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Neurosciences: NeurologyDementia II - Differential Diagnosis and Follow Up |
1 Centre for PET, Austin Hospital, Melbourne, Victoria, Australia; ; 2 National Ageing Research Institute, Melbourne, Victoria, Australia; ; 3 Psychiatry; ; 4 The Mental Health Research Institute, University of Melbourne, Melbourne, Victoria, Australia
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Objectives: In-vivo amyloid imaging with PET is allowing new insights into Aβ deposition in the brain. Longitudinal studies allow researchers to more clearly define the role of Aβ deposition in the development of dementias where Aβ may play a role.
Methods: Fifty-one subjects -15 with Alzheimer’s disease (AD), 8 with Mild Cognitive Impairment (MCI) and 28 age-matched healthy controls (HC)- were re-assessed 21±5 months after their first 11C-PiB-PET scan. Aβ burden was quantified using SUVR normalized to cerebellar cortex.
Results: Cortical PiB binding was markedly elevated in every AD subject. In the MCI group, PiB binding was either "AD-like" (50%) or "HC-like". At baseline, 8 out of the 28 HC (29%) showed cortical binding, predominantly in the prefrontal and posterior cingulate/precuneus regions, though to a lesser degree than AD patients. Though no significant difference in PiB binding was attained between baseline and follow-up in the groups examined, 12 out of 15 AD showed an increase ranging from 3 to 18% (mean 9.5%). Furthermore, 3/8 PiB+ve (38%) HC and 4/4 (100%) PiB+ve MCI declined at follow-up and their clinical classification was changed to either MCI or AD at the repeat visit. Only one PiB -ve HC showed decline to MCI.
Conclusions: PiB binding changed little over 2 years, though there was a slight increase in the AD group. The presence of Aβ deposits in the brain, even at presymptomatic stages, seems to be a strong predictor of cognitive decline and conversion to AD.
Research Support: Neurosciences Victoria
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