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1. Neopterin Levels and Immune Activation in the Blood of Children with Down’s Syndrome

Author

Licastro F., Chiappelli M., Porcellini E., Rustica M., and Corsi M.M.

Subjects
down's syndrome. alzheimer's disease, il-6, crp, neopterin, plasma levels, Crystallography, QD901-999
Abstract

Patients with AD often show altered levels of some immune molecules in their peripheral blood which correlate with cognitive impairment. Downs' syndrome (DS) subjects are at high risk of developing Alzheimer's disease (AD). Here we studied immune molecules, such as interleukin-6 (IL-6), C reactive protein (CRP) and neopterin, in the blood of non demented children with DS to investigate whether altered peripheral immune phenotype could be present in this subjects without dementia, many years before the presentation of clinical signs of cognitive deterioration. Plasma levels of neopterin and IL-6 were measured by commercially available ELISA kits, whereas plasma CRP concentration was evaluated by nephelometric immunoassay technique. We studied a group of 40 patients with DS, 20 healthy controls and 100 patients w ith AD. Plasma levels of IL-6 and CRP were significantly higher in DS than in control children. The increase of IL-6 and CRP from DS children was similar to that found in elderly patients with clinical AD. In the present research we have also studied blood levels of neopterin which were in the normal range either in DS or control. Increased or normal levels of this metabolite have been found in the blood of AD patients. However, increased blood neopterin was likely to be only elevated in patients with advanced clinical stage of AD. Peripheral altered immune phenotype in healthy young subjects with DS might be an early sign of CNS alterations leading many years later to cognitive deterioration and dementia.

Published
2005
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4. APOE and Alzheimer disease: a major gene with semi-dominant inheritance

Author

Genin, E, Hannequin, D, Wallon, D, Sleegers, K, Hiltunen, M, Combarros, O, Bullido, M J, Engelborghs, S, De Deyn, P, Berr, C, Pasquier, F, Dubois, B, Tognoni, G, Fiévet, N, Brouwers, N, Bettens, K, Arosio, B, Coto, E, Del Zompo, M, Mateo, I, Epelbaum, J, Frank-Garcia, A, Helisalmi, S, Porcellini, E, Pilotto, A, Forti, P, Ferri, R, Scarpini, E, Siciliano, G, Solfrizzi, V, Sorbi, S, Spalletta, G, Valdivieso, F, Vepsäläinen, S, Alvarez, V, Bosco, P, Mancuso, M, Panza, F, Nacmias, B, Bossù, P, Hanon, O, Piccardi, P, Annoni, G, Seripa, D, Galimberti, D, Licastro, F, Soininen, H, Dartigues, J-F, Kamboh, M I, Van Broeckhoven, C, Lambert, J C, Amouyel, P, and Campion, D

Published
2011
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16. Genome-wide association study indentifies variants at CLU and CR1 associated with Alzheimer’s disease

Author

Lambert JC, Heath S, Even G, Campion D, Sleegers K, Hiltunen M, Combarros O, Zelenika D, Bullido MJ, Tavernier B, Letenneur L, Bettens K, Berr C, Pasquier F, Fiévet N, Barberger-Gateau P, Engelborghs S, De Deyn P, Mateo I, Franck A, Helisalmi S, Porcellini E, Hanon O, European Alzheimer's Disease Initiative Investigators, de Pancorbo MM, Lendon C, Dufouil C, Jaillard C, Leveillard T, Alvarez V, Bosco P, Mancuso M, Panza F, Nacmias B, Bossù P, Piccardi P, Annoni G, Seripa D, Galimberti D, Hannequin D, Licastro F, Soininen H, Ritchie K, Blanché H, Dartigues JF, Tzourio C, Gut I, Van Broeckhoven C, Alpérovitch A, Lathrop M, Amouyel P, FORTI, PAOLA, Lambert, J, Heath, S, Even, G, Campion, D, Sleegers, K, Hiltunen, M, Cambarros, O, Zelenika, D, Bullido, M, Tavernier, B, Letenneur, L, Bettens, K, Berr, C, Pasquier, F, Fiévet, N, Barbager Gateau, P, Engelborghs, S, De Deyn, P, Mateo, I, Franck, A, Helisalmi, S, Porcellini, E, Hanon, O, the European Alzheimer’s disease Initiative, I, de Pancorbo, M, Lendon, C, Dufouil, C, Jaillard, C, Leveillard, T, Alvarez, V, Bosco, P, Mancuso, M, Panza, F, Nacmias, B, Bossù, P, Piccardi, P, Annoni, G, Seripa, D, Galimberti, D, Hannequin, D, Licastro, F, Soininen, H, Ritchie, K, Blanché, H, Dartigues, J, Tzourio, C, Gut, I, Broeckhoven, C, Alpérovitch, A, Lathrop, M, Amouyel, P, Lambert JC, Heath S, Even G, Campion D, Sleegers K, Hiltunen M, Combarros O, Zelenika D, Bullido MJ, Tavernier B, Letenneur L, Bettens K, Berr C, Pasquier F, Fiévet N, Barberger-Gateau P, Engelborghs S, De Deyn P, Mateo I, Franck A, Helisalmi S, Porcellini E, Hanon O, European Alzheimer's Disease Initiative Investigator, de Pancorbo MM, Lendon C, Dufouil C, Jaillard C, Leveillard T, Alvarez V, Bosco P, Mancuso M, Panza F, Nacmias B, Bossù P, Piccardi P, Annoni G, Seripa D, Galimberti D, Hannequin D, Licastro F, Soininen H, Ritchie K, Blanché H, Dartigues JF, Tzourio C, Gut I, Van Broeckhoven C, Alpérovitch A, Lathrop M, Amouyel P, Electronics and Informatics, Clinical sciences, Neurology, and Pathologic Biochemistry and Physiology

