EPIDEMIOLOGY OF DEMENTIA IN OLDER JAPANESE AMERICANS

现有的研究表明，虽然总的患病率 痴呆症在日本和美国相似，相对患病率 阿尔茨海默病(AD)到血管性痴呆(VAD)在 目前尚不清楚这些差异是否源于不同的 研究方法或它们是否反映了 两国痴呆症亚型的发病率及其伴随关系 遗传易感性和/或暴露在环境中的差异 风险因素。对总人口的流行率调查的结果 居住在华盛顿州金县的65岁及以上的日裔美国人表明 患病率更接近于高加索人群 而不是日语母语。我们建议(1)在下一年遵循这一队列 五年(2)确定特定年龄和性别的发病率 痴呆及其亚型；(3)遵循现有流行和发展趋势 监测临床和神经心理进展的事件病例 并描述AD和VAD病例的生存情况，(4)进行前瞻性风险 遗传(载脂蛋白)的因素分析，包括生存分析 E和家族史)和环境因素对AD和VAD的影响， 尤其是那些受生活方式和饮食影响的人，并检查潜力 基因和环境之间的相互作用对痴呆风险的影响 其亚型；(5)比较患病率、发病率以及相对和 年方法学标准化研究的归因风险 檀香山、广岛和真田市。基线检查(1992- 1994年)包含近2,000个个体；认知完好无损的队列 人员总数约为1,650人。认知完好的队列将 每两年进行一次筛查，有认知障碍的人 每年跟进一次。等待我们筛查的分析结果 策略在目前获拨款的资助期内，我们计划 认知完好的队列每两年使用81/100的截止值 关于认知能力筛查量表(CASI)和/或衰退 在任何CASI水平上的7个点，以估计年龄和性别特定的发病率 费率。得分低于分数线的患者将会有常规， 标准化的神经学和神经心理学评估。后续行动 到2001年将产生大约127例新病例 痴呆症。痴呆症亚型的危险因素将在本课程中进行研究 组，包括可能的保护因素，初步显示 与认知障碍和流行疾病的关系，如 雌激素替代疗法、头围与载脂蛋白 E-e2(ApoE)等位基因。认知能力的CASI得分随时间的变化 完整的队列还将分析载脂蛋白E基因和 其他寄主因素。最后，标准化研究之间的努力 现场将重点加强诊断的一致性 方法和跨点资料分析，比较患病率和危险因素。

Existing studies suggest that, while the overall prevalence rates of dementia in Japan and the U.S. are similar, the relative prevalence of Alzheimer's disease (AD) to vascular dementia (VaD) is much greater in the U.S. It is not known whether these differences result from differing study methods or whether they reflect underlying differences in the incidence of dementia subtypes in the two countries with concomitant differences in genetic susceptibility and/or exposure to environmental risk factors. Results from a prevalence survey of a total population of Japanese-Americans aged 65 and over living in King County, WA show that prevalence rates more closely resemble those of Caucasian populations than native Japanese. We propose to (1) follow this cohort over the next five years to (2) determine age- and sex-specific incidence rates of dementia and its subtypes; (3) follow existing prevalent and developing incident cases to monitor the clinical and neuropsychological progression and describe survival in AD and VaD cases, (4) conduct prospective risk factor analyses, including survival analyses, of genetic (apolipoprotein E and family history) and environmental factors for AD and VaD, particularly those affected by lifestyle and diet, and examine potential interactions between genes and environment on the risk of dementia and its subtypes; (5) compare prevalence, incidence as well as relative and attributable risks with methodologically standardized studies in Honolulu, Hiroshima and Machida City. The baseline examination (1992- 1994) contained nearly 2,000 individuals; to cohort of cognitively intact persons contains approximately 1,650. The cognitively intact cohort will be screened every two years, the persons with cognitive impairment are followed annually. Pending the results of an analysis of our screening strategy during the currently funded grant period, we plan to screen the cognitively intact cohort every two years using a cutoff score of 81/100 on the Cognitive Abilities Screening Instrument (CASI) and/or a decline of 7 points at any CASI level, to estimate age and sex-specific incidence rates. Patients scoring below the cut scores will have routine, standardized neurologic and neuropsychological evaluations. The followup of the cohort to the year 2001 will yield approximately 127 new cases of dementia. Risk factors for dementia subtypes will be examined in this group, including possible protective factors which show preliminary associations with cognitive impairment and prevalent disease, such as estrogen therapy replacement, head circumference and the apolipoprotein E-e2 (apoE) allele. Changes over time in CASI scores in the cognitively intact cohort also will be analyzed with regard to apoE genotype and other host factors. Finally, standardization efforts between the study sites will focus on the enhancement of the uniformity of diagnostic methods, and cross-site data analysis to compare rates and risk factors.