Memory Deficits in Parkinson's Disease Are Associated with Impaired Attentional Filtering and Memory Consolidation Processes

The present study examined mechanisms underlying memory deficits in Parkinson's disease (PD) and their associations with brain structural metrics. Nineteen PD patients and twenty-two matched controls underwent two memory experiments. In Experiment 1 (delayed memory task), subjects were asked to remember an array of colored rectangles with varying memory set sizes (Low-Load (2 items), Low-Load (relevant 2 items) with Distractor (irrelevant 3 items), and High-Load (5 items)). After a 7 s delay period, they reported whether the orientation of any relevant figures had changed (test period). In Experiment 2 (working memory task), memory arrays were presented in varying set sizes (2 to 6 items) without distractors, followed by a 2 s delay period and a subsequent test period. Brain MRI data were acquired to assess structural differences (volumes and cortical thickness) in areas related to attention, working memory storage capacity, and episodic memory. Multivariate analyses of covariance revealed that, compared with controls, PD patients had lower memory capacity scores in all memory load conditions for Experiment 1 ( < 0.021), whereas there were no group differences in any memory load conditions for Experiment 2 ( > 0.06). In addition, PD patients had lower cortical thickness in the left superior temporal gyrus ( = 0.02), a region related to the ventral attentional system. Moreover, regression analyses revealed that lower cortical thickness values in the left superior temporal gyrus significantly predicted lower memory scores of Low-Load and Low-Load with Distractor conditions in Experiment 1 ( < 0.044) and lower scores of memory load conditions of 4 and 5 items in Experiment 2 ( < 0.012). These findings suggest that memory deficits in PD may partly be due to impaired attentional filtering and memory consolidation processes that may be related to superior temporal neurodegeneration. Future studies are warranted to confirm the current findings to guide the development of effective treatments for memory deficits in PD.