Long-term evaluation of amyloid deposition in basal ganglia in patients with mild cognitive impairment by 11C-PIB PET/CT. Correlation with cortical brain amyloid load and clinical evolutionY

1066 Objectives: To evaluate 11C-PIB amyloid deposition in basal ganglia in amnestic and non-amnestic MCI patients (A-MCI and NA-MCI) and their evolutive changes in comparison with cortical brain amyloid load (BAL) and their clinical outcome. Methods: We examined 32 A- MCI, 9 NA-MCI and 5 with multi-domain MCI (MD-MCI) at MCI diagnosis clinically and by 11C-PIB PET/CT and 5 years later by clinical re-evaluation and a new 11C-PIB PET/CT. Severity of global cognitive impairment, presence of extrapyramidal abnormalities and neuropsychiatric symptoms were correlated with PIB scan findings. All 11C-PIB positive scans were visualy classified in two paterns (A-pattern: predominantly in frontal, basal ganglia and anterior cingulated; B-pattern: global). All 11C-PIB PET/CT were also semiquantitatively analyzed obtaining subcortical SUV mean values in basal ganglia (caudate and caudate-striatum complex) and in 6 regional cortical ROIS to obtain a cortical BAL and a subcortical BAL values using the cerebellum as reference region. Results: In A-MCI group (n= 32) 24 patients were initially PIB positive (5 showing A-pattern and 17 B-pattern) and 8 were PIB negative; in NA-MCI group, all were PIB negative and in MD-MCI group (n=5) 1 was PIB positive (A-pattern) and 4 were PIB negative. At MCI diagnosis, the mean of subcortical BAL in A-MCI group with A-pattern was 2,227 + 0,567 and in B-pattern group 2,298 + 0,553 (p= ns); and cortical BAL in A-pattern group 1,808 + 0,371 and in B-pattern 2,019 + 0,378. Five years later, of the 5 PIB positive A-pattern, 1 evolved to B-pattern, and 4 rest as A-pattern. Semiquantitative analysis showed increase of subcortical BAL in A-pattern group (mean SUV mean 2,646 + 0,3371; % of increment basal-5y 15,83%); and in B-pattern group (2,414 + 0,447; % of increment basal-5y was 4,80%) and also increase the mean cortical BAL in A-pattern group (2,123 + 0.615; % increment 14,83% and in B-pattern (2,321 + 0,484; % of increment was 9,13%). More interesting was the change from a negative pattern to A-pattern in 3 patients (1 NPHi with aprobably AD co-patology and 2 A­-MCI initially negative There were no differences between final GDS in A and B pattern groups. There were only 2 patients with extrapyramidal symptoms and psychiatric symptoms at 5-year follow-up, both showing an initial B pattern and suggesting a phenotipic lewy’s body dementia. Conclusions: Dynamic processes of amyloid brain deposition have significant differences along time between A and B visual patterns of PIB distribution observed at MCI stage. A-Pattern seems to be an early positive stage of brain amyloidosis, but not always progress to a B-pattern. Amyloid deposition in basal ganglia mainly involve to caudate nucleus and striatum seem to be preserved. This findings may be related with the scarce developed extrapyramidal symptoms at follow-up.