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Franziska T Scheiwein, Kazunari Ishii, Chisa Hosokawa, Hayato Kaida, Tomoko Hyodo, Kohei Hanaoka, Matthias Brendel, Peter Bartenstein, Axel Rominger and Takamichi Murakami
Purpose: In subjects showing an increased level of 11C-Pittsburgh compound B (PiB) in positron emission tomography (PET) imaging of the brain, two groups can be distinguished: those with and without elevated PiB uptake in the striatum. We examined regional PiB uptake differences between these groups, and additionally compared them with PiB-negative subjects. Methods: This study included 141 subjects complaining of cognitive impairment. Their clinical diagnoses were Alzheimer’s disease (AD), mild cognitive impairment, dementia with Lewy bodies, frontotemporal lobar degeneration, or subjective cognitive impairment. PiB and 18F-fluorodeoxy-D-glucose (FDG) PET were performed in all subjects. PiB PET images were visually classified into three groups: 1) PiB-positive with uptake in any region of the cortex accompanied by striatal PiB uptake (STRPOS), 2) PiB-positive with cortical uptake but without striatal PiB uptake (STRNEG), and 3) both cortex and striatum PiB-negative (PiBNEG). Standardised uptake value ratios (SUVR) and regional differences in PiB uptake were evaluated using voxelbased analysis of PiB and FDG uptake images. Results: Eighty subjects were visually rated as PiB-positive: 11 had no increased PiB uptake in the striatal area, while 69 showed an elevated striatal PiB level. Sixty-one subjects were PiB-negative. Mean cortical SUVR was 1.46 ± 0.23 for STRNEG, 2.00 ± 0.44 for STRPOS and 0.99 ± 0.19 for PiBNEG. Apart from the striatum, PiB accumulation in the medial orbitofrontal cortex of STRPOS subjects was higher than in STRNEG subjects. No significant differences in regional FDG distribution were observed. Conclusion: PiB-positive cases with high striatal PiB uptake have an increased mean cortical SUVR in comparison to PiB-positive subjects without striatal uptake. This difference is most distinctive in the orbitofrontal cortex. We conclude that a high amyloid load in the striatum is linked to amyloid deposition occurring mostly in the frontal region, and may occur later in the course of AD progression.