is involved in regulated α-secretase cleavage of the Alzheimer amyloid protein precursor. J. Biol. Chem.273(43), 27765–27767 (1998).
  • Barger SW, Harmon AD. Microglial activation by Alzheimer amyloid precursor protein and modulation by apolipoprotein E. Nature388(6645), 878–881 (1997).
  • Giulian D, Woodward J, Young DG, Krebs JF, Lachman LB. Interleukin-1 injected into mammalian brain stimulates astrogliosis and neovascularization. J. Neurosci.8(7), 2485–2490 (1988).
  • Das S, Potter H. Expression of the Alzheimer amyloid-promoting factor antichymotrypsin is induced in human astrocytes by IL-1. Neuron14(2), 447–456 (1995).
  • McGeer PL, Akiyama H, Itagaki S, McGeer EG. Activation of the classical complement pathway in brain tissue of Alzheimer patients. Neurosci. Lett.107(1–3), 341–346 (1989).
  • Sheng JG, Ito K, Skinner RD, et al. In vivo and in vitro evidence supporting a role for the inflammatory cytokine interleukin-1 as a driving force in Alzheimer pathogenesis. Neurobiol. Aging17(5), 761–766 (1996).
  • Nicoll JAR, Mrak RE, Graham DI et al. Association of interleukin-1 gene polymorphisms in Alzheimer’s disease. Ann. Neurol.47, 365–368 (2000).
  • Combarros O, Sanchez-Guerra M, Infante J, Llorca J, Berciano J. Gene dose-dependent association of interleukin-1α (-889) allele 2 polymorphism with Alzheimer’s disease. J. Neurol.249(9), 1242–1245 (2002).
  • Grimaldi LME, Casadei VM, Ferri C et al. Association of early-onset Alzheimer’s disease with an interleukin-1α gene polymorphism. Ann. Neurol.47, 361–365 (2000).
  • Rebeck GW. Confirmation of genetic association of interleukin-1A with early onset sporadic Alzheimer’s disease. Neurosci. Lett.293, 75–77 (2000).
  • Du Y, Dodel RC, Eastwood BJ et al. Association of an interleukin-1α polymorphism with Alzheimer’s disease. Neurology55, 480–483 (2000).
  • Hedley R, Hallmayer J, Groth DM, Brooks WS, Gandy SE, Martins RN. Association of interleukin-1 polymorphisms with Alzheimer’s disease in Australia. Ann. Neurol.51(6), 795–797 (2002).
  • Kuo YM, Liao PC, Lin C et al. Lack of association between interleukin-1α polymorphism and Alzheimer disease or vascular dementia. Alzheimer Dis. Assoc. Disord.17(2), 94–97 (2003).
  • Pirskanen M, Hiltunen M, Mannermaa A et al. Interleukin 1 α gene polymorphism as a susceptibility factor in Alzheimer’s disease and its influence on the extent of histopathological hallmark lesions of Alzheimer’s disease. Dement. Geriatr. Cogn. Disord.14(3), 123–127 (2002).
  • Green EK, Harris JM, Lemmon H et al. Are interleukin-1 gene polymorphisms risk factors or disease modifiers in AD? Neurology58(10), 1566–1568 (2002).
  • Fidani L, Goulas A, Mirtsou V et al. Interleukin-1A polymorphism is not associated with late onset Alzheimer’s disease. Neurosci. Lett.323(1), 81–83 (2002).
  • Combarros O, Llorca J, Sanchez-Guerra M, Infante J, Berciano J. Age-dependent association between interleukin-1A (-889) genetic polymorphism and sporadic Alzheimer's disease. A meta-analysis. J. Neurol.250(8), 987–989 (2003).
  • Sciacca FL, Ferri C, Licastro F et al. Interleukin-1B polymorphism is associated with age at onset of Alzheimer's disease. Neurobiol. Aging24(7), 927–931 (2003)
  • Licastro F, Veglia F, Chiappelli M, Grimaldi LM, Masliah E. A polymorphism of the interleukin-1 β gene at position +3953 influences progression and neuro-pathological hallmarks of Alzheimer's disease. Neurobiol. Aging25(8), 1017–1022 (2004).
