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Cognitive and neuroimaging evidence of impaired interaction between self and memory in Alzheimer's disease
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International audience. In human cognition, self and memory processes strongly interact, as evidenced by the memory advantage for self-referential materials [Self-Reference Effect (SRE) and Self-Reference Recollection Effect (SRRE)]. The current study examined this interaction at the behavioural level and its neural correlates in patients with Alzheimer's disease (AD). Healthy older controls (HC) and AD patients performed trait-adjectives judgements either for self-relevance or for other-relevance (encoding phase). In a first experiment, the encoding and subsequent yes–no recognition phases were administrated in a Magnetic Resonance Imaging (MRI) scanner. Brain activation as measured by functional MRI (fMRI) was examined during self-relevance judgements and anatomical images were used to search for correlation between the memory advantage for self-related items and grey matter density (GMD). In a second experiment, participants described the retrieval experience that had driven their recognition decisions (familiarity vs recollective experience). The behavioural results revealed that the SRE and SRRE were impaired in AD patients compared to HC participants. Furthermore, verbal reports revealed that the retrieval of self-related information was preferentially associated with the retrieval of contextual details, such as source memory in the HC participants, but less so in the AD patients. Our imaging findings revealed that both groups activated the medial prefrontal cortex (MPFC) at encoding during self-relevance judgements. However, the variable and limited memory advantage for self-related information was associated with GMD in the lateral prefrontal cortex in the AD patients, a region supporting high-order processes linking self and memory. These findings suggest that even if AD patients engage MPFC during self-referential judgements, the retrieval of self-related memories is qualitatively and quantitatively impaired in relation with altered high-order processes in the lateral PFC.
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