Interleukin-10 promoter polymorphism in sporadic Alzheimer's disease

Lio, Domenico; Licastro, Federico; Scola, Letizia; Chiappelli, Martina; Grimaldi, Luigi Maria Edoardo; Crivello, Antonino; Colonna‐Romano, Giuseppina; Candore, Giuseppina; Franceschi, Claudio; Caruso, Calogero

doi:10.1038/sj.gene.6363964

Cited by 119 publications

(93 citation statements)

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“…Despite there being no significant differences in genotype and allele frequencies of -1082 G/A (p = 0.61 and p = 0.33, respectively), -819 C/T and -592 C/A SNPs (p = 0.47 and p = 0.24, respectively), there is a trend toward AD patients having a higher frequency of the low/intermediate IL-10-producing genotypes (−1082 AA/GA: 77%) and lower frequency of −1082GG genotype (23%) compared to controls (65% and 35%, respectively) [19,20,23,25,26]. AD fast showed a lower frequency of high IL-10 producing genotype compared to AD slow (25.0% versus 18.2%).…”

Section: Resultsmentioning

confidence: 97%

“…Ex vivo, LPS-and A␤-induced IL-10 production by PBMCs of AD patients and age-matched controls. PBMCs (3.10 6 cells / ml) from AD patients (n = 30) and age-matched controls (n = 18) were cultured either in complete medium alone (open symbol), supplemented with 1 ng/ml of LPS (full symbol, A) during two days or supplemented with a pool of three A␤ peptides: 1 g/ml of fragment (1-16), 10 g/ml of fragment (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35), and 25 g/ml of fragment (1-40) (full symbol, B) during five days. Results have been showed as scatter plot and the median value is indicated by a black plain line.…”

Section: Resultsmentioning

confidence: 99%

“…Blood from all individuals was collected at the same time in the morning and employed for biochemical tests and PBMCs isolation. PBMCs were cultured in medium, medium+LPS (1 ng/ml), or medium+pool of three A␤ peptides: 1 g/ml of fragment (1-16), 10 g/ml of fragment (25)(26)(27)(28)(29)(30)(31)(32)(33)(34)(35), and 25 g/ml of fragment (1-40) (Innovagen, Lund, Sweden). IL-10 production was measured with ELISA (Ready-SET-Go!…”

Section: Methodsmentioning

confidence: 99%

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Interleukin-10 Production in Response to Amyloid-β Differs between Slow and Fast Decliners in Patients with Alzheimer’s Disease

Asselineau

Benlhassan²,

Arosio

et al. 2015

JAD

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Abstract. We investigated IL-10 and IL-6 production in amyloid-␤ (A␤) stimulated peripheral blood mononuclear cells (PBMCs) in twenty Alzheimer's disease (AD) patients with slow progression, eleven with fast progression, and twenty age-matched controls. Promoter polymorphisms in IL-10 (position −592, −819, −1082), IL-6 (−174), transforming growth factor-␤1 (TGF-␤1) (−10, −25), interferon-␥ (IFN-␥) (−874), and tumor necrosis factor-␣ (TNF-␣) (−308) genes were analyzed. IL-10 production after A␤ stimulation was high in PBMCs from slow decliners and almost completely abrogated in fast decliners. Association between AA IFN-␥ low-producing genotype and fast progression was demonstrated. Investigations in a larger sample will clarify these findings.

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Section: Resultsmentioning

confidence: 97%

Section: Resultsmentioning

confidence: 99%

Section: Methodsmentioning

confidence: 99%

See 1 more Smart Citation

Interleukin-10 Production in Response to Amyloid-β Differs between Slow and Fast Decliners in Patients with Alzheimer’s Disease

Asselineau

Benlhassan²,

Arosio

et al. 2015

JAD

View full text Add to dashboard Cite

show abstract

“…Intriguing clues have come from genetic mutations that cause such diseases to recur sporadically in pedigrees, even though familial cases typically comprise only a small fraction of the total (Lio et al ., 2003; Cardenas et al ., 2012; Abdel‐Salam, 2014; Barmada, 2015; Heneka et al ., 2015). Those mutations may render a single ‘seed’ protein susceptible to aggregation in whichever brain regions it is chiefly expressed.…”

