title: Impaired metabolic activation in Alzheimer's disease: a PET study during continuous visual recognition.
abstract: Regional cerebral metabolic rate of glucose (rCMRGl) was studied in 21 patients with probable Alzheimer's disease (AD) and nine age-matched normal controls by positron emission tomography (PET) of 2(18F)-fluoro-deoxy-D-glucose (FDG) at rest and during stimulation with a continuous visual recognition task. While global metabolism at rest was comparable in both groups, rCMRGl in the temporo-parietal junction area, the mid-temporal and the frontal cortex was typically decreased in the AD patients. The continuous visual recognition task adapted to the individual performance capacity increased the global metabolic rate in the controls by 21 +/- 18%, while in the AD patients the metabolic change (5.7 +/- 11.1%) during activation was significantly weaker (P = 0.023). Due to the tasks chosen the activation of rCMRGl in both groups was most prominent in the visual cortex and the temporo-parietal association areas, although the recognition task additionally involved widespread brain structures with varying rCMRGl. A significant correlation was found between rCMRGl in areas usually severely affected by AD pathology, e.g. the temporo-parietal cortex, and GDS scores, and became stronger during metabolic activation. Neither at rest nor during stimulation was there a relationship between the rCMRGl of structures usually less involved in AD, e.g. the sensorimotor cortex, and the severity of dementia as assessed by the global deterioration scale (GDS). From these results it can be concluded that metabolic rate at rest reflects the extent of morphologic damage, while PET studies during activation indicate the brain's reserve capacity to respond to functional tasks. Since metabolism in AD patients during activation is more severely impaired than at rest, PET studies during functional tests could help in the selection of patients with a potential to benefit from therapeutic intervention.
authors.affiliation: Max-Planck-Institut für neurologische Forschung, Köln, F.R.G.
authors.forename: J
authors.initials: J
authors.lastname: Kessler
authors.forename: K
authors.initials: K
authors.lastname: Herholz
authors.forename: M
authors.initials: M
authors.lastname: Grond
authors.forename: W D
authors.initials: WD
authors.lastname: Heiss
mesh_terms: D000544:Alzheimer Disease / Q000000981:diagnostic imaging / Q000378:metabolism* / Q000503:physiopathology; D001923:Brain Chemistry / Q000502:physiology*; D003071:Cognition / Q000502:physiology*; D003847:Deoxyglucose / Q000031:analogs & derivatives; D005260:Female; D019788:Fluorodeoxyglucose F18; D005947:Glucose / Q000378:metabolism; D006801:Humans; D008297:Male; D008875:Middle Aged; D011581:Psychological Tests; D011597:Psychomotor Performance / Q000502:physiology; D014055:Tomography, Emission-Computed; D014785:Vision, Ocular / Q000502:physiology*
chemical_list: D019788:Fluorodeoxyglucose F18; D003847:Deoxyglucose; D005947:Glucose