Subjects
Apolipoprotein E, SORL1, Genome-wide association study, Disease, Polymorphism, Single Nucleotide, White People, ABCA7, PICALM, Alzheimer Disease, Genetics, Humans, Genetic Predisposition to Disease, European Continental Ancestry Group/genetics, Alzheimer's disease, genome-wide association, APOE, APOJ, Medicine(all), Alzheimer Disease/genetics, biology, Phosphatidylinositol binding, Clusterin, Haplotypes, Receptors, Complement 3b, biology.protein, Human medicine, Clusterin/genetics, Receptors, Complement 3b/genetics, Genome-Wide Association Study
Abstract

The gene encoding apolipoprotein E (APOE) on chromosome 19 is the only confirmed susceptibility locus for late-onset Alzheimer's disease. To identify other risk loci, we conducted a large genome-wide association study of 2,032 individuals from France with Alzheimer's disease (cases) and 5,328 controls. Markers outside APOE with suggestive evidence of association (P 10 5) were examined in collections from Belgium, Finland, Italy and Spain totaling 3,978 Alzheimer's disease cases and 3,297 controls. Two loci gave replicated evidence of association: one within CLU (also called APOJ), encoding clusterin or apolipoprotein J, on chromosome 8 (rs11136000, OR = 0.86, 95% CI 0.81-0.90, P = 7.5 × 10 9 for combined data) and the other within CR1, encoding the complement component (3b/4b) receptor 1, on chromosome 1 (rs6656401, OR = 1.21, 95% CI 1.14-1.29, P = 3.7 × 10 9 for combined data). Previous biological studies support roles of CLU and CR1 in the clearance of Β amyloid (AΒ) peptide, the principal constituent of amyloid plaques, which are one of the major brain lesions of individuals with Alzheimer's disease. © 2009 Nature America, Inc. All rights reserved.

Published
2009

19. Polymorphisms of pro-inflammatory genes and Alzheimer's disease risk

Author

CANDORE, Giuseppina, BALISTRERI, Carmela Rita, GRIMALDI, Maria Paola, LISTI', Florinda, VASTO, Sonya, ORLANDO, Valentina, LIO, Domenico, FRANCESCHI C, LICASTRO F, CARUSO C., CANDORE G, BALISTRERI CR, GRIMALDI MP, LISTI' F, VASTO S, ORLANDO V, LIO D, FRANCESCHI C, LICASTRO F, and CARUSO C

Published
2006

25. Gene Polymorphism affecting Alpha-1-Antichymotrypsin and interleukin 1 Plasma Levels increases Alzheimer Disease Risk

Author

Licastro, F, Pedrini, S, Ferri, C, Casadei, V, Govoni, M, Pession, A, Sciacca, FL, Veglia, F, Bonafe, M, Olivieri, F, Franceschi, C, Grimaldi, LME, ANNONI, GIORGIO, Licastro, F, Pedrini, S, Ferri, C, Casadei, V, Govoni, M, Pession, A, Sciacca, F, Veglia, F, Annoni, G, Bonafe, M, Olivieri, F, Franceschi, C, and Grimaldi, L