  • Yucesoy B, Peila R, White LR et al. Association of interleukin-1 polymorphisms with dementia in a community-based sample: the Honolulu-Asia Aging Study. Neurobiol. Aging27(2), 211–217 (2006).
  • Ehl C, Kolsch H, Ptok U et al. Association of an interleukin-1β polymorphism at position –511 with Alzheimer’s disease. Int. J. Mol. Med.11(2), 235–238 (2003).
  • Fagiolo U, Cossarizza A, Scala E et al. Increased cytokine production in mononuclear cells of elderly people. Eur. J. Immunol.23, 2375–2378 (1993).
  • Marz P, Cheng JG, Gadient RA et al. Sympathetic neurons can produce and respond to interleukin 6. Proc. Natl Acad. Sci. USA95(6), 3251–3256 (1998).
  • Van Wagoner NJ, Oh JW, Repovic P, Benveniste EN. Interleukin-6 (IL-6) production by astrocytes: autocrine regulation by IL-6 and the soluble IL-6 receptor. J. Neurosci.19(13), 5236–5244 (1999)
  • Gadient RA, Otten UH. Interleukin-6 (IL-6) – a molecule with both beneficial and destructive potentials. Prog. Neurobiol.52(5), 379–390 (1997).
  • Gruol DL, Nelson TE. Physiological and pathological roles of interleukin-6 in the central nervous system. Mol. Neurobiol.15(3), 307–339 (1997).
  • Nakashima K, Wiese S, Yanagisawa M et al. Developmental requirement of gp130 signaling in neuronal survival and astrocyte differentiation. J. Neurosci.19(13), 5429–5434 (1999).
  • Strauss S, Bauer J, Ganter U, Jonas U, Berger M, Volk B. Detection of interleukin-6 and α-2-macroglobulin immunoreactivity in cortex and hippocampus of Alzheimer’s disease patients. Lab. Invest.66, 223–230 (1992).
  • Huell M, Strauss S, Volk B, Berger M, Bauer J. Interleukin-6 present in early stage of plaque formation and is restricted to the brain of Alzheimer’s disease patients. Acta Neuropathol.89, 544–551 (1995).
  • Fishman D, Faulds G, Jeffery R et al. The effect of novel polymorphisms in the interleukin-6 (IL-6) gene on IL-6 transcription and plasma IL-6 levels, and an association with systemic-onset juvenile chronic arthritis. J. Clin. Invest.102(7), 1369–1376 (1998).
  • Licastro F, Grimaldi LM, Bonafe M et al. Interleukin-6 gene alleles affect the risk of Alzheimer’s disease and levels of the cytokine in blood and brain. Neurobiol. Aging24(7), 921–926 (2003).
  • Bagli M, Papassotiropoulos A, Knapp M et al. Association between an interleukin-6 promoter and 3' flanking region haplotype and reduced Alzheimer’s disease risk in a German population. Neurosci. Lett.283(2), 109–112 (2000).
  • Papassotiropoulos A, Bagli M, Jessen F et al. A genetic variation of the inflammatory cytokine interleukin-6 delays the initial onset and reduces the risk for sporadic Alzheimer's disease. Ann. Neurol.45(5), 666–668 (1999).
  • Pola R, Flex A, Gaetani E et al. The -174 G/C polymorphism of the interleukin-6 gene promoter is associated with Alzheimer’s disease in an Italian population [corrected]. Neuroreport13(13), 1645–1647 (2002).
  • Faltraco F, Burger K, Zill P et al. Interleukin-6–174 G/C promoter gene polymorphism C allele reduces Alzheimer’s disease risk. J. Am. Geriatr. Soc.51(4), 578–579 (2003).
  • Depboylu C, Lohmuller F, Gocke P et al. An interleukin-6 promoter variant is not associated with an increased risk for Alzheimer’s disease. Dement. Geriatr. Cogn. Disord.17(3), 170–173 (2004).