Section: Introductionmentioning

confidence: 99%

Proteins that mediate protein aggregation and cytotoxicity distinguish Alzheimer's hippocampus from normal controls

et al. 2016

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SummaryNeurodegenerative diseases are distinguished by characteristic protein aggregates initiated by disease‐specific ‘seed’ proteins; however, roles of other co‐aggregated proteins remain largely unexplored. Compact hippocampal aggregates were purified from Alzheimer's and control‐subject pools using magnetic‐bead immunoaffinity pulldowns. Their components were fractionated by electrophoretic mobility and analyzed by high‐resolution proteomics. Although total detergent‐insoluble aggregates from Alzheimer's and controls had similar protein content, within the fractions isolated by tau or Aβ1–42 pulldown, the protein constituents of Alzheimer‐derived aggregates were more abundant, diverse, and post‐translationally modified than those from controls. Tau‐ and Aβ‐containing aggregates were distinguished by multiple components, and yet shared >90% of their protein constituents, implying similar accretion mechanisms. Alzheimer‐specific protein enrichment in tau‐containing aggregates was corroborated for individuals by three analyses. Five proteins inferred to co‐aggregate with tau were confirmed by precise in situ methods, including proximity ligation amplification that requires co‐localization within 40 nm. Nematode orthologs of 21 proteins, which showed Alzheimer‐specific enrichment in tau‐containing aggregates, were assessed for aggregation‐promoting roles in C. elegans by RNA‐interference ‘knockdown’. Fifteen knockdowns (71%) rescued paralysis of worms expressing muscle Aβ, and 12 (57%) rescued chemotaxis disrupted by neuronal Aβ expression. Proteins identified in compact human aggregates, bound by antibody to total tau, were thus shown to play causal roles in aggregation based on nematode models triggered by Aβ1–42. These observations imply shared mechanisms driving both types of aggregation, and/or aggregate‐mediated cross‐talk between tau and Aβ. Knowledge of protein components that promote protein accrual in diverse aggregate types implicates common mechanisms and identifies novel targets for drug intervention.

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“…Exploring the interactions between AD-related phenotypes and polymorphisms of IL-10 will help understand its roles in AD. The -1082G/A polymorphism has been extensively investigated, and the GG genotype has been suggested to decrease [86,117], increase [38], or have no influence on AD risk [118]. According to the two recent meta-analyses, IL-10 -1082G may be associated with reduced AD risk, particularly among Europeans [40,41].…”

Section: Il-10mentioning

confidence: 99%

Inflammatory Cytokines and Alzheimer’s Disease: A Review from the Perspective of Genetic Polymorphisms

2016

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Neuroinflammatory processes are a central feature of Alzheimer's disease (AD) in which microglia are over-activated, resulting in the increased production of proinflammatory cytokines. Moreover, deficiencies in the antiinflammatory system may also contribute to neuroinflammation. Recently, advanced methods for the analysis of genetic polymorphisms have further supported the relationship between neuroinflammatory factors and AD risk because a series of polymorphisms in inflammation-related genes have been shown to be associated with AD. In this review, we summarize the polymorphisms of both pro-and anti-inflammatory cytokines related to AD, primarily interleukin-1 (IL-1), IL-6, tumor necrosis factor alpha, IL-4, IL-10, and transforming growth factor beta, as well as their functional activity in AD pathology. Exploration of the relationship between inflammatory cytokine polymorphisms and AD risk may facilitate our understanding of AD pathogenesis and contribute to improved treatment strategies.

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Interleukin-10 promoter polymorphism in sporadic Alzheimer's disease

Cited by 119 publications

References 50 publications

Interleukin-10 Production in Response to Amyloid-β Differs between Slow and Fast Decliners in Patients with Alzheimer’s Disease

Interleukin-10 Production in Response to Amyloid-β Differs between Slow and Fast Decliners in Patients with Alzheimer’s Disease

Proteins that mediate protein aggregation and cytotoxicity distinguish Alzheimer's hippocampus from normal controls

Inflammatory Cytokines and Alzheimer’s Disease: A Review from the Perspective of Genetic Polymorphisms

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