Subjects
ALPHA, ALLELE, ALPHA(1)-ANTICHYMOTRYPSIN, BRAIN, MED/09 - MEDICINA INTERNA, APOLIPOPROTEIN-E, APOE
Abstract

Plasma levels of al-antichymotrypsin (ACT) and interleukin-1 beta (IL-1 beta) were increased in patients with probable Alzheimer's disease (AD). A common polymorphism within ACT and IL-IP genes affected plasma levels of ACT or IL-1 beta, and AD patients with the ACT T,T or IL-1 beta T,T genotype show-ed the highest levels of plasma ACT or IL-1 beta, respectively. The concomitant presence of the ACT T,T and IL-1 beta T,T genotypes increased the risk of AD (odds ratio: 5.606, confidence interval: 1.654-18.996) and decreased the age at onset of the disease

Published
2000

26. Association of Early-Onset Alzheimer¿s Disease with an Interleukin-1 alpha Polymorphism

Author

Grimaldi, LME, Casadei, VM, Ferri, C, Veglia, F, Licastro, F, Biunno, I, De Bellis, G, Sorbi, S, Mariani, C, Canal, N, Griffin, WST, Franceschi, M., ANNONI, GIORGIO, Grimaldi, L, Casadei, V, Ferri, C, Veglia, F, Licastro, F, Annoni, G, Biunno, I, De Bellis, G, Sorbi, S, Mariani, C, Canal, N, Griffin, W, and Franceschi, M

Subjects
MICROGLIA, PROTEIN-PRECURSOR, GLIAL-NEURONAL INTERACTIONS, MED/09 - MEDICINA INTERNA
Abstract

Overexpression of the pluripotent cytokine interleukin-l (IL-I) by microglial cells correlates with formation of neuritic P-amyloid plaques in Alzheimer's disease (AD). We evaluated polymorphisms in the genes coding for the IL-1 alpha, IL-IP, and IL-1 receptor antagonist cytokines, and tested their association with the occurrence and age at onset of sporadic AD. We found a strong association between the IL-IA T/T genotype and AD onset before 65 years of age (odds ratio, 4.86), with carriers of this genotype showing an onset of disease 9 years earlier than IL-1A CIC carriers. A weaker association with the age at onset was also shown for the IL-1B and IL-1RN genes. These data suggest either a direct effect of the IL-I gene family, mainly IL-1A, on the clinical onset of AD, or a linkage dysequilibrium with an unknown locus relevant to AD on chromosome 2.

Published
2000

27. APOE-491 Promoter Polymorphism is a Risk Factor for late-onset Alzheimer's Disease

Author

Casadei, VM, Ferri, C, Veglia, F, Gavazzi, A, Salani, G, Cattaneo, M, Sorbi, S, Licastro, F, Mariani, C, Franceschi, M, Grimaldi, LME, ANNONI, GIORGIO, Casadei, V, Ferri, C, Veglia, F, Gavazzi, A, Salani, G, Cattaneo, M, Sorbi, S, Annoni, G, Licastro, F, Mariani, C, Franceschi, M, and Grimaldi, L

Subjects
Gene polymorphism, APOE-491, Alzheimer's Disease
Published
1999

28. The CALHM1 P86L polymorphism is a genetic modifier of age at onset in Alzheimer's disease: a meta-analysis study

Author

Lambert, J., Sleegers, K., Gonzalez-Perez, A., Ingelsson, M., Beecham, G., Hiltunen, M., Combarros, O., Bullido, M., Brouwers, N., Bettens, K., Berr, C., Pasquier, F., Richard, F., Dekosky, S., Hannequin, D., Haines, J., Tognoni, G., Fievet, N., Dartigues, J., Tzourio, C., Engelborghs, S., Arosio, B., Coto, E., De Deyn, P., Del Zompo, M., Mateo, I., Boada, M., Antunez, C., Lopez-Arrieta, J., Epelbaum, J., Schjeide, B., Frank-Garcia, A., Giedraitis, V., Helisalmi, S., Porcellini, E., Pilotto, A., Forti, P., Ferri, R., Delepine, M., Zelenika, D., Lathrop, M., Scarpini, E., Siciliano, G., Solfrizzi, V., Sorbi, S., Spalletta, G., Ravaglia, G., Valdivieso, F., Vepsalainen, S., Alvarez, V., Bosco, P., Mancuso, M., Panza, F., Nacmias, B., Bossu, P., Hanon, O., Piccardi, P., Annoni, G., Mann, D., Marambaud, P., Seripa, D., Galimberti, D., Tanzi, R., Bertram, L., Lendon, C., Lannfelt, L., Licastro, F., Campion, D., Pericak-Vance, M., Soininen, H., Van Broeckhoven, C., Alperovitch, A., Ruiz, A., Kamboh, M., and Amouyel, P.

