Brain, Vol 121, Issue 4 611-631, Copyright © 1998 by Oxford University Press
B Desgranges, JC Baron, V de la Sayette, MC Petit-Taboue, K Benali, B Landeau, B Lechevalier and F Eustache
The aim of this study was to determine the neuronal basis for memory
impairment in Alzheimer's disease by taking advantage of the clinical and
metabolic heterogeneity of this pathology. To this end, 19 patients
satisfying the NINCDSADRDA criteria for probably Alzheimer's disease of
mild-to-moderate severity underwent a detailed examination of the five
memory systems according to Tulving's model, together with a PET
measurement of resting regional cerebral glucose utilization (CMRGlc).
Compared with controls, the patients as a group showed the expected memory
and metabolic profiles of impairment. Correlations (corrected for the
effects of ageing) were calculated between memory scores and CMRGlc
(normalized by the vermis CMRGlc) using two methods: (i) the classic
regions-of-interest method, based on a priori hypotheses and individual
coregistered structural MRI; and (ii) the statistical parametric mapping
method which allows a systematic voxel-by-voxel analysis, in a more
descriptive and exploratory way. Significant correlations were above chance
levels and largely consistent between the two methods. They were almost
exclusively positive (i.e. in the neurobiologically expected direction) and
their distribution showed striking differences according to each memory
system. Thus, verbal episodic memory impairment was related to changes in a
large neuronal network including not only the limbic structures (mesial
temporal cortex, thalamus and cingulate gyrus, with left side predominance)
but also the parietotemporal and frontal association cortices of the right
hemisphere, possibly on a compensatory basis. Regardless of modality,
short-term memory tests were mainly correlated with bilateral activity in
posterior association cortex, and also with activity in left prefrontal
cortex for the visuospatial span, possibly indicating essentially uniform
strategies for the performance of the different tasks. As predicted,
semantic memory scores correlated with activity in temporoparietal and
frontal association cortices of the left hemisphere, and also with activity
in left cingulate cortex. Thus, for episodic, short-term and semantic
memory, many findings fit classical neuropsychology, while most of the less
expected ones were consistent with recent results from functional
neuro-imaging in healthy subjects, notably with the hemispheric encoding/
retrieval asymmetry (HERA) model; only few findings suggested possible
reorganization processes and/or recourse to unexpected cognitive strategy.
Finally, only negative correlations were found for perceptual priming and
procedural memory; although they could arise by chance, some of these
unexpected findings give rise to interesting hypotheses about the cognitive
relationships between the most and least affected memory systems. This
study documents the validity and usefulness of our approach in unravelling
the neural substrates of cognitive impairment in brain pathology without
focal tissue loss such as that seen in neurodegenerative diseases.
ARTICLES
The neural substrates of memory systems impairment in Alzheimer's disease. A PET study of resting brain glucose utilization
INSERM U320, Cote de Nacre, France.
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