Intereleukin-10 Promoter Polymorphism in Mild Cognitive Impairment and in Its Clinical Evolution
Author(s) -
Beatrice Arosio,
L. Mastronardi,
Carlo Vergani,
Giorgio Ani
Publication year - 2010
Publication title -
international journal of alzheimer s disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.657
H-Index - 49
eISSN - 2090-8024
pISSN - 2090-0252
DOI - 10.4061/2010/854527
Subject(s) - genotype , allele , neurodegeneration , polymorphism (computer science) , allele frequency , medicine , alzheimer's disease , disease , genetics , biology , gene
Specific proinflammatory alleles are associated with higher risk of Alzheimer disease (AD) in different onset age. The homozygosis for the A allele of -1082 polymorphism (G/A) of interleukin-10 (IL-10) promotes a higher risk of AD and reduced IL-10 generation in peripheral cells after amyloid stimulation. In this paper we analysed genotype and allele frequencies of this polymorphism in 138 subjects with mild cognitive impairment (MCI) diagnosed, respectively, as amnestic (a-MCI) and multiple impaired cognitive domains (mcd-MCI). The genotype frequencies were similar in a-MCI and AD subjects, whereas in mcd-MCI comparable to controls (AA genotype: 50% in a-MCI, 49.2% in AD, 28.7% in mcd-MCI and 31.8% in controls). Consequently, both allele and genotype distributions were significantly different between a-MCI and mcd-MCI (allele: P = .02, genotype: P < .05). These results support the theory that polymorphisms of cytokine genes can affect neurodegeneration and its clinical progression. IL-10 may partly explain the conversion of a-MCI to AD or be a genetic marker of susceptibility.
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