In vivo amyloid imaging with PET in frontotemporal dementia

Department of Public Health and Caring Sciences, Uppsala University, Uppsala, Uppsala, Sweden
European Journal of Nuclear Medicine (Impact Factor: 5.38). 02/2008; 35(1):100-6. DOI: 10.1007/s00259-007-0523-1
Source: PubMed


N-methyl[11C]2-(4'methylaminophenyl)-6-hydroxy-benzothiazole (PIB) is a positron emission tomography (PET) tracer with amyloid binding properties which allows in vivo measurement of cerebral amyloid load in Alzheimer's disease (AD). Frontotemporal dementia (FTD) is a syndrome that can be clinically difficult to distinguish from AD, but in FTD amyloid deposition is not a characteristic pathological finding.
The aim of this study is to investigate PIB retention in FTD.
Ten patients with the diagnosis of FTD participated. The diagnosis was based on clinical and neuropsychological examination, computed tomography or magnetic resonance imaging scan, and PET with 18 Fluoro-2-deoxy-d-glucose (FDG). The PIB retention, measured in regions of interest, was normalised to a reference region (cerebellum). The results were compared with PIB retention data previously obtained from 17 AD patients with positive PIB retention and eight healthy controls (HC) with negative PIB retention. Statistical analysis was performed with a students t-test with significance level set to 0.00625 after Bonferroni correction.
Eight FTD patients showed significantly lower PIB retention compared to AD in frontal (p < 0.0001), parietal (p < 0.0001), temporal (p = 0.0001), and occipital (p = 0.0003) cortices as well as in putamina (p < 0.0001). The PIB uptake in these FTD patients did not differ significantly from the HC in any region. However, two of the 10 FTD patients showed PIB retention similar to AD patients.
The majority of FTD patients displayed no PIB retention. Thus, PIB could potentially aid in differentiating between FTD and AD.

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    • "Future in FTLD are very similar to imaging in AD–early detection, molecular diagnosis, monitor disease progression and validate and implement disease modifying therapies. Specific anatomic patterns in FTLD, and an amyloid-PET neuroimaging, which uses the amyloid-β-detecting 11C-Pittsburgh compound B, has shown promising results in discriminating or rule-out atypical AD and FTD cases [38,39] particularly those presenting with language deficits rather than behavioural changes. Micro PET with 18 F-THK523 in Tau transgenic mice have been reported [40]. "
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    • "While the clinical distinction between AD and fully expressed FTLD may not be difficult, this can be challenging in the mild stages of disease. Hypometabolism in the frontal lobes on PET (Ishii et al. 1998) and amyloid imaging using PET with Pittsburgh Compound B (PET- PIB) (Engler et al. 2008) may assist in the differentiation between FTLD and AD in these cases. "
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    • "The set of ROI applied was the same as used in other studies and has been described in detail before [9] [14] [15] [16] [17]. The following areas were included in the analyses: frontal, parietal, temporal , occipital and cerebellar cortices, pons, white matter and striatum. "
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