Subjects
lipids (amino acids, peptides, and proteins)
Abstract

The only established genetic determinant of non-Mendelian forms of Alzheimer's disease (AD) is the epsilon4 allele of the apolipoprotein E gene (APOE). Recently, it has been reported that the P86L polymorphism of the calcium homeostasis modulator 1 gene (CALHM1) is associated with the risk of developing AD. In order to independently assess this association, we performed a meta-analysis of 7,873 AD cases and 13,274 controls of Caucasian origin (from a total of 24 centers in Belgium, Finland, France, Italy, Spain, Sweden, the UK, and the USA). Our results indicate that the CALHM1 P86L polymorphism is likely not a genetic determinant of AD but may modulate age of onset by interacting with the effect of the epsilon4 allele of the APOE gene.

Published
2010

29. Genome-wide association study identifies variants at CLU and CR1 associated with Alzheimer's disease

Author

Lambert, Jc, Heath, S, Even, G, Campion, D, Sleegers, K, Hiltunen, M, Combarros, O, Zelenika, D, Bullido, Mj, Tavernier, B, Letenneur, L, Bettens, K, Berr, C, Pasquier, F, Fiévet, N, BARBERGER GATEAU, P, Engelborghs, S, DE DEYN, P, Mateo, I, Franck, A, Helisalmi, S, Porcellini, E, Hanon, O, Siciliano, Gabriele, DE PANCORBO MM, Lendon, C, Dufouil, C, Jaillard, C, Leveillard, T, Alvarez, V, Bosco, P, Mancuso, Michelangelo, Panza, F, Nacmias, B, Bossù, P, Piccardi, P, Annoni, G, Seripa, D, Galimberti, D, Hannequin, D, Licastro, F, Soininen, H, Ritchie, K, Blanché, H, Dartigues, Jf, Tzourio, C, Gut, I, VAN BROECKHOVEN, C, Alpérovitch, A, Lathrop, M, and Amouyel, P.

Published
2009

32. Proapoptotic activated T-cells in the blood of children with Down's syndrome: relationship with dietary antigens and intestinal alterations

Author

Corsi, M. M., Ponti, W., Venditti, A., Ferrara, F., Chiara Baldo, Chiappelli, M., and Licastro, F.

Subjects
Male, Adolescent, CD3 Complex, Interleukin-6, Incidence, T-Lymphocytes, Apoptosis, HLA-DR Antigens, Lymphocyte Activation, Gliadin, Immunoglobulin A, Celiac Disease, Intestinal Diseases, Immunoglobulin G, CD4 Antigens, Humans, Female, Settore VET/05 - Malattie Infettive degli Animali Domestici, fas Receptor, Annexin A5, Antigens, Down Syndrome, Coloring Agents, Cells, Cultured, Propidium
Abstract

Immune defects, thyroid abnormalities, infections and coeliac disease are often associated with Down's syndrome (DS). However, the basis of the immune defects is still unclear in DS. In the present study, we show that peripheral CD4 T-cells were decreased in children with DS, while mean values of cytotoxic CD8 T-cells were comparable with those from healthy children. Circulating activated (CD3/HLA-DR positive) T-cells were increased and a large proportion of purified T-cells from DS were also positive for APO-I/FAS (CD95) antigen. To further explore the functional status of circulating activated T-cells, enriched CD3 lymphocytes were cultured for 3 h and were tested for positivity to annexin-V (ANX-V) and propidium iodide. T-cells with the early apoptotic phenotype were increased in cell cultures from DS children. Plasma levels of inteleukin-6 (IL-6) were higher in DS children than in healthy children. The incidence of coeliac disease was also increased in this group of children. Most DS children showed increased levels of circulating IgG or IgA specific for gliadin, and their plasma IL-6 levels correlated with those of antigliadin IgG. The number of CD4 circulating cells was very low in DS children with coeliac disease, was low in those with serum antigliadin antibodies and was normal in DS without antigliadin antibodies. An overload of dietary antigens and impaired nutrient absorption secondary to altered functioning of the gastrointestinal mucosa might interfere with normal immune responses by inducing programmed cell death in CD4 T-cells.

