Studies on emotional processing in Alzheimer's disease (AD) have reported abnormalities in emotional decoding. However, it remains unclear whether the impairment depends on a general cognitive decline that characterizes these patients or is an independent deficit. We conducted a comprehensive meta-analysis of existing studies that compared AD patients with age-matched healthy older adults (HOA) on measures of emotional decoding abilities. Our first goal was to quantify the magnitude of the AD patients' deficit. The second goal was to identify variables that may modulate the deficit, including emotional task design and participants' characteristics. The random-effects model analysis on 212 effect sizes indicated that AD patients showed significant impairment in emotional decoding abilities. This deficit is consistent regardless of the emotional task, stimuli, type of emotion considered, or disease severity. After we controlled for cognitive status, the emotional performance in AD patients was still poorer than that in HOA. The effect size of emotional performance was significantly lower when the cognitive status was considered than when it was not. Thus, our results suggest that impaired emotion processing in AD patients cannot be solely explained by the cognitive deficit. These findings provide evidence that progressive neuropathological changes characterizing the disease could affect emotional processing, which may suggest that clinicians should be sensitive to the emergence of impairments in emotional decoding. Further research that addresses the limitations of existing studies is needed to draw conclusions about methodological issues and the impact of the AD patient's depression symptoms on emotional decoding.

Patients with early atrophy of both limbic structures involved in memory and emotion processing in Alzheimer’s disease (AD) provide a unique clinical population for investigating how emotion is able to modulate retention processes. This review focuses on the emotional enhancement effect (EEE), defined as the improvement of memory for emotional events compared with neutral ones. The assessment of the EEE for different memory systems in AD suggests that the EEE could be preserved under specific retrieval instructions. The first part of this review examines these data in light of compelling evidence that the amygdala can modulate processes of hippocampus-dependent memory. We argue that the EEE could be a useful paradigm to reduce impairment in episodic memory tasks. In the second part, we discuss theoretical consequences of the findings in favor of an EEE, according to which a compensatory mechanism in patients with AD solicits greater amygdala functioning or additional networks, even when amygdala atrophy is present. These considerations emphasize the relevance of investigating patients with AD to understand the relationship between emotion and memory processes.

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Current research suggests that amygdalar volumes in patients with Alzheimer's disease (AD) may be a relevant measure for its early diagnosis. However, findings are still inconclusive and controversial, partly because studies did not focus on the earliest stage of the disease. In this study, we measured amygdalar atrophy in 48 AD patients and 82 healthy controls (HC) by using a multi-atlas procedure, MAPER. Both hippocampal and amygdalar volumes, normalized by intracranial volume, were significantly reduced in AD compared with HC. The volume loss in the two structures was of similar magnitude (~24%). Amygdalar volume loss in AD predicted memory impairment after we controlled for age, gender, education, and, more important, hippocampal volume, indicating that memory decline correlates with amygdalar atrophy over and above hippocampal atrophy. Amygdalar volume may thus be as useful as hippocampal volume for the diagnosis of early AD. In addition, it could be an independent marker of cognitive decline. The role of the amygdala in AD should be reconsidered to guide further research and clinical practice.

Background: The aim of the present study was to assess the possibility of compensating early facial expression recognition impairments in amnestic Mild Cognitive Impairment (a-MCI) patients. Methods: Twelve patients with a-MCI and 17 healthy participants matched according to age and education participated in the study. The originality of the present study was to cue the recognition of facial expressions (happiness, anger, fear, and neutral) by comparing eye region expressions and entire facial expressions. Results: A deficit in the recognition of fearful expressions was observed in a-MCI patients relative to the control group, whereas recognition of all the other emotional expressions was spared. Nevertheless, when eye expressions cued the recognition of fearful facial expressions, the performance of normal controls and a-MCI patients was comparable. Conclusion: The present paper indicates a selective impairment in fear recognition in the prodromal state of Alzheimer’s disease, and the possibility of compensating this deficit by orienting selective attention on specific facial features.

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