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The effect of delay on conceptual and perceptual priming in Alzheimer's disease : relationship to attention and cortical activation

Abstract

Repetition priming in which the initial presentation of a stimulus facilitates its subsequent processing through activation of its visual/auditory form (perceptual priming) is often normal in Alzheimer's disease (AD), whereas priming that depends upon activation of lexical/ semantic associations (conceptual priming) is often impaired. This pattern of implicit memory deficits could reflect differential degradation of cortically-mediated conceptual versus perceptual representations, a general deficit in attention/alerting, or cortical activation deficiencies that interact with the integrity of representations. To explore these possibilities, the present study compared the performances of 20 AD and 20 normal elderly control (EC) subjects on word-stem completion (WSC) and perceptual identification (PI) priming tasks with either no delay or a 10-minute delay between study and test phases. Explicit memory, visual attention, and phasic alerting (i.e., stimulus-driven enhancement of sensory processing that may reflect cortical activation) were also assessed. Results showed that AD patients were impaired in both delay conditions of the WSC test, but had a normal rate of decay of priming. The magnitude and rate of decay of priming in the PI task was normal in the AD patients. As expected, AD patients were impaired and exhibited abnormally rapid forgetting on explicit memory measures, but these effects did not correlate with the magnitude or rate of decay of WSC or PI priming. Alerting and orienting of attention was normal in AD patients and did not correlate with WSC or PI priming effects. WSC priming correlated with performance on a language/semantic memory test. These results confirm previously observed dissociations between impaired conceptual and preserved perceptual priming in AD and further show that priming in both tasks dissipates at a normal rate. This normal rate of decay of priming, along with normal attention and alerting effects, suggests that insufficient cortical activation does not underlie the priming deficit in AD. Rather, impaired conceptual priming may be better explained by degradation of cortically- mediated conceptual representations that must be activated in the WSC task but not in the PI task. Thus, the integrity of priming in AD may depend upon the nature of the representation rather than the fate of cortical activation.

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