K. Ishii et al., RELATIVELY PRESERVED HIPPOCAMPAL GLUCOSE-METABOLISM IN MILD ALZHEIMERS-DISEASE, Dementia and geriatric cognitive disorders, 9(6), 1998, pp. 317-322
The purpose of this study was to clarify the changes in hippocampal gl
ucose metabolism in mild Alzheimer's disease (AD) using positron emiss
ion tomography (PET) and 2-(F-18)fluoro-2-deoxy-D-glucose (FDG). Forty
-one patients with probable mild AD (age: 69.0 +/- 8.0 years; MMSE: 22
.6 +/- 2.1) and 22 normal volunteers (age: 67.7 +/- 7.1 years) were st
udied. The regional cerebral metabolic rate for glucose (CMRglc) was m
easured using FDG and PET, Although the mean CMRglc in the parietal re
gion was significantly lower in the AD group (right: 6.35 +/- 1.26 mg/
100 g/min; left: 6.37 +/- 1.21 mg/100 gl min) than in the control grou
p (right: 7.73 +/- 1.02 mg/100 g/min; left: 7.63 +/- 0.95 mg/100 g/min
), the mean CMRglc in the hippocampus did not show a significant diffe
rence between the AD group (right: 4.58 +/- 0.70 mg/100 g/min; left: 4
.63 +/- 0.67 mg/100 g/min) and the control group (right: 5.22 +/- 0.65
mg/100 g/min; left: 5.22 +/- 0.67 mg/100 g/min) by analysis of varian
ce and post-hoc Tukey's test. The magnitude of the hippocampal CMRglc
reduction was not as large as that of parietal CMRglc reduction. Stati
stical parametric maps (SPM) analysis also did not significantly demon
strate reduced hippocampal CMRglc in AD patients, although it did show
a significant reduction in parietal CMRglc in AD patients. Hippocampa
l CMRglc was not significantly decreased in mild AD. This was unexpect
ed in view of previous studies that have shown atrophy and clinical dy
sfunction concerning hippocampus in AD, and suggests that the pathophy
siology of the hippocampus in AD may be more complex than was previous
ly thought.