[11C]PIB imaging in primary progressive aphasia and Alzheimer disease

192 Objectives: Progressive non-fluent aphasia (PNFA) is a neurodegenerative disorder characterized by gradually deteriorating expressive language function and variable progression to a more generalized dementia. There is currently no antemortem method to distinguish cases of PNFA related to Alzheimer’s from those caused by other disorders. In an effort to make this distinction, we examined whether PET imaging using the Pittsburgh Compound B, [11C]PIB revealed distinctive patterns of amyloid deposition in clinically diagnosed PNFA versus AD. Methods: Three patients with a clinical diagnosis of PNFA and three age- and gender-matched patients with mild probable AD were included in this study. All subjects underwent FDG-PET, PIB-PET and CT scans under an IRB-approved protocol. With both tracers, venous samples were used to generate blood time activity curves. Quantitative cerebral glucose utilization images were derived from the FDG scans and blood data. Modified Logan plots were generated with cerebellar references for the analysis of the PIB scans. Results: All subjects showed decreased cerebral metabolism, but in two PNFA patients hypometabolism was asymmetric with accentuated left-sided abnormalities in language-related cortical regions. All PNFA patients demonstrated bilateral cortical PIB retention, but the two patients with asymmetric FDG hypometabolism retained PIB to lesser degree. The one PNFA patient who progressed to a more generalized dementia showed FDG and PIB activity patterns similar to that of AD. Conclusions: The asymmetric distribution of PIB and lateralized cerebral hypometabolism observed in patients with PNFA may be useful in identifying this entity. The finding of PIB retention in all three PNFA subjects was unexpected given the lack of plaque pathology in as many as 2/3 of PNFA patients who have come to autopsy. This could reflect underlying AD pathology in these three cases, or binding of PIB to fibrillar proteins other than beta amyloid. Further studies of PIB binding in other PNFA cases are therefore warranted.