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. 2005;19(1):24-30.
doi: 10.1159/000080967. Epub 2004 Sep 21.

[18F]FDG-PET in patients with Alzheimer's disease: marker of disease spread

Affiliations

[18F]FDG-PET in patients with Alzheimer's disease: marker of disease spread

D Bittner et al. Dement Geriatr Cogn Disord. 2005.

Abstract

Background: It is not known yet whether temporoparietal glucose hypometabolism in patients with probable Alzheimer's disease (AD) reflects disease severity or different subtypes of patients.

Methods: Twenty-five subjects with mild probable AD [NINCDS-ADRDA criteria; age 65.8 +/- 9.3 years (mean +/- SD); Mini-Mental State Examination (MMSE) 26.0 +/- 3.3] were investigated. [(18)F]FDG-PET data were analyzed visually with raters blinded to the diagnosis and with a quantitative analysis in the region of interest on individual anatomically normalized PET scans.

Results: Thirteen of 25 patients showed temporoparietal hypometabolism on visual inspection (PET+; age 65.7 +/- 10.7), 12 patients had normal FDG-PET results (PET-; age 65.9 +/- 8.0; n.s.). The MMSE and immediate reproduction of the Wechsler Memory Scale (WMS-R-I) were 27.7 +/- 1.9 and 31.1 +/- 6.1 in the PET- vs. 24.5 +/- 3.6 (p = 0.012) and 22.0 +/- 7.4 (p = 0.006) in the PET+ group. Immediate and delayed recall in the California Verbal Learning Test and delayed reproduction in the Wechsler Memory Scale were alike. Regression analysis revealed a significant correlation of temporoparietal glucose metabolism with the block span (r = 0.60; p < 0.01) and the WMS-R-I (r = 0.68; p < 0.01) but not with measures of hippocampal function.

Conclusions: Temporoparietal glucose metabolism in patients with very mild AD is a sign of disease spread beyond the temporal lobe. This may aid in establishing objective parameters for future therapeutic studies.

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