Published
2004

35. Evidence of the association of BIN1 and PICALM with the AD risk in contrasting European populations

Author

Lambert, J, Zelenika, D, Hiltunen, M, Chouraki, V, Combarros, O, Bullido, M, Tognoni, G, Fiévet, N, Boland, A, Arosio, B, Coto, E, Zompo, M, Mateo, I, Frank Garcia, A, Helisalmi, S, Porcellini, E, Pilotto, A, Forti, P, Ferri, R, Delepine, M, Scarpini, E, Siciliano, G, Solfrizzi, V, Sorbi, S, Spalletta, G, Ravaglia, G, Valdivieso, F, Alvarez, V, Bosco, P, Mancuso, M, Panza, F, Nacmias, B, Bossù, P, Piccardi, P, Annoni, G, Seripa, D, Galimberti, D, Licastro, F, Lathrop, M, Soininen, H, Amouyel, P, Bullido, MJ, Zompo, MD, ANNONI, GIORGIO, Amouyel, P., Lambert, J, Zelenika, D, Hiltunen, M, Chouraki, V, Combarros, O, Bullido, M, Tognoni, G, Fiévet, N, Boland, A, Arosio, B, Coto, E, Zompo, M, Mateo, I, Frank Garcia, A, Helisalmi, S, Porcellini, E, Pilotto, A, Forti, P, Ferri, R, Delepine, M, Scarpini, E, Siciliano, G, Solfrizzi, V, Sorbi, S, Spalletta, G, Ravaglia, G, Valdivieso, F, Alvarez, V, Bosco, P, Mancuso, M, Panza, F, Nacmias, B, Bossù, P, Piccardi, P, Annoni, G, Seripa, D, Galimberti, D, Licastro, F, Lathrop, M, Soininen, H, Amouyel, P, Bullido, MJ, Zompo, MD, ANNONI, GIORGIO, and Amouyel, P.

Abstract

Recent genome-wide association studies have identified 5 loci (BIN1, CLU, CR1, EXOC3L2, and PICALM) as genetic determinants of Alzheimer's disease (AD). We attempted to confirm the association between these genes and the AD risk in 3 contrasting European populations (from Finland, Italy, and Spain). Because CLU and CR1 had already been analyzed in these populations, we restricted our investigation to BIN1, EXO2CL3, and PICALM. In a total of 2816 AD cases and 2706 controls, we unambiguously replicated the association of rs744373 (for BIN1) and rs541458 (for PICALM) polymorphisms with the AD risk (odds ratio [OR] = 1.26, 95% confidence interval [CI] [1.15-1.38], p = 2.9 × 10-7, and OR = 0.80, 95% CI [0.74-0.88], p = 4.6 × 10-7, respectively). In a meta-analysis, rs597668 (EXOC3L2) was also associated with the AD risk, albeit to a lesser extent (OR = 1.19, 95% CI [1.06-1.32], p = 2.0 × 10-3). However, this signal did not appear to be independent of APOE. In conclusion, we confirmed that BIN1 and PICALM are genetic determinants of AD, whereas the potential involvement of EXOC3L2 requires further investigation. © 2011 Elsevier Inc.

