MEMORY MECHANISMS IN AGING, PRECLINICAL AND EARLY DEMENTIA

因为记忆障碍往往是阿尔茨海默氏症的最早影响 阿尔茨海默病(AD)、痴呆症相关的记忆损害必须检测到 与增龄相关的记忆改变相区别。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。特定的 目的是：1)通过检测特定的AD来提高临床AD的预测性 临床前阿尔茨海默病患者的记忆损害类型(即编码特异性) 而不是次要于更基本的认知能力的下降(例如， 处理速度)；2)区分记忆和认知变化 来自记忆的健康衰老和临床前的认知障碍 AD；3)检验未被识别的临床前AD有助于 推测非痴呆患者与年龄相关的认知功能下降的估计 以及4)确定横断面年龄的介体是否 差异也在个体的纵向认知衰退中起中介作用。 我们的具体假设是：1)发现临床前阿尔茨海默病 通过检测编码特异性中的特异性记忆缺陷而得到改善； 2)临床前AD将占表观年龄的很大一部分- 认知测量的相关差异；3)在认知测量中的个体差异 处理速度和其他基本中介因素将考虑交叉 各年龄段的差异；4)年龄之间会有直接的关系 以及不受处理速度影响的编码专一性；5) 年龄相关认知差异的中介因素不会解释 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部 记忆力下降，但与年龄相关的纵向显著下降 在考虑处理过程中的状态和更改后，内存将保留 速度和其他力量中介的横截面年龄差异。 将使用回归分析和结构建模来解释记忆 老年和阿尔茨海默病患者其他认知过程损害的变化 测试记忆力、编码专一性、处理速度、言语能力、 处理能力、注意力和执行功能。结果将会是 提供检测临床前AD和预测临床所需的信息 AD，区分年龄与AD相关的认知变化，调查 认知老化而非痴呆症，提供AD的早期治疗，以及 认知、生理、生化、神经病理和 衰老和阿尔茨海默病的神经影像改变。

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.