Abstract
Mechanisms underlying working (WM) and long-term memory (LTM) are not entirely coextensive: although both depend on the hippocampus for feature binding, WM also utilises frontoparietal regions for information maintenance. Hence, disorders that affect the hippocampus, such as Alzheimer’s disease (AD), may affect WM and LTM differently. Apolipoprotein E (APOE) e4 allele is the highest genetic risk factor for late-onset AD. Previous research demonstrates that even healthy older carriers of this allele show impairments in LTM as compared to non-carriers, while their WM may be better, suggesting a different pattern of WM versus LTM performance in later adulthood. Therefore, we aimed at investigating whether APOE e4 alters the relationship between WM and LTM.
In a double-blind study, we tested over 80 middle-aged adults genotyped for three different APOE allele combinations: e3/e3, e3/e4 and e4/e4. We used a recently developed delayed-report contextual spatial memory task to measure WM and LTM in an analogous way. In each trial, participants viewed a photograph with either one or three objects superimposed on it, followed by a memory delay. They were then either probed to report the location of one of the objects (WM trials) or asked to tap on a centrally presented fixation cross (learning trials). The LTM stage followed 20 minutes later with an identical memory probe of all previously seen stimuli, supplemented by confidence rating scales (LTM trials). We measured response times and memory errors, the Euclidian distances between the original and the reported locations.
The analysis per gene group is soon to be completed following the unblinding. However, a preliminary analysis of all data showed that the task worked as expected: larger set size increased reaction times in WM and memory errors in WM and LTM trials, while WM performance significantly predicted LTM performance. This promises interesting results for gene group analysis.