Abstract
Background: Recent findings from a genome wide association investigation in a large cohort of patients with Alzheimer's disease (AD) and non demented controls (CTR) showed that a limited set of genes was in a strong association (p > l0-5) with the disease.Presentation of the hypothesis: In this report we suggest that the polymorphism association in 8 of these genes is consistent with a non conventional interpretation of AD etiology.Nectin-2 (NC-2), apolipoprotein E (APOE), glycoprotein carcinoembryonic antigen related cell adhesion molecule- 16 (CEACAM-16), B-cell lymphoma-3 (Bcl-3), translocase of outer mitochondrial membrane 40 homolog (T0MM-40), complement receptor-1 (CR-l), APOJ or clusterin and C-type lectin domain A family-16 member (CLEC-16A) result in a genetic signature that might affect individual brain susceptibility to infection by herpes virus family during aging, leading to neuronal loss, inflammation and amyloid deposition.Implications of the hypothesis: We hypothesized that such genetic trait may predispose to AD via complex and diverse mechanisms each contributing to an increase of individual susceptibility to brain viral infections. © 2010 Porcellini et al; licensee BioMed Central Ltd.
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Porcellini, E., Carbone, I., Ianni, M., & Licastro, F. (2010). Alzheimer’s disease gene signature says: Beware of brain viral infections. Immunity and Ageing, 7. https://doi.org/10.1186/1742-4933-7-16
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