Published
2011

36. Common variants at ABCA7, MS4A6A/MS4A4E, EPHA1, CD33 and CD2AP are associated with Alzheimer's disease

Author

Hollingworth, P, Harold, D, Sims, R, Gerrish, A, Lambert, J, Carrasquillo, M, Abraham, R, Hamshere, M, Pahwa, J, Moskvina, V, Dowzell, K, Jones, N, Stretton, A, Thomas, C, Richards, A, Ivanov, D, Widdowson, C, Chapman, J, Lovestone, S, Powell, J, Proitsi, P, Lupton, M, Brayne, C, Rubinsztein, D, Gill, M, Lawlor, B, Lynch, A, Brown, K, Passmore, P, Craig, D, Mcguinness, B, Todd, S, Holmes, C, Mann, D, Smith, A, Beaumont, H, Warden, D, Wilcock, G, Love, S, Kehoe, P, Hooper, N, Vardy, E, Hardy, J, Mead, S, Fox, N, Rossor, M, Collinge, J, Maier, W, Jessen, F, Rüther, E, Schürmann, B, Heun, R, Kölsch, H, van den Bussche, H, Heuser, I, Kornhuber, J, Wiltfang, J, Dichgans, M, Frölich, L, Hampel, H, Gallacher, J, Hüll, M, Rujescu, D, Giegling, I, Goate, A, Kauwe, J, Cruchaga, C, Nowotny, P, Morris, J, Mayo, K, Sleegers, K, Bettens, K, Engelborghs, S, De Deyn, P, Van Broeckhoven, C, Livingston, G, Bass, N, Gurling, H, Mcquillin, A, Gwilliam, R, Deloukas, P, Al Chalabi, A, Shaw, C, Tsolaki, M, Singleton, A, Guerreiro, R, Mühleisen, T, Nöthen, M, Moebus, S, Jöckel, K, Klopp, N, Wichmann, H, Pankratz, V, Sando, S, Aasly, J, Barcikowska, M, Wszolek, Z, Dickson, D, Graff Radford, N, Petersen, R, van Duijn, C, Breteler, M, Ikram, M, Destefano, A, Fitzpatrick, A, Lopez, O, Launer, L, Seshadri, S, Berr, C, Campion, D, Epelbaum, J, Dartigues, J, Tzourio, C, Alpérovitch, A, Lathrop, M, Feulner, T, Friedrich, P, Riehle, C, Krawczak, M, Schreiber, S, Mayhaus, M, Nicolhaus, S, Wagenpfeil, S, Steinberg, S, Stefansson, H, Stefansson, K, Snædal, J, Björnsson, S, Jonsson, P, Chouraki, V, Genier Boley, B, Hiltunen, M, Soininen, H, Combarros, O, Zelenika, D, Delepine, M, Bullido, M, Pasquier, F, Mateo, I, Frank Garcia, A, Porcellini, E, Hanon, O, Coto, E, Alvarez, V, Bosco, P, Siciliano, G, Mancuso, M, Panza, F, Solfrizzi, V, Nacmias, B, Sorbi, S, Bossù, P, Piccardi, P, Arosio, B, Annoni, G, Seripa, D, Pilotto, A, Scarpini, E, Galimberti, D, Brice, A, Hannequin, D, Licastro, F, Jones, L, Holmans, P, Jonsson, T, Riemenschneider, M, Morgan, K, Younkin, S, Owen, M, O'Donovan, M, Amouyel, P, Williams, J, Carrasquillo, MM, Hamshere, ML, Pahwa, JS, Lupton, MK, Rubinsztein, DC, Brown, KS, Passmore, PA, McGuinness, B, Smith, AD, Kehoe, PG, Hooper, NM, Vardy, ERLC, Fox, NC, Goate, AM, Kauwe, JSK, Morris, JC, De Deyn, PP, Bass, NJ, McQuillin, A, Shaw, CE, Singleton, AB, Mühleisen, TW, Nöthen, MM, Pankratz, VS, Sando, SB, Aasly, JO, Wszolek, ZK, Dickson, DW, Graff Radford, NR, Petersen, RC, van Duijn, CM, Breteler, MMB, Ikram, MA, DeStefano, AL, Fitzpatrick, AL, Launer, LJ, Feulner, TM, Jonsson, PV, Bullido, MJ, ANNONI, GIORGIO, Holmans, PA, Younkin, SG, Owen, MJ, Williams, J., Hollingworth, P, Harold, D, Sims, R, Gerrish, A, Lambert, J, Carrasquillo, M, Abraham, R, Hamshere, M, Pahwa, J, Moskvina, V, Dowzell, K, Jones, N, Stretton, A, Thomas, C, Richards, A, Ivanov, D, Widdowson, C, Chapman, J, Lovestone, S, Powell, J, Proitsi, P, Lupton, M, Brayne, C, Rubinsztein, D, Gill, M, Lawlor, B, Lynch, A, Brown, K, Passmore, P, Craig, D, Mcguinness, B, Todd, S, Holmes, C, Mann, D, Smith, A, Beaumont, H, Warden, D, Wilcock, G, Love, S, Kehoe, P, Hooper, N, Vardy, E, Hardy, J, Mead, S, Fox, N, Rossor, M, Collinge, J, Maier, W, Jessen, F, Rüther, E, Schürmann, B, Heun, R, Kölsch, H, van den Bussche, H, Heuser, I, Kornhuber, J, Wiltfang, J, Dichgans, M, Frölich, L, Hampel, H, Gallacher, J, Hüll, M, Rujescu, D, Giegling, I, Goate, A, Kauwe, J, Cruchaga, C, Nowotny, P, Morris, J, Mayo, K, Sleegers, K, Bettens, K, Engelborghs, S, De Deyn, P, Van Broeckhoven, C, Livingston, G, Bass, N, Gurling, H, Mcquillin, A, Gwilliam, R, Deloukas, P, Al Chalabi, A, Shaw, C, Tsolaki, M, Singleton, A, Guerreiro, R, Mühleisen, T, Nöthen, M, Moebus, S, Jöckel, K, Klopp, N, Wichmann, H, Pankratz, V, Sando, S, Aasly, J, Barcikowska, M, Wszolek, Z, Dickson, D, Graff Radford, N, Petersen, R, van Duijn, C, Breteler, M, Ikram, M, Destefano, A, Fitzpatrick, A, Lopez, O, Launer, L, Seshadri, S, Berr, C, Campion, D, Epelbaum, J, Dartigues, J, Tzourio, C, Alpérovitch, A, Lathrop, M, Feulner, T, Friedrich, P, Riehle, C, Krawczak, M, Schreiber, S, Mayhaus, M, Nicolhaus, S, Wagenpfeil, S, Steinberg, S, Stefansson, H, Stefansson, K, Snædal, J, Björnsson, S, Jonsson, P, Chouraki, V, Genier Boley, B, Hiltunen, M, Soininen, H, Combarros, O, Zelenika, D, Delepine, M, Bullido, M, Pasquier, F, Mateo, I, Frank Garcia, A, Porcellini, E, Hanon, O, Coto, E, Alvarez, V, Bosco, P, Siciliano, G, Mancuso, M, Panza, F, Solfrizzi, V, Nacmias, B, Sorbi, S, Bossù, P, Piccardi, P, Arosio, B, Annoni, G, Seripa, D, Pilotto, A, Scarpini, E, Galimberti, D, Brice, A, Hannequin, D, Licastro, F, Jones, L, Holmans, P, Jonsson, T, Riemenschneider, M, Morgan, K, Younkin, S, Owen, M, O'Donovan, M, Amouyel, P, Williams, J, Carrasquillo, MM, Hamshere, ML, Pahwa, JS, Lupton, MK, Rubinsztein, DC, Brown, KS, Passmore, PA, McGuinness, B, Smith, AD, Kehoe, PG, Hooper, NM, Vardy, ERLC, Fox, NC, Goate, AM, Kauwe, JSK, Morris, JC, De Deyn, PP, Bass, NJ, McQuillin, A, Shaw, CE, Singleton, AB, Mühleisen, TW, Nöthen, MM, Pankratz, VS, Sando, SB, Aasly, JO, Wszolek, ZK, Dickson, DW, Graff Radford, NR, Petersen, RC, van Duijn, CM, Breteler, MMB, Ikram, MA, DeStefano, AL, Fitzpatrick, AL, Launer, LJ, Feulner, TM, Jonsson, PV, Bullido, MJ, ANNONI, GIORGIO, Holmans, PA, Younkin, SG, Owen, MJ, and Williams, J.

