In the pathogenesis of Alzheimer disease (AD), it has been proposed that the anti-inflammatory interleukins such as IL-10 regulate β-amyloid-induced microglial inflammatory responses inhibiting the proinflammatory cytokine IL-6. Since the promoters of the IL-10 and IL-6 genes show single nucleotide polymorphisms (SNPs) (IL-10: -1082 G→A; IL-6: -174 G→C), we investigated these SNPs and cytokine production by peripheral blood mononuclear cells in 65 AD patients and 65 controls (HC). In AD there was a significant increase of the -1082A IL-10 allele (P=0.009) and a decrease of -1082GG genotype (P=0.019). The frequency of the GG IL-6 genotype in AD was lower and the C allele significantly higher (P<0.005). The co-occurrence of IL-10 A and IL-6 C alleles significantly raised the odds ratio (OR 11.2, confidence interval: CI 1.3-97.3; P<0.05) independently of apolipoprotein E4 (adjusted OR 10.3, CI 1-108; P<0.05). Only amyloid-stimulated IL-10 production differed between the groups (P=0.023). These results raise questions regarding the inflammatory theory in AD, pointing to a pivotal role of IL-10 and IL-6 and a selective alteration in this network.

Interleukin-10 and interleukin-6 gene polymorphisms as risk factors for Alzheimer’s disease / B. Arosio, D. Trabattoni, L. Galimberti, P. Bucciarelli, F. Fasano, C. Calabresi, C.L. Cazzullo, C. Vergani, G. Annoni, M. Clerici. - In: NEUROBIOLOGY OF AGING. - ISSN 0197-4580. - 25:8(2004), pp. 1009-1015.

Interleukin-10 and interleukin-6 gene polymorphisms as risk factors for Alzheimer’s disease

B. Arosio
Primo
;
D. Trabattoni
Secondo
;
L. Galimberti;P. Bucciarelli;F. Fasano;C. Calabresi;C. Vergani;M. Clerici
Ultimo
2004

Abstract

In the pathogenesis of Alzheimer disease (AD), it has been proposed that the anti-inflammatory interleukins such as IL-10 regulate β-amyloid-induced microglial inflammatory responses inhibiting the proinflammatory cytokine IL-6. Since the promoters of the IL-10 and IL-6 genes show single nucleotide polymorphisms (SNPs) (IL-10: -1082 G→A; IL-6: -174 G→C), we investigated these SNPs and cytokine production by peripheral blood mononuclear cells in 65 AD patients and 65 controls (HC). In AD there was a significant increase of the -1082A IL-10 allele (P=0.009) and a decrease of -1082GG genotype (P=0.019). The frequency of the GG IL-6 genotype in AD was lower and the C allele significantly higher (P<0.005). The co-occurrence of IL-10 A and IL-6 C alleles significantly raised the odds ratio (OR 11.2, confidence interval: CI 1.3-97.3; P<0.05) independently of apolipoprotein E4 (adjusted OR 10.3, CI 1-108; P<0.05). Only amyloid-stimulated IL-10 production differed between the groups (P=0.023). These results raise questions regarding the inflammatory theory in AD, pointing to a pivotal role of IL-10 and IL-6 and a selective alteration in this network.
Alzheimer's disease; Apolipoprotein E; Inflammation; Interleukin-10; Interleukin-6; Single nucleotide polymorphism; T lymphocytes
Settore MED/04 - Patologia Generale
2004
Article (author)
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/2434/10132
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