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Impaired recollection and preserved familiarity in Alzheimer’s disease : an fMRI study

hospital lion « which one is the biggest? ». moon scissors « which one is the biggest? ». mouse factory «which one is the biggest? ». plate fox « old or new? ». Recombined (50). moon lion « old or new? ». Intact (50). mouse factory « old or new? ». P < .000005.

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Impaired recollection and preserved familiarity in Alzheimer’s disease : an fMRI study

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  1. hospital lion « which one is the biggest? » moon scissors « which one is the biggest? » mousefactory «which one is the biggest? » plate fox « old or new? » Recombined (50) moon lion « old or new? » Intact (50) mouse factory « old or new? » P < .000005 Impaired recollection and preserved familiarity in Alzheimer’s disease : an fMRI study S. Genon§, E. Salmon *§, F. Collette§ & C. Bastin§ *Memory Clinic,CHU Liege, Belgium. §Cyclotron Research Centre, University of Liege, Belgium. INTRODUCTION According to the dual-process models of memory, two independent processes support memory recognition performance: recollection and familiarity. Recollection reflects the controlled and conscious retrieval of information including the recovery of the context related to the encoding of the information. Familiarity reflects a relatively automatic process of global assessment of memory strength (Yonelinas, 2002). The memory profile in early Alzheimer’s disease (AD) is characterized by severe impairment of recollection but relatively preserved familiarity processes (Tse, Balota, Moynan, Duchek & Jacoby, 2010; Dalla Barba, 1997; Piolino et al., 2003; Rauchs et al., 2007). The objective of this study was to investigate if the preserved familiarity process is supported by the same brain regions in AD and healthy older populations and to examine the brain regions related to impaired recollection in AD patients in comparison to healthy older participants. METHODS RESULTS Participants: 28 mild AD patients (Mattis DRS:124 ± 9.4) 17 healthy older participants (HC) 3 groups: AD without recollection (AD-): n = 12 AD with recollection (AD+): n = 16 HC: n = 17 Imaging method: event-related fMRI, 3T head-only Siemens scanner Task: associative memory task (1) Incidental encoding of unrelated word pairs (n = 103) FAMILIARITY Groups conjunction: HC ∩ AD+ ∩ AD-masked by Correct Rejection of new pairs in the 3 groups; P <.05 corrected (2) Recognition (old-new): 3 types of pairs (total n = 150) New (50) RECOLLECTION Groups conjunction: HC ∩ AD+, P <.001uncorrected Process Dissociation Procedure: inclusion condition: intact pairs exclusion condition: recombined pairs fMRI data analyses: SPM8, t-tests: voxel-wise analyses thresholded at p<.05 FWE corrected or p < .001 uncorrected with a-priori hypotheses Familiarity: Mean effect: hits to intact pairs & false alarms to recombined pairs Recollection: Hits to intact pairs > false alarms to recombined pairs DISCUSSION In AD, recollection was severely impaired whereas familiarity was intact. The intact familiarity process was related to activation along the intraparietal sulcus (IPS), a region frequently found to be related to familiarity process in the healthy population and that is supposed to be engaged when top-down attention to memory retrieval is needed (Ciaramelli et al., 2008). The recollection process was related in both healthy older and AD with residual recollection groups to an activation in the posterior cingulate cortex (PCC), a region frequently found to be related to the conscious retrieval of contextual information (Kim et al., 2010). It is now well known that the PCC is a site of atrophy and metabolic abnormalities very early in AD (see notably Buckner et al., 2005). In parallel, recent studies have found that the objective recollection process was specifically impaired at very early stages of AD (Tse et al. 2010; Bastin et al., 2010). Thus, our results as well as current knowledge on neuropathology of AD suggest that early PCC alterations may play an important role in early deficit of controlled retrieval of episodic memories in AD patients. References: C. Bastin et al. , Journal of Alzheimer’s disease 20, 547 (2010). R. Buckner et al., Neurobiology of Disease25, 7709 (2005) E. Ciaramelli, C.L. Grady, M. Moscovitch, Neuropsychologia46, 1828 (2008) G. Della Barba, Memory 5,143 (1997) H. Kim, NeuroImage 50, 1648 (2010) P. Piolino et al.,Brain10, 2203 (2003) G. Rauchs et al., Neurobiology of Aging28, 1410 (2007) C. Tse, D.A. Balota, S.C. Moynan, J.M. Duchek, L.L. Jacoby, Neuropsychology 24, 49 (2010) A.P. Yonelinas, Journal of memory and langage 46, 441 (2002) This work was supported by grants from the Foundation for Research on Alzheimer’s disease (SAO-FRMA); from the Inter-University Attraction Pole (PAI) and from the Belgian National Funds for Scientific Research (FNRS). Contact: sarah.genon@ulg.ac.be

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