Abstract

We sought to identify new susceptibility loci for Alzheimer's disease through a staged association study (GERAD+) and by testing suggestive loci reported by the Alzheimer's Disease Genetic Consortium (ADGC) in a companion paper. We undertook a combined analysis of four genome-wide association datasets (stage 1) and identified ten newly associated variants with P ĝ‰Currency sign 1 × 10 -5. We tested these variants for association in an independent sample (stage 2). Three SNPs at two loci replicated and showed evidence for association in a further sample (stage 3). Meta-analyses of all data provided compelling evidence that ABCA7 (rs3764650, meta P = 4.5 × 10 -17; including ADGC data, meta P = 5.0 × 10 -21) and the MS4A gene cluster (rs610932, meta P = 1.8 × 10 -14; including ADGC data, meta P = 1.2 × 10 -16) are new Alzheimer's disease susceptibility loci. We also found independent evidence for association for three loci reported by the ADGC, which, when combined, showed genome-wide significance: CD2AP (GERAD+, P = 8.0 × 10 -4; including ADGC data, meta P = 8.6 × 10 -9), CD33 (GERAD+, P = 2.2 × 10 -4; including ADGC data, meta P = 1.6 × 10 -9) and EPHA1 (GERAD+, P = 3.4 × 10 -4; including ADGC data, meta P = 6.0 × 10 -10). © 2011 Nature America, Inc. All rights reserved.

