FRONTAL CONTROL /MEMORY IN AGING & SENILE DEMENTIA OF THE ALZHEIMER'S TYPE

阿尔茨海默型老年痴呆症(SDAT)正在成为 破坏社会面临的健康问题。在项目的最初阶段， 疾病，个人会经历一些记忆障碍，随后 大多数认知功能普遍崩溃。此外，虽然 赤字没有那么严重和渐进，也有证据表明 对健康的老年人认知障碍的影响。的目标是 目前的建议是研究一种认知机制，它可能是 在健康老年人和SDAT个人中都表现出缺陷，以及 着手开发一个能够解释这些赤字的正式模型。 本提案中涉及的具体目标机制是 以抑制部分激活和竞争信息。近期工作 来自我们实验室(P01AG03991，项目3)的研究表明，健康的老年人 个人和SDAT个人在更大程度上表现出崩溃 在抑制性老年个体和更大程度上SDAT个体中 在一系列实验中显示出抑制控制的崩溃 范例。在第一系列提议的实验中(实验1-7， 系列I)，抑制过程在健康衰老和 SDAT将在多个不同的级别上进行审查 信息处理系统：知觉、记忆提取、词汇 消解歧义和句子理解。此外，这些 实验将涉及到允许人们追踪 受试者抑制过程的时间进程的变化 组。第二系列实验(实验1-4，系列II) 将向健康的老年人和SDAT个人推广一套正式的 由Cohen和Servan-Schreiber发展的连接主义模型 (1992)解释了抑制效率的细分 精神分裂症个体的过程以及模拟多巴胺能 前额叶皮质出现故障。拟议中的实验将 为正式建模认知变化提供经验基础 发生在健康的老年人和SDAT个体中，也提供了独特的 有机会比较以下特定模型参数的变化 有必要解释以下三种情况下认知表现的变化 不同的人群(精神分裂症患者、健康老年人和SDAT个人)。 因此，在与J.Cohen和D.Servan-Schreiber的合作中，我们打算 利用基本认知理论进行三管齐下的攻击，正式 连接主义建模和神经学证据，以更好地理解 与健康老龄化相关的认知变化 阿尔茨海默氏症。

Senile dementia of the Alzheimer type (SDAT) is becoming one of the most devasting health problems facing society. In the initial stages of the disease, individuals experience some memory impairment followed later by widespread breakdown in most cognitive functions. In addition, although the deficits are not as severe and progressive, there is also evidence of cognitive breakdowns in healthy aged individuals. The goal of the present proposal is to examine a cognitive mechanism which may underlie the deficits exhibited in both healthy aged and in SDAT individuals, and to begin to develop a formal model which can account for these deficits. The specific target mechanism addressed in this proposal is the ability to inhibit partially activated and competitive information. Recent work from our lab (P01AG03991, Project 3) indicates that healthy aged individuals and to a greater extent SDAT individuals exhibit a breakdown in inhibitory aged individuals and to a greater extent SDAT individuals exhibit a breakdown in inhibitory control across a number of experimental paradigms. In the first series of proposed experiments (Experiments 1-7, Series I), the efficiency of inhibitory processes in healthy aging and SDAT will be examined at a number of distinct levels within the information processing system: perception, memory retrieval, lexical disambiguation, and sentence comprehension. In addition, these experiments will involve manipulations that will allow one to track changes in the time course of inhibitory processes across our subjects groups. The second series of experiments (Experiments 1-4, Series II) will extend to healthy aged and SDAT individuals a set of formal connectionist models that were developed by Cohen and Servan-Schreiber (1992) to account for breakdowns in the efficiency of inhibitory processes in schizophrenic individuals and also to simulate dopaminergic breakdowns in the prefrontal cortex. The proposed experiments will provide an empirical base for formally modelling cognitive changes that occur in healthy aged and SDAT individuals, and also provide a unique opportunity to compare changes in the specific model parameters that are necessary to account for changes in cognitive performance across three distinct populations (schizophrenic, healthy aged, and SDAT individuals). Hence, in collaboration with J. Cohen and D. Servan-Schreiber we intend to use a three-pronged attack utilizing basic cognitive theory, formal connectionist modelling, and neurological evidence to better understand the cognitive changes that are associated with healthy aging and Alzheimer's Disease.