  • Bhojak TJ, DeKosky ST, Ganguli M, Kamboh MI. Genetic polymorphisms in the cathespin D and interleukin-6 genes and the risk of Alzheimer’s disease. Neurosci. Lett.288(1), 21–24 (2000).
  • Licastro F, Porcellini E, Caruso C, Lio D, Corder EH. Genetic risk profiles foe Alzheimer’s disease: integration of APOE genotype and gene variants that up-regulate inflammation. Neurobiol. Aging (2006) (In press).
  • Moore KW, de Waal MR, Coffman RL, O'Garra A. Interleukin-10 and the interleukin-10 receptor. Annu. Rev. Immunol.19, 683–765 (2001).
  • Sato K, Nagayama H, Tadokoro K, Juji T, Takahashi TA. Extracellular signal-regulated kinase, stress-activated protein kinase/c-Jun N-terminal kinase, and p38mapk are involved in IL-10-mediated selective repression of TNF-alpha-induced activation and maturation of human peripheral blood monocyte-derived dendritic cells. J. Immunol.162(7), 3865–3872 (1999).
  • Mizuno T, Sawada M, Marunouchi T, Suzumura A. Production of interleukin-10 by mouse glial cells in culture. Biochem. Biophys. Res. Commun.205(3), 1907–1915 (1994).
  • Strle K, Zhou JH, Shen WH et al. Interleukin-10 in the brain. Crit. Rev. Immunol.21(5), 427–449 (2001).
  • Gibson AW, Edberg JC, Wu J, Westendorp RG, Huizinga TW, Kimberly RP. Novel single nucleotide polymorphisms in the distal IL-10 promoter affect IL-10 production and enhance the risk of systemic lupus erythematosus. J. Immunol.166(6), 3915–3922 (2001).
  • Tagore A, Gonsalkorale WM, Pravica V et al. Interleukin-10 (IL-10) genotypes in inflammatory bowel disease. Tissue Antigens54(4), 386–390 (1999).
  • Lio D, Licastro F, Scola L et al. Interleukin-10 promoter polymorphism in sporadic Alzheimer’s disease. Genes Immun.4(3), 234–238 (2003).
  • Depboylu C, Du Y, Muller U et al. Lack of association of interleukin-10 promoter region polymorphisms with Alzheimer’s disease. Neurosci. Lett.342(1–2), 132–134 (2003).
  • Arosio B, Trabattoni D, Galimberti L et al. Interleukin-10 and interleukin-6 gene polymorphisms as risk factors for Alzheimer’s disease. Neurobiol. Aging25(8), 1009–1015 (2004)
  • Scassellati C, Zanardini R, Squitti R et al. Promoter haplotypes of interleukin-10 gene and sporadic Alzheimer’s disease. Neurosci. Lett.356(2), 119–122 (2004).
  • Travis J, Salvelsen GS. Human plasma proteinase inhibitors. Annu. Rev. Biochem.52, 655–709 (1983).
  • Furby A, Leys D, Delacourte A, Buee L, Soetaert G, Petit H. Are α-1-antichymotrypsin and inter-α-trypsin inhibitor peripheral markers of Alzheimer’s disease? J. Neurol. Neurosurg. Psychiatry54(5), 469 (1991).
  • Eriksson S, Janciauskiene S, Lannfelt L. Alpha 1-antichymotrypsin regulates Alzheimer beta-amyloid peptide fibril formation. Proc. Natl Acad. Sci. USA92(6), 2313–2317 (1995).
  • Licastro F, Morini MC, Polazzi E, Davis LJ. Increased serum a-1-antichymotrypsin in patients with probable Alzheimer’s disease: an acute-phase reactant without the peripheral acute-phase response. J. Neuroimmunol.57, 71–75 (1995).
  • Licastro F, Parnetti L, Morini MC et al. acute-phase reactant α-1-antichymotrypsin is increased in cerebrospinal fluid and serum of patients with probable Alzheimer’s disease. Alzheimer Dis. Assoc. Disord.9, 112–118 (1995).
