Brain, Vol. 125, No. 5, 1116-1124,
May 2002
© 2002 Guarantors of Brain
The neural substrates of episodic memory impairment in Alzheimer’s disease as revealed by FDG–PET: relationship to degree of deterioration
1 EMI INSERM-Unive Laboratoire de Neuropsychologie, CHU Côte de Nacre, Centre CYCERON, France and 2 Department of Neurology, University of Cambridge, Cambridge, UK
Correspondence to: Béatrice Desgranges, EMI INSERM, Université de Caen Laboratoire de Neuropsychologie, CHU, Côte de Nacre, 14033 Caen Cedex, France E-mail: desgranges-b{at}chu-caen.fr
In a previous investigation, we raised the hypothesis that in Alzheimer’s disease the cerebral structures implicated in episodic memory deficits may differ according to the severity of cognitive impairment. To test this hypothesis, Story Recall test scores and PET measurements of resting cerebral glucose utilization, a measure of synaptic integrity, were obtained in 40 patients. Using SPM96 (statistical parametric mapping 1996), positive correlations between the two sets of data were calculated on a voxel basis, first in the whole patient sample and then separately in the two subgroups of 20 patients differing in Mini-Mental State Examination score, i.e. those with least impaired and those with most impaired performance (‘less severe’ and ‘more severe’ subgroups, respectively). In the whole sample, significant correlations (P < 0.05, corrected for multiple tests) involved bilaterally not only several limbic structures (the hippocampal/rhinal cortex regions, posterior cingulate gyrus and retrosplenial cortex) but also, and less expectedly, some temporo-occipital association areas. However, the subgroup analysis disclosed that, in the less severe subgroup, all significant correlations (P < 0.005, uncorrected) were restricted to the parahippocampal gyrus and retrosplenial cortex, in accordance with both the distribution of changes in tau in early Alzheimer’s disease and the known involvement of this network in normal and impaired memory function, while in the more severe subgroup they mainly involved the left temporal neocortex, which is known to be implicated in semantic memory. These findings suggest that, when episodic memory is mildly impaired, limbic functions are still sufficient to subserve the remaining performance, whereas with more severe memory deficit resulting from accumulated pathology the neocortical areas that are normally involved in semantic memory are recruited, perhaps as a form of (inadequate) compensatory mechanism.
CiteULike 
Connotea 
Del.icio.us What's this?
This article has been cited by other articles:
|
|
 |
|
  N. Abe, T. Fujii, K. Hirayama, A. Takeda, Y. Hosokai, T. Ishioka, Y. Nishio, K. Suzuki, Y. Itoyama, S. Takahashi, et al. Do parkinsonian patients have trouble telling lies? The neurobiological basis of deceptive behaviour Brain, May 1, 2009; 132(5): 1386 - 1395. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J. R. Binder, R. H. Desai, W. W. Graves, and L. L. Conant Where Is the Semantic System? A Critical Review and Meta-Analysis of 120 Functional Neuroimaging Studies Cereb Cortex, March 27, 2009; (2009) bhp055v1. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 O. Colliot, G. Chetelat, M. Chupin, B. Desgranges, B. Magnin, H. Benali, B. Dubois, L. Garnero, F. Eustache, and S. Lehericy Discrimination between Alzheimer Disease, Mild Cognitive Impairment, and Normal Aging by Using Automated Segmentation of the Hippocampus Radiology, July 1, 2008; 248(1): 194 - 201. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
H.-J. Lee, A.-L. Giraud, E. Kang, S.-H. Oh, H. Kang, C.-S. Kim, and D. S. Lee Cortical Activity at Rest Predicts Cochlear Implantation Outcome Cereb Cortex, April 1, 2007; 17(4): 909 - 917. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 E. H. Chang, M. J. Savage, D. G. Flood, J. M. Thomas, R. B. Levy, V. Mahadomrongkul, T. Shirao, C. Aoki, and P. T. Huerta AMPA receptor downscaling at the onset of Alzheimer's disease pathology in double knockin mice PNAS, February 28, 2006; 103(9): 3410 - 3415. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 J.-F. Demonet, G. Thierry, and D. Cardebat Renewal of the Neurophysiology of Language: Functional Neuroimaging Physiol Rev, January 1, 2005; 85(1): 49 - 95. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Eustache, P. Piolino, B. Giffard, F. Viader, V. D. L. Sayette, J.-C. Baron, and B. Desgranges 'In the course of time': a PET study of the cerebral substrates of autobiographical amnesia in Alzheimer's disease Brain, July 1, 2004; 127(7): 1549 - 1560. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
C. Lustig, A. Z. Snyder, M. Bhakta, K. C. O'Brien, M. McAvoy, M. E. Raichle, J. C. Morris, and R. L. Buckner Functional deactivations: Change with age and dementia of the Alzheimer type PNAS, November 25, 2003; 100(24): 14504 - 14509. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. Chetelat, B. Desgranges, V. de la Sayette, F. Viader, K. Berkouk, B. Landeau, C. Lalevee, F. Le Doze, B. Dupuy, D. Hannequin, et al. Dissociating atrophy and hypometabolism impact on episodic memory in mild cognitive impairment Brain, September 1, 2003; 126(9): 1955 - 1967. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
F. Vargha-Khadem, C. H. Salmond, K. E. Watkins, K. J. Friston, D. G. Gadian, and M. Mishkin Developmental amnesia: Effect of age at injury PNAS, August 19, 2003; 100(17): 10055 - 10060. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G. Chetelat, B. Desgranges, V. de la Sayette, F. Viader, F. Eustache, and J.-C. Baron Mild cognitive impairment: Can FDG-PET predict who is to rapidly convert to Alzheimer's disease? Neurology, April 22, 2003; 60(8): 1374 - 1377. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 C. L. Grady, A. R. McIntosh, S. Beig, M. L. Keightley, H. Burian, and S. E. Black Evidence from Functional Neuroimaging of a Compensatory Prefrontal Network in Alzheimer's Disease J. Neurosci., February 1, 2003; 23(3): 986 - 993. [Abstract] [Full Text] [PDF]
|
|