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Neurosciences: Neurology |
1 Centre for PET, Austin Hospital, Melbourne, Victoria, Australia; ; 2 School of Psychology, Psychiatry and Psychological Medicine, Monash University, Melbourne, Victoria, Australia; ; 3 Cogstate Pty Ltd, Melbourne, Victoria, Australia; ; 4 Pathology, University of Melbourne, Melbourne, Victoria, Australia; ; 5 The Mental Health Research Institute of Victoria, Melbourne, Victoria, Australia
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Objectives: Up to 30% of healthy persons aged over 75 years show Aß deposition at autopsy. It is postulated that this represents preclinical Alzheimers disease (AD). We evaluated the relationship between Aß burden as assessed by PIB PET and cognitive decline in a predominantly normal elderly population. Methods: PIB PET and cognitive tests were performed on 33 elderly participants (age 73 ± 6) from the longitudinal Melbourne Healthy Ageing Study (MHAS). Subjects were classified as being cognitively "stable" or "declining" by an independent behavioral neurologist based on clinical assessment and annual word-list recall scores from the preceding six years. Rate of decline was calculated from the word-list recall scores. Aß burden was quantified using Standardized Uptake Value normalized to cerebellar cortex (SUVR). Results: Nine subjects were classified as declining. At the time of the PET scan, three subjects had MCI, one had Alzheimers disease (AD), and five