EPIDEMIOLOGY OF DEMENTIA IN OLDER JAPANESE AMERICANS

现有的研究表明，虽然总体患病率 痴呆症在日本和美国是相似的， 阿尔茨海默病（AD）到血管性痴呆（VaD）的发病率要高得多， 目前尚不清楚这些差异是否是由不同的 研究方法，或者它们是否反映了 两个国家痴呆亚型的发病率， 遗传易感性和/或暴露于环境中的差异 危险因素 结果来自对1999 - 2000年总人口的流行率调查， 居住在华盛顿州金县的65岁及以上的日裔美国人显示， 患病率更接近于高加索人群 比日本本土的 我们建议（1）在下一个 （2）确定特定年龄和性别的发病率， 痴呆及其亚型;（3）遵循现有的流行和发展 监测临床和神经心理学进展的事件病例 并描述AD和VaD病例的生存情况，（4）进行前瞻性风险评估 遗传因素分析，包括生存分析（载脂蛋白 E和家族史）和AD和VaD的环境因素， 特别是那些受生活方式和饮食影响的人， 基因和环境之间的相互作用对痴呆症的风险， （5）比较其患病率、发病率以及相对和 方法标准化研究的归因风险， 檀香山、广岛和町田市。 基线检查（1992- 1994年）包含近2,000人;认知完整的队列 约有1，650人。 认知完整的队列将 每两年进行一次筛查，有认知障碍的人 每年跟踪。 在我们的筛选分析结果出来之前 在目前资助的补助金期间，我们计划筛选 每两年使用81/100的临界评分进行一次认知完整队列研究 认知能力筛查工具（CASI）和/或下降 任何CASI水平的7分，以估计年龄和性别特异性发病率 rates. 评分低于临界值的患者将接受常规治疗， 标准化的神经学和神经心理学评估。 的后续行动 到2001年，将产生大约127个新病例， 痴呆 痴呆亚型的危险因素将在本研究中进行检查。 组，包括可能的保护因素，显示初步 与认知障碍和流行疾病的关系，如 雌激素替代治疗，头围与载脂蛋白 E-e2（apoE）等位基因。 认知障碍患者CASI评分随时间的变化 还将分析完整队列的apoE基因型， 其他宿主因素。 最后，标准化之间的努力研究 各研究中心将重点加强诊断的一致性， 方法和跨站点数据分析来比较比率和风险因素。

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.