Published
2011

38. Is immunotherapy an effective treatment for Alzheimer's disease?

Author

LICASTRO F, CARUSO, Calogero, LICASTRO F, and CARUSO C

Subjects
lcsh:Immunologic diseases. Allergy, lcsh:RC952-954.6, Commentary, lcsh:Geriatrics, lcsh:RC581-607
Abstract

Immunotherapy in patients with Alzheimer's disease (AD) is rapidly becoming a hot topic of modern geriatric and clinical gerontology. Current views see immunization with Aβ peptide, the amyloidogenic protein found in senile plaque of AD patient's brains, or the infusion of preformed antibody specific for human Aβ, as possible therapeutic approaches to improve the cognitive status in the disease. Animal models of the disease have provided positive results from both approaches. Thus, an initial clinical trial using immunization with human Aβ in AD patients was started, but then shortly halted because of an unusually high incidence (6%) of meningoencephalitis. A long and currently ongoing debate in the scientific community about the pro or contra of vaccination or passive immunization with Aβ in AD is thereafter started. Here, the authors would like to stress few points of concern regarding these approaches in clinical practice.

Published
2004

39. Tumor Necrosis Factor-alpha-308a/G Polymorphism is Associated with Age at Onset of Alzheimer Disease

Author

Lio, D, Annoni, G, Licastro, F, Crivello, A, Forte, G, Scola, L, Colonna Romano, G, Candore, G, Arosio, B, Galimberti, L, Vergani, C, Caruso, C, Forte, GI, Caruso, C., ANNONI, GIORGIO, Lio, D, Annoni, G, Licastro, F, Crivello, A, Forte, G, Scola, L, Colonna Romano, G, Candore, G, Arosio, B, Galimberti, L, Vergani, C, Caruso, C, Forte, GI, Caruso, C., and ANNONI, GIORGIO

Abstract

Pro-inflammatory cytokines and acute-phase proteins play an important role in Alzheimer's disease (AD) neurodegeneration, and common polymorphisms of genes controlling their production have been shown to be associated with AD. Tumor necrosis factor (TNF)-alpha is an inflammatory cytokine involved in the local immune response occurring in the central nervous system of AD patients. Genetic variation could contribute to the risk of developing AD or influence the age at the onset of the disease. We genotyped 222 patients (152 women, 70 men; age range 60-87) and 240 non-demented age-matched healthy controls for TNF-alpha -308G/A single nucleotide polymorphism (SNP). No significant differences were observed in genotyped frequencies between patients and controls, whereas carriers of -308A showed a significantly lower mean age at onset than non-carriers of this allele. This difference was more evident taking into account ApolipoproteinE (ApoE) status since the lowest age at onset was observed in patients carrying the -308ATNF+/APOE4+ genotypes. In conclusion, our data support previous suggestions that, at least in Caucasians, the TNF gene is a disease modifier gene in patients in which AD is rising, bringing to light the importance of genetic variation at the pro-inflammatory components in the progression of AD

Published
2006

45. alpha-1-Antichymotrypsin and Oxidative Stress in the Peripheral Blood From Patients With Probable Alzheimer Disease: A Short-Term Longitudinal Study

Author

Licastro, F, Pedrini, S, Davis, L, Caputo, L, Tagliabue, J, Savorani, G, Cucinotta, D, Annoni, G, Davis, LJ, ANNONI, GIORGIO, Licastro, F, Pedrini, S, Davis, L, Caputo, L, Tagliabue, J, Savorani, G, Cucinotta, D, Annoni, G, Davis, LJ, and ANNONI, GIORGIO

Abstract

To evaluate the stability and reproducibility of selected peripheral oxidative stress markers and their possible relation to cognitive performance, three different blood samples were taken at 7- to 10-day intervals from 11 patients with probable Alzheimer disease (AD) and 11 nondemented controls. Blood samples were also collected once from 6 patients with vascular dementia (VT). alpha -1-Antichymotrypsin (ACT), C-reactive protein (CRP), glutathione peroxidase (GSH-Px), superoxide dismutase (SOD), lactoferrin (LTF), and total lipid peroxidation (LPO) were then measured. Blood levels of ACT and GSH-Px were increased in AD patients but not in patients with VD. Levels of LTF, CRP, and LPO were comparable between AD patients and controls. Erythrocyte SOD activity was increased in AD patients. Blood levels of ACT negatively correlated with LPO levels and positively correlated with scores of the Global Deterioration Scale of AD patients. ACT might be implicated in controlling oxidative damage of blood lipids and their turnover during the progression of AD.

Published
2001

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