[Brain substrates of episodic memory disorders in Alzheimer’s disease].

Resting state PET measurement is useful to unravel brain regions whose dysfunction is responsible for impairment of episodic memory in Alzheimer’s disease. First, the consistent hypometabolism of posterior cingulate cortex, temporo-parietal cortex and frontal cortex contrasts with the frequent lack of hippocampal hypometabolism, although it is first to be concerned by neurofibrillary tangles. Several hypotheses are proposed to explain this paradoxical result. Second, the correlative approach (correlations between memory performances and metabolic values on a voxel basis) shows that dysfunction of the hippocampal region is responsible for the earliest deficits of episodic memory, and then suggests the recruitment of neocortical temporal areas normally involved in semantic memory, perhaps as a form of a compensatory mechanism. When applied to the study of Mild Cognitive Impairment, this approach is also very fruitful.