  • Kamboh MI, Sanghera DK, Ferrel RE, DeKosky ST. APOE 4 associated Alzheimer’s disease risk is modified by α-1-antichymotrypsin polymorphism. Nat. Genet.10, 486–488 (1995).
  • Haines JL, Prochard ML, Saunders AM et al. No genetic effect of α-1-antichymotrypsin in Alzheimer’s disease. Genomics33, 53–56 (1996).
  • Licastro F, Pedrini S, Govoni M et al. Apolipoprotein E and α-1-antichymotrypsin allele polymorphism in sporadic and familiar Alzheimer’s disease. Neurosci. Lett.270, 129–132 (1999).
  • Kamboh MI, Minster RL, Kenney M et al. α-1-antichymotrypsin (ACT or SERPINA3) polymorphism may affect age-at-onset and disease duration of Alzheimer’s disease. Neurobiol. Aging27(10), 1435–1439 (2005).
  • Licastro F, Pedrini S, Ferri C et al. Gene polymorphism affecting α-1-antichymotrypsin and interleukin-1 plasma levels increases Alzheimer’s disease risk. Ann. Neurol.48, 388–391 (2000).
  • Morgan K, Licastro F, Tilley L, Ritchie A, Pedrini S, Kalsheker N. Polymorphism in the α-1-antichymotrypsin (ACT) gene promoter: effect on expression in transfected glial and liver cells lines and plasma ACT concentrations. Hum. Genet.109, 303–310 (2001).
  • Licastro F, Chiappelli M, Grimaldi LM et al. A new promoter polymorphism in the alpha-1-antichymotrypsin gene is a disease modifier of Alzheimer's disease. Neurobiol. Aging26(4), 449–53 (2005).
  • Goldstein JL, Brown MS. Regulation of the mevalonate pathway. Nature343, 425–430 (2000).
  • Zhang FL, Casey PJ. Protein prenylation: molecular mechanisms and functional consequences. Annu. Rev. Biochem.65, 241–269 (1996).
  • Chong PH, Kezele R, Franklin C. High-density lipoprotein cholesterol and the role of statins. Circ. J.66, 1037–1044 (2002).
  • Rockwood K, Kirkland S, Hogan DB et al. Use of lipid-lowering agents, indication bias, and the risk of dementia in community-dwelling elderly people. Arch. Neurol.59, 223–227 (2002).
  • Kuodinov AR, Berezov TT, Kuodinova NV. Alzheimer’s amyloid beta and lipid metabolism: a missing link? FASEB12, 1097–1099 (1998).
  • Ignatius MJ, Shooter EM, Pitas RE, Mahley RW. Lipoprotein uptake by neuronal growth cones in vitro. Science236, 959–962 (1987).
  • Frears ER, Stephens DJ, Walters CE, Davies H, Austen BM. The role of cholesterol in the biosynthesis of β-amyloid. Neuroreport10, 1699–1705 (1999).
  • Grimm MO, Grimm HS, Patzold AJ et al. Regulation of cholesterol and sphingomyelin metabolism by amyloid-β and presenilin. Nat. Cell. Biol.7(11), 1118–1123 (2005).
  • Sorrentino S, Landmesser U. Nonlipid-lowering effects of statins. Curr. Treat. Options Cardiovasc. Med.7(6), 459–566 (2005).
  • Cordle A, Landreth G. 3-hydroxy-3-methylglutaryl-coenzyme A reductase inhibitors attenuate β-amyloid-induced microglial inflammatory responses. J. Neurosci.25(2), 299–307 (2005).
  • Stuve O, Youssef S, Steinman L, Zamvil SS. Statins as potential therapeutic agents in neuroinflammatory disorders. Curr. Opin. Neurol.16(3), 393–401 (2003).
  • Walsh S, Aisen P. Inflammatory processes and Alzheimer’s disease. Expert Rev. Neurotherapeutics4(5), 793–798 (2004).

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