背景:证据表明单纯疱疹病毒(HSV)参与了阿尔茨海默病(AD)的发病机制。
目的:我们根据疱疹病毒抗体的存在,研究了AD和痴呆的风险,这些抗体与抗疱疹病毒治疗和潜在的APOE®4载体相互作用有关。
方法:这项研究是对2001-2005年生活在瑞典的1002名无痴呆症的70岁儿童进行的,他们被随访了15年。分析血清样本以检测抗HSV和抗HSV-1免疫球蛋白(Ig)G,抗巨细胞病毒(CMV)IgG,抗HSVIgM,以及抗HSV和抗CMVIgG水平。从医疗记录中收集诊断和药物处方。应用Cox比例风险回归模型。
结果:累积AD和全因痴呆发生率分别为4%和7%,分别。82%的参与者是抗HSVIgG携带者,其中6%接受了抗疱疹病毒治疗。抗HSVIgG与痴呆风险增加了一倍以上相关(完全校正风险比=2.26,p=0.031)。与AD无显著关联,但风险比与痴呆症的风险比相同。抗HSVIgM和抗CMVIgG患病率,抗疱疹病毒治疗,抗HSV和-CMVIgG水平与AD或痴呆无关,抗HSVIgG与APOEº4或抗CMVIgG之间也没有相互作用。对于HSV-1获得了类似的结果。
结论:HSV(而非CMV)感染可能是痴呆风险加倍的指标。该队列中的低AD发病率可能损害了检测与AD关联的统计能力。
UNASSIGNED: Evidence indicates that herpes simplex virus (HSV) participates in the pathogenesis of Alzheimer\'s disease (AD).
UNASSIGNED: We investigated AD and dementia risks according to the presence of herpesvirus antibodies in relation to anti-herpesvirus treatment and potential APOE ɛ4 carriership interaction.
UNASSIGNED: This study was conducted with 1002 dementia-free 70-year-olds living in Sweden in 2001-2005 who were followed for 15 years. Serum samples were analyzed to detect anti-HSV and anti-HSV-1 immunoglobulin (Ig) G, anti-cytomegalovirus (CMV) IgG, anti-HSV IgM, and anti-HSV and anti-CMV IgG levels. Diagnoses and drug prescriptions were collected from medical records. Cox proportional-hazards regression models were applied.
UNASSIGNED: Cumulative AD and all-cause dementia incidences were 4% and 7%, respectively. Eighty-two percent of participants were anti-HSV IgG carriers, of whom 6% received anti-herpesvirus treatment. Anti-HSV IgG was associated with a more than doubled dementia risk (fully adjusted hazard ratio = 2.26, p = 0.031). No significant association was found with AD, but the hazard ratio was of the same magnitude as for dementia. Anti-HSV IgM and anti-CMV IgG prevalence, anti-herpesvirus treatment, and anti-HSV and -CMV IgG levels were not associated with AD or dementia, nor were interactions between anti-HSV IgG and APOE ɛ4 or anti-CMV IgG. Similar results were obtained for HSV-1.
UNASSIGNED: HSV (but not CMV) infection may be indicative of doubled dementia risk. The low AD incidence in this cohort may have impaired the statistical power to detect associations with AD.