(Department of Psychology, Uppsala University, Sweden)

In this presentation I will discuss the cognitive consequences of Alzheimers disease (AD), focusing largely on memory problems ? the cardinal symptom of the disease. Although I will spend some time in discussing how different forms of memory are affected in clinical AD, a major part of the presentation deals with the transition from normal aging to dementia, the preclinical phase of AD. In early clinical AD, there is evidence that primary memory, procedural memory, as well as various forms of priming are relatively little affected. Moderate dementia-related deficits early on in the pathogenesis are seen for tasks assessing semantic memory and working memory. However, the largest and most consistent impairment is observed in episodic memory tasks. Nevertheless, contrary to previous assertions, AD patients are able to benefit from cognitive support (e.g., a rich stimulus input, instructions, cues) to improve episodic memory, although they need more support than the healthy aged to show memory facilitation. Several recent studies demonstrate that persons who will develop AD within a few years exhibit preclinical deficits, particularly in episodic memory tasks. Interestingly, a global deficit in episodic memory appears to precede reductions in cognitive reserve capacity in the early development of AD. Recent research indicates that, although preclinical episodic memory deficits may be documented more than 6 years prior to diagnosis, those who will develop AD do not show disproportionate decline from 6 to 3 years prior to diagnosis. However, during the last 3 years before diagnosis precipitous decline is seen in these persons. It is noteworthy that measures of both free recall and recognition make independent contributions to the differentiation of preclinical AD and nondemented subjects 6 and 3 years before diagnosis. To the extent that free recall draws largely on conscious recollection, whereas recognition involves a blend of conscious and unconscious operations, these findings suggest that both these classes of operations are implicated long before the dementia diagnosis. Thus, there is emerging evidence that the preclinical phase of AD spans several years, perhaps decades, although selective decline is not seen until a few years prior to diagnosis. It may be speculated that the threshold eventually leading to diagnosis is reached when multiple biological alterations have occurred (e.g., accumulation of plaques and tangles, shrinkage of medial-temporal regions, radiation of histopathological changes to the neocortical association areas). Finally, there is converging evidence from histopathological, structural imaging, and functional imaging data that early changes in the hippocampus and related structures play a critical role in AD-related memory problems.

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