Research agenda for understanding Alzheimer disease in diverse populations: Work group on cultural diversity, Alzheimer's Association

Research agenda for understanding Alzheimer disease in diverse populations: Work group on cultural diversity, Alzheimer's Association
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DOI:
10.1097/00002093-200200002-00012
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发表时间:
2002-01-01
影响因子:
2.1
通讯作者:
Larson, EB
Larson, EB
中科院分区:
医学4区
文献类型:
--
作者:
Shadlen, MF;McCormick, WC;Larson, EB

文献摘要

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载脂蛋白多态性和阿尔茨海默病风险的种族差异的新证据表明,不能过于广泛地概括基于单一文化群体的发现(Tang et al.,2001年)。在白人和亚洲人中,一个载脂蛋白E β 4等位基因的存在是比黑人更强的阿尔茨海默病的危险因素(Farrer等人,1997年)。环境或遗传辅因子可能在不同亚群中不同地调节β-淀粉样蛋白4对β-淀粉样蛋白代谢的影响(Shadlen,1998)。认识到这一点,阿尔茨海默病协会扩大了其目标,以加强人口多样性和阿尔茨海默病异质性相互作用的科学信息基础(NIA,1998年)。这一新的重点是及时的,因为少数民族老年人是老年人口中增长最快的部分(Lilienfeld和Perl,1994年,Brookmeyer等人,1998年)。在这篇文章中,作者强调了在文化多样性人群中阿尔茨海默病研究的最新进展,特别强调了知识基础的差距。作者建议未来阿尔茨海默病研究的四个优先事项:(1)确定遗传致病因素在不同人群中是否有不同的相互作用;(2)重新检查脑缺血和梗死的性质和作用以及阿尔茨海默病症状严重程度的变化;(3)探索基因和环境影响的相互作用对阿尔茨海默病的保护作用;和(4)在阿尔茨海默病临床试验中招募和登记种族多样的受试者。
The emerging evidence of ethnic variations in apolipoprotein polymorphism and Alzheimer disease risk shows that one cannot generalize findings based on a single cultural group too broadly (Tang et al., 2001). Presence of one apolipoprotein E epsilon 4 allele is a stronger risk factor for Alzheimer disease in whites and Asians than in blacks (Farrer et al., 1997). Environmental or genetic cofactors may modulate the effects of epsilon 4 on beta-amyloid metabolism differently in different subpopulations (Shadlen, 1998). Recognizing this, the Alzheimer's Association has extended its goals to strengthen the scientific information base on the interactions of population diversity and Alzheimer disease heterogeneity (NIA, 1998). This new focus is timely since minority elderly are the most rapidly increasing segment of the elderly population (Lilienfeld and Perl, 1994, Brookmeyer et al., 1998). In this article, the authors highlight recent progress in research on Alzheimer disease among culturally diverse populations with a special emphasis on gaps in the knowledge base. The authors recommend four priorities for future Alzheimer disease research: (1) determine whether genetic causative factors interact differently in different populations; (2) reexamine the nature and role of cerebral ischemia and infarction and variations in symptom severity of Alzheimer disease; (3) explore the interaction of genes and environmental influences that are protective against Alzheimer disease; and (4) recruit and enroll ethnically diverse subjects in Alzheimer disease clinical trials.