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.
Intereleukin-10 promoter polymorphism in mild cognitive impairment and in its clinical evolution / G. Annoni, B. Arosio, L. Mastronardi, C. Vergani. - In: INTERNATIONAL JOURNAL OF ALZHEIMER'S DISEASE. - ISSN 2090-0252. - 2010:(2010), pp. 854527.1-854527.5. [10.4061/2010/854527]
Intereleukin-10 promoter polymorphism in mild cognitive impairment and in its clinical evolution
B. ArosioSecondo
;
2010
Abstract
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.File | Dimensione | Formato | |
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