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- W2536512868 abstract "Though Alzheimer’ s Disease (AD) has long been considered as a gray matter disease, recently white matter abnormalities are also reported. In this study our purpose is to evaluate influence of [18F] THK-5351 and connectivity in AD brain. Participants were 8 PIB-positive AD patients and 7 PIB-negative, age and gender matched cognitively normal healthy controls (CN). We performed [18F] THK-5351 PET, [11C] PIB PET, structural MRI and diffusion kurtosis image (DKI) for each participant. We first coregistered all the image modalities. Then extracted left and right hippocampi and the posterior cingulate cortex (PCC) VOI from structural MRI. Within these regions we identified significantly higher [18F] THK-5351 accumulation in AD patients comparing with CN. Selected VOIs were divided using standardized uptake value ratio (SUVR) grades as a threshold. SUVR was calculated for each PET image using the whole cerebellum as a reference region. Finally, we calculated fractional anisotropy in diffusion kurtosis imaging (DKI-FA) for each VOI at range of SUVR thresholds (starting at 0.5 to 4 in 0.25 increments). We used two way repeated measures ANOVA to evaluate influence of: group factor (AD and CN), SUVR factor (range of thresholds) and their interaction. Group effect was significant both in bilateral hippocampi and PCC, with AD having significantly lower (p < 0.05) FA value than CN. Moreover, SUVR factor was also significant in all the VOIs; higher SUVR values led to higher FA values (p < 10-4). Group×SUVR interaction was significant only for the PCC (p < 10-4); CN showed steeper rise in FA values as SUVR increased, as compared to AD. Group difference suggests that [18F] THK-5351 accumulation in AD patients is pathological, and not related to aging. Moreover, higher tau concentration values yield higher DKI-FA values, which reflects greater number of axons or increased myelination. Lastly, the presence of Group×SUVR interaction in PCC, but not in bilateral hippocampi suggests the presence of compensatory mechanisms in hippocampus area, previously reported by Matsuda (J Nucl Med. 2007; 48:1289-300). PCC has both SUVR factor and interaction influence, suggesting a different compensatory mechanism to regulate for increased tau concentration." @default.
- W2536512868 created "2016-10-28" @default.
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- W2536512868 date "2016-07-01" @default.
- W2536512868 modified "2023-09-27" @default.
- W2536512868 title "IC-P-183: Diffusion Kurtosis Image Analysis Associated with TAU Accumulation Measured by [18 F] THK-5351 in Alzheimer’s Disease" @default.
- W2536512868 doi "https://doi.org/10.1016/j.jalz.2016.06.214" @default.
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