Healthy participants remember emotional stimuli better than neutral stimuli. In normal, older adults this emotional enhancement of memory (EEM) was mostly seen in respect of positive stimuli (positivity bias) after rich and deep encoding. The results relating to this effect in Alzheimer's disease (AD) patients are fairly inconsistent. The goal of the present study was to ascertain whether EEM in AD patients depends on the depth and the richness of encoding. Twenty-one patients with mild-to-moderate AD and 23 age-and-education-matched controls completed two study phases, each followed by a retrieval phase. The first study phase consisted of a natural/man-made categorization task followed by a recognition task, whereas the second, which involved the stimuli used in the recognition task, allowed for richer and deeper encoding as a result of repetition and naming of the stimuli and presentation of the same semantic cues at encoding and retrieval. The second study phase was followed by free and cued recall tasks and a recognition task. After the first study phase we observed EEM in respect of negative and positive stimuli in controls, but not in AD patients. After the second study phase, the positivity bias was observed in the free recall task in controls but not in AD patients. In the cued recall and recognition tasks, however, both groups showed the positivity bias. Based on our results, AD patients present a positivity memory bias when encoding is sufficiently rich and deep, and when support is provided at the time of retrieval (cued recall or recognition tasks).
In healthy young and older participants declarative memory for emotional information is typically better than memory for non-emotional information (LaBar and Cabeza, 2006 and Reisberg and Heuer, 2004). Numerous neuroimaging and neuropsychology studies have suggested that emotional enhancement of memory (EEM) relies on several cerebral structures, especially the amygdala, which recruits sensory-processing regions in order to increase attention paid to emotional information and, thus, encoding of these stimuli (attention-mediation hypothesis) (Talmi, Anderson, Riggs, Caplan, & Moscovitch, 2008), and modulates the hippocampal long-term memory consolidation processes (consolidation-mediation hypothesis) (McGaugh, 2000 and Vuilleumier et al., 2004).
EEM has also been studied in Alzheimer's disease (AD), a condition characterised by a gradual decline in declarative memory (Greene, Baddeley, & Hodges, 1996) attributable to neuropathological changes in the medial temporal lobes, notably the amygdala and hippocampus (Braack and Braack, 1991 and Poulin et al., 2011). Despite early atrophy of the amygdala, emotion processing is relatively spared in AD (Boller et al., 2002 and Hamann et al., 2000), whereas data regarding the presence of EEM are fairly inconsistent (see Klein-Koerkamp, Baciu, & Hot, 2012 for a review). Therefore, it seems factors other than impaired emotional processing can account for the contradictory results concerning the presence of EEM in AD. In the present study we investigated whether rich and deep encoding might permit the emergence of EEM in AD.
