The acquisition process is impaired in AD patients even at a very early stage of the disease (MCI_AD). This deficit is linked to metabolic changes in the hippocampal formation. In contrast, variations of relatively intact performances of controls and participants with stable MCI are related to metabolic variations in a fronto-parietal attentional network. The consolidation process is specifically impaired in AD patients at the dementia stage of the disease. However, this deficit was not significantly correlated to brain metabolism in our participant groups at the selected statistical threshold.
**
***
*
Verbal Learning in Alzheimer’s disease and Mild
Cognitive Impairment: neuroanatomic correlates of
acquisition and consolidation performances.
S. Genon
§, F. Collette
§, C. Moulin
#, F. Lekeu
*, E. Salmon
*§, C. Bastin
§.
#
Leeds Memory Group, University of Leeds, UK.
*Centre de la Mémoire, CHU de Liège. §Centre de
Recherches du Cyclotron, Université de Liège, Belgique.
Episodic memory impairment is a key feature of cognitive decline in Alzheimer’s disease (AD). Indeed, episodic memory is generally the first cognitive function to be altered even at Mild Cognitive Impairment (MCI) stage.
Moulin et al. (2004) have shown that acquisition and consolidation deficits can account for episodic impairment in AD patients and in patients with MCI. However, little is known about cerebral alterations associated with these particular deficits.
Objective: The aim of this study was to examine correlations
between impaired memory acquisition/consolidation and brain metabolism at rest in Alzheimer’s disease.
CYCLOTRON RESEARCH CENTRE
INTRODUCTION
METHODS
RESULTS
44 AD
31 MCI
T1
Brain examination + cognitive assessment4-8 years follow-up
15 stables
(MCI_S)
16 AD
(MCI_AD)
12 CTRL
T2
Analysis of cognitive-metabolic correlationsDISCUSSION
Measures:
acquisition = mean proportion of gained access across the 5 study-test trials of the California Verbal Learning Test.
consolidation = total proportion of lost access across the 5 study-test trials of the California Verbal Learning Test.
18FDG-PET
Analyses:
Cognitive-metabolic correlations (SPM8): gained/lost access performances - metabolic TEP T1; covariates: age, MMSE;
statistic threshold: p uncorrected with a priori hypotheses <.001.
Acquisition (gained access performances) :
Behavioral results
ANCOVA : F(3,80) = 9.08 ; P < .00005 POST-HOC (HSD different N):
*P < 0.005, **P < 0.001, P*** <. 0.0005
Cognitive-metabolic correlations
Consolidation (lost access performances) :
Behavioral results
ANCOVA : F(3,80) = 4.04 ; P < .01 POST-HOC (HSD different N):p = .052
18FDG-TEP
CVLT:
GAINED ACCESS (acquisition)
LOST ACCESS (consolidation)
Cognitive-metabolic correlations: no significant correlation
44 AD
12 CTRL
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).