APOLIPOPROTEIN-E ALLELE EPSILON-4, DEMENTIA, AND COGNITIVE DECLINE IN A POPULATION-SAMPLE
APOLIPOPROTEIN-E ALLELE EPSILON-4, DEMENTIA, AND COGNITIVE DECLINE IN A POPULATION-SAMPLE
复制标题
DOI：
10.1016/s0140-6736(95)92405-1
复制
发表时间：
1995-11-25
期刊：
影响因子：
168.9
通讯作者：
JACOMB, PA
中科院分区：
文献类型：
--
作者：
HENDERSON, AS;EASTEAL, S;JACOMB, PA
基于临床的系列研究表明，载脂蛋白E ε 4 （apoE ε 4）等位基因的纯合子，到80岁时阿尔茨海默病几乎是不可避免的。在1990-91年期间，对70岁及以上的人口样本进行了访谈，以确定是否存在痴呆或认知障碍。1994年再次对样本进行了访问，同时确定了载脂蛋白e基因型。完成第二次检查的638人的患病率数据显示，apoE ε 4等位基因与痴呆和认知障碍之间存在线性关联（对于杂合子，痴呆的比值比为1.89,95%置信区间为1.04-3.44；对于纯合子，比值比为3.58,95% CI为1.82-11.82；两者都经过年龄调整）。然而，即使在ε 4纯合子的受试者中，到90岁时痴呆症的估计患病率也只有50%左右。有一个或两个ε 4等位基因的人比没有等位基因的人更有可能有痴呆家族史。这项研究在人群样本中证实了epsilon 4等位基因是痴呆症的一个危险因素，但反驳了epsilon 4等位基因的纯合性足以导致阿尔茨海默病的说法：拥有一个或两个epsilon 4等位基因的人可能会在没有认知障碍的情况下进入老年。
From clinically based series it has been proposed that, in homozygotes for the apolipoprotein E epsilon 4 (apoE epsilon 4) allele, Alzheimer's disease is almost inevitable by the age of 80. A population sample of persons aged 70 years and over was interviewed in 1990-91 to ascertain the presence of dementia or cognitive impairment. The sample was re-interviewed in 1994, when the apoE genotype was also determined.Prevalence data for the 638 persons who completed the second examination revealed a linear association between having an apoE epsilon 4 allele and both dementia and cognitive impairment (for heterozygotes, odds ratio for dementia 1.89, 95% confidence interval 1.04-3.44 and for homozygotes OR 3.58, 95% CI 1.82-11.82; both adjusted for age). However, even in subjects homozygous for epsilon 4 the estimated prevalence of dementia by age 90 was only about 50%. Persons with one or two epsilon 4 alleles were more likely to have a family history of dementia than those with none.This study confirms in a population sample that the epsilon 4 allele is a risk factor for dementia, but refutes the suggestion that homozygosity for the epsilon 4 allele is sufficient for the development of Alzheimer's disease: persons with either one or two epsilon 4 alleles may reach late old age without cognitive impairment.