Affiliations: Department of Experimental Pathology, School of Medicine, University of Bologna, Bologna, Italy
Correspondence:
[*]
Correspondence to: Prof. Federico Licastro, MD, Department of Experimental Pathology, School of Medicine, University of Bologna, Via S. Giacomo 14, 40126 Bologna, Italy. Tel.: +39 051 2094730; Fax: +39 051 2094746; E-mail: [email protected].
Abstract: Genome wide association investigations from large cohorts of patients with Alzheimer's disease (AD) and non demented controls (CTR) showed that a limited set of genes were associated (p > 10−5) with the disease. A very recent study from our group showed that an additional limited group of SNP in selected genes were associated with AD. In this report we argue that the association of these genes with AD is suggestive of a pivotal role of environmental factors in the pathogenesis of the disease and one of these factors is virus infection. In other words, the genetic signature revealed by genome wide association (GWA) studies discloses a network of genes that might influence the ability of the central nervous system to cope with and fight against the invasion by virus of the herpes family. In fact, 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); Phosphatidyl inositol- binding clathrin assembly protein gene (PICALM); ATP-bonding cassette, sub family A, member 7 (ABCA7); membrane spanning A4 (MSA4); CD2 associated protein (CD2AP); cluster of differentiation 33 (CD33); and ephrin receptor A1 (EPHA1) result in a genetic signature that might affect individual brain susceptibility to infection by the herpes virus family during aging, leading to neuronal loss, inflammation, and amyloid deposition.
