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Abstract :
[en] Introduction. Memory deficits are the clinical hallmark of typical Alzheimer’s disease. The precise nature of these deficits however remains to be fully characterized. In this study, we investigated binding in long-term episodic memory. Relational binding processes in memory create an associative link between independent items or between items and context into episodic memories (Cohen et al., 1999). An alternative process, conjunctive binding, allows associations to be encoded as a united representation of features into a single entity (O'Reilly and Rudy, 2001; Mayes et al., 2007). The current study (1) assessed whether Alzheimer’s disease disrupt both conjunctive and relational memory, and (2) related patients’ memory performance to cerebral metabolism.
Methods. Thirty patients with mild Alzheimer’s disease and 24 healthy older adults performed a source memory task where items were associated to a background color (Diana et al., 2008, 2010). In one condition, relational binding was promoted by the instruction to associate the item with another object of the same color as the background. In the other condition, color had to be integrated as an item feature (conjunctive binding). Patients’ brain metabolic activity at rest (FDG-PET) was analysed with spatio-temporal Partial Least Squares (McIntosh et al., 1996) in order to assess the relation of behavioral performance and activity in functional cerebral networks.
Results. Alzheimer’s disease patients had an impaired capacity to remember item-color associations, with deficits in both relational and conjunctive memory. However, performance in the two kinds of associative memory varied independently across patients. Partial least square analyses revealed a significant pattern of metabolic activity that correlated specifically with each condition (accounting for 76.48 % of the covariance in the data; p< .05). More specifically, poor conjunctive memory was related to hypometabolism in an anterior temporal-posterior fusiform brain network, whereas relational memory correlated with metabolism in regions of the default mode network.
Conclusions. These findings support the hypothesis of distinct neural systems specialized in different types of associative memory and point to heterogeneous profiles of memory alteration in Alzheimer’s disease as a function of damage to the respective neural networks.