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International Journal of Alzheimer’s Disease
Volume 2010, Article ID 854527, 5 pages
Research Article

Intereleukin-10 Promoter Polymorphism in Mild Cognitive Impairment and in Its Clinical Evolution

1Department of Internal Medicine, Università degli Studi di Milano, Geriatric Unit, Fondazione IRCCS Cà Granda Ospedale Maggiore Policlinico, Via Pace 9, 20122 Milano, Italy
2Department of Internal Medicine and Prevention, Università degli Studi di Milano-Bicocca, Geriatric Clinic, San Gerardo Hospital, Via Pergolesi 33, 20052 Monza, Italy

Received 1 April 2010; Accepted 17 June 2010

Academic Editor: Diana Paleacu

Copyright © 2010 Beatrice Arosio et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


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 = . 0 2 , genotype: 𝑃 < . 0 5 ). 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.