IC-P1-030: Does Amyloid β accumulation modify clinical feature of frontotemporal dementia?

Abstract

The PET tracer 11C labeled Pittsburgh Compound-B (11C-PIB) specifically binds to amyloid-β (Aβ) and has been reported to be useful to differentiate Alzheimer's disease (AD) from frontotemporal dementia (FTD). Serial neuropathological investigation of our Gerontology Hospital autopsy cases has revealed the Aβ accumulation is observed as a continuous profile among normal aging and even in non-AD degenerative disorders such as FTD. The purpose of this study is to evaluate the role of Aβ accumulation in FTD patients. We studied fifteen patients of FTD and fifteen patients with AD meeting the diagnostic criteria and six subjects as healthy controls. All the subjects underwent PET study with 11C-PIB and 18F-FDG. All the patients were followed up clinically at least one year. Three FTD patients had two 11C-PIB scans with one-year interval, and nine FTD patients had multiple 18F-FDG PET scans to monitor the disease progression. The 11C-PIB accumulation was evaluated with the summing image from 40 to 60 min after the injection with the cerebellar cortex was used as a reference region. The images were evaluated by visual inspection, measurements with regions of interest, and statistical analysis with statistical parametric mapping (SPM). Three FTD patients had 11C-PIB accumulation as high as the level of AD group. Those patients may be the contamination of AD as the limitation of clinical diagnostic criteria. In the rest of 12 FTD patients, the average of 11C-PIB accumulation was not significantly higher than that of healthy controls. However, four of them had mild 11C-PIB accumulation, and three of them underwent follow up 11C-PIB scan revealing increasing 11C-PIB accumulation in one-year follow up. The FTD patients with increasing 11C-PIB accumulation have a trend to demonstrate relatively rapid progression of the clinical symptoms in comparison with the patients with negative 11C-PIB accumulation. Mild increase in 11C-PIB accumulation was observed in about a quarter of FTD patients who showed relatively rapid progression of the symptoms. Besides normal aging, Aβ burden may have some pathological role in FTD. Further prospective study and pathological correlation study are required.