PDF(Pubmed)
Abstract：
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.
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.
摘要：
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。
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。
