FEATURE INTEGRATION AND ATTENTION IN ALZHEIMER'S DISEASE

这项拟议的项目旨在系统地研究阿尔茨海默病(AD)中调节物体表征和注意之间相互作用的神经心理学过程。尽管最近的研究表明，AD患者在基于对象的注意过程中存在特定的缺陷，但在将视觉信息整合到连贯的对象表征中，高阶关联区内皮质连接的中断也可能导致前注意障碍。因此，阿尔茨海默病患者在视觉注意力测试中表现出的明显缺陷可能既与注意力本身的损害有关，也与物体表征方面的损害有关。识别AD中物体表征和注意过程的相互作用方式，不仅可以更好地了解与该疾病相关的认知缺陷，而且还可以获得有关调节正常物体表征和注意的神经心理学基础的重要信息。该提案分为两个部分。首先，将使用一系列分类和检查时间任务，其中包括几种不同类型的多维刺激，它们的特征完整性程度不同，将被用来系统地评估AD患者和正常对照组在调节物体知觉的表征上的差异。其次，这些相同的刺激将被用于一系列视觉搜索和幻觉连接任务，以便直接评估AD患者注意缺陷和代表缺陷之间的交互作用。

The proposed project is designed to systematically examine the neuropsychological processes mediating interactions between object representation and attention in Alzheimer's disease (AD). Although recent studies suggest that AD patients possess specific deficits in object-based attentional processes, it is possible that disruption of corticocortical connections within higher- order association areas may also produce pre-attentive impairment in the integration of visual information into coherent object representations. Thus, the apparent deficits exhibited by AD patients on tests of visual attention may be attributable as much to impairments in object representation as to impairments in attention per se. Identification of the ways in which object representation and attentional processes interact in AD should not only provide a better understanding of the cognitive deficits associated with this disease, but should also lead to important information about the neuropsychological substrates mediating normal object representation and attention. The proposal is divided into two sections. First, a series of classification and inspection time tasks incorporating several types of multidimensional stimuli that vary in their degree of feature integrality will be used to systematically assess differences between AD patients and normal controls in the representations mediating object perception. Second, these same stimuli will be used in a series of visual search and illusory conjunction tasks in order directly assess interactions between attentional and representional deficits in AD.