MEMORY MECHANISMS IN AGING, PRECLINICAL AND EARLY DEMENTIA

衰老、临床前和早期痴呆的记忆机制

• 批准号: 6324493
• 负责人: HERMAN BUSCHKE
• 金额: $ 27.09万
• 依托单位: ALBERT EINSTEIN COLLEGE OF MEDICINE
• 依托单位国家: 美国
• 财政年份: 2000
• 资助国家: 美国
• 起止时间: 2000-07-01 至 2001-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6324493
• 关键词: Alzheimer's disease; age difference; aging; behavioral /social science research tag; clinical research; cognition disorders; cues; dementia; diagnosis design /evaluation; disease /disorder classification; early diagnosis; human old age (65+); human subject; interview; learning disorders; longitudinal human study; memory disorders; mental disorder diagnosis; neural information processing; neuropsychological tests; performance; questionnaires

Because memory impairment is often the earliest effect of Alzheimer's disease (AD), dementia-related memory impairment must be detected and discriminated from aged related memory change. Long-term objectives are to distinguish memory changes in aging and early AD, detect preclinical and early AD, and validate criteria for diagnosis of preclinical AD. Specific aims are to: 1) improve prediction of clinical AD by detecting specific kinds of memory impairment in preclinical AD (i.e., encoding specificity) that are not secondary to decline of more basic cognitive abilities (e.g., processing speed); 2) distinguish memory and cognitive changes due to healthy aging from the memory and cognitive impairment due to preclinical AD; 3) test the hypothesis that unrecognized preclinical AD contributes to estimates of age-related cognitive decline in presumably non-demented adults; and 4) to determine if the mediators of cross-sectional age differences also mediate longitudinal cognitive decline in individuals. Our specific hypothesis are that: 1) identification of preclinical AD can be improved by detecting specific memory deficits in encoding specificity; 2) Preclinical AD will account for a significant amount of apparent age- related variance in cognitive measures; 3) Individual differences in processing speed and other basic mediators will account for cross- sectional age differences; 4) There will be a direct relation between age and encoding specificity that is not mediated by processing speed; 5) Mediators of age-related cognitive differences will not account for the cognitive differences related to preclinical AD; 6) Intra-individual age- related decline in basic cognitive abilities will predict intra-individual decline in memory, but 7) Significant longitudinal age-related decline in memory will remain after accounting for status and change in processing speed and other power mediators of cross-sectional age differences. Regression analysis and structural modeling will be used to explain memory changes in aging and AD by impairment of other cognitive processes in tests of memory, encoding specificity, processing speed, verbal ability, processing capacity, attention, and executive function. The results will provide information needed to detect preclinical AD and predict clinical AD, discriminate age-from AD-related cognitive changes, investigate cognitive aging without dementia, provide early treatment of AD, and correlate cognitive, physiologic, biochemical, neuropathologic, and neuroimaging changes in aging and AD.

因为记忆障碍通常是老年痴呆症的最早影响 疾病（AD），必须检测痴呆相关的记忆障碍， 与年龄相关的记忆变化。长期目标是 区分衰老和早期AD的记忆变化，检测临床前和 早期AD，并验证临床前AD的诊断标准。具体 目的是：1）通过检测特异性抗体， 临床前AD中的各种记忆损伤（即，编码特异性） 不继发于更基本的认知能力下降（例如， 处理速度）; 2）区分记忆和认知变化， 健康老龄化从记忆和认知障碍由于临床前 AD; 3）检验未被识别的临床前AD有助于 估计与年龄相关的认知能力下降， 成年人;和4）以确定是否调解人的横截面年龄 差异还介导个体的纵向认知下降。 我们的具体假设是：1）临床前AD的鉴定可以 通过检测编码特异性的特定记忆缺陷来改善; 2)临床前AD将占表观年龄的显著量- 认知测量的相关方差; 3） 处理速度和其他基本介质将占交叉- 年龄段差异; 4）年龄与年龄之间存在直接关系 和不受加工速度介导的编码特异性; 5） 年龄相关认知差异的中介者不会解释 与临床前AD相关的认知差异; 6）个体内年龄- 基本认知能力的相关下降将预测个体内 记忆力下降，但7）显著的纵向年龄相关性下降， 在处理中考虑状态和变化后，内存将保留 速度和其他权力的调解人的横截面年龄差异。 回归分析和结构建模将被用来解释记忆 通过损害其他认知过程的衰老和AD变化， 记忆力、编码特异性、处理速度、语言能力、 处理能力、注意力和执行功能。结果将 提供检测临床前AD和预测临床 AD，区分年龄与AD相关的认知变化，调查 无痴呆症的认知衰老，提供AD的早期治疗，并且 将认知、生理、生化、神经病理和 神经影像学变化的老化和AD。