%0 Journal Article
%T Alzheimer's disease gene signature says: beware of brain viral infections
%A Elisa Porcellini
%A Ilaria Carbone
%A Manuela Ianni
%A Federico Licastro
%J Immunity & Ageing
%D 2010
%I BioMed Central
%R 10.1186/1742-4933-7-16
%X 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.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 infectionsThe incidence of Alzheimer's disease (AD) is rising sharply and a large fraction of the elderly population will ultimately be affected by the disease. Because of an urgent need for effective preventative and therapeutic measures, extensive research has focused on pathogenetic mechanisms of the disease. However, effective therapy is not already available. AD pathology is characterized by neuronal loss leading to brain atrophy and a decrement of the cerebral metabolism. Major neuropathologic lesions are: (i) synapse and neuron loss; (ii) extracellular amyloid deposits and amyloid plaques, principally composed of amyloid beta (A¦Â) peptide; (iii) intraneuronal accumulation of hyperphosphorylated Tau proteins leading to neurofibrillary degeneration; (iv) reactive astrogliosis; (v) brain inflammation. Current views of AD pathogenetic mechanisms describe amyloid deposition and neuritic plaque formation as a central mechanisms leading to neuro-degeneration, cognitive impairment and sporadic AD [1]. Therefore, therapeutic approaches have focused on reducing amyloid load and plaque deposition or clearance of brain amyloid. Other mechanisms may b
%U http://www.immunityageing.com/content/7/1/16