Department of Experimental Pathology, School of Medicine, University of Bologna Italy.
Immun Ageing. 2010 Dec 14;7:16. doi: 10.1186/1742-4933-7-16.
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.
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 infections.
最近在一项针对大量阿尔茨海默病(AD)患者和非痴呆对照(CTR)的全基因组关联研究中发现,一组有限的基因与该疾病存在强烈关联(p > l0-5)。
在本报告中,我们提出这 8 个基因中的多态性关联与 AD 病因的一种非传统解释一致。神经细胞黏附分子 2(NC-2)、载脂蛋白 E(APOE)、糖蛋白癌胚抗原相关细胞黏附分子 16(CEACAM-16)、B 细胞淋巴瘤-3(Bcl-3)、外膜线粒体转位酶 40 同源物(T0MM-40)、补体受体 1(CR-1)、APOJ 或簇蛋白和 C 型凝集素域 A 家族 16 成员(CLEC-16A)导致遗传特征,可能会影响个体大脑在衰老过程中对疱疹病毒家族感染的易感性,导致神经元丧失、炎症和淀粉样蛋白沉积。
我们假设这种遗传特征可能通过复杂多样的机制导致 AD,每种机制都增加个体对大脑病毒感染的易感性。