Recent work has shown that patients with Alzheimer's disease (AD) have a normal visual working memory (VWM) capacity for simple visual features when compared to healthy older adults. In contrast, AD patients have reduced VWM capacity for complex objects, resulting from an impaired ability to bind the visual features of complex objects together. Understanding the cognitive and neural basis underlying this binding impairment is critical because VWM is vitally important for basic visual tasks, such as navigating new environments, noting changes in the landscape, finding objects in a cluttered space, and driving. Decades of previous research have indicated that VWM is a complex process that can be divided into several processing stages. These include an early stage of encoding that creates a mental representation of previously viewed information and a later stage of maintenance that stores the representation without requiring external stimulation. Multiple factors mediate each of these stages, including those involving perception, attention, and memory. Importantly, a deficit of attention stands out as a candidate source of VWM binding impairments because AD patients are known to have deficits of visual attention under certain conditions, and visual attention is involved in both encoding and maintenance stages. This proposal employs behavioral and electroencephalogram (EEG) methods to determine whether changes in visual attention, rather than perception and memory, underlie AD patients' diminished ability to bind features in VWM. The specific aims target the different factors that mediate VWM stages of encoding and maintenance. Aim 1 will test the hypothesis that AD-related impairments in VWM binding result from diminished visual attention during the encoding of information into VWM. One behavioral and one event-related potential (ERP) experiment under Aim 1 will use variations of the rapid serial visual presentation (RSVP) task to determine whether AD patients' binding errors result from perceptual deficits that lead to the loss of information or attentional deficits that lead to poor binding of information. Aim 2 will test the hypothesis that AD-related impairments in VWM binding result from diminished visual attention during the maintenance of information in VWM. One ERP experiment under Aim 2 will use a change detection task to determine whether AD patients' reduced VWM capacity for complex objects results from memory decay or impaired attentional binding, while one behavioral experiment will examine whether attention-based rehearsal will reduce VWM binding errors in AD patients and result in their improved VWM capacity for complex objects. The results of this research could potentially inform behavioral applications for accommodating the living environments for AD patients according to changes in their visual cognition. The results could also provide a potential target for pharmacological management. Such applications could help to ameliorate financial burdens on the family and the healthcare system in general by prolonging independent living and improving the quality of life of patients living with AD.
NIH ExPorter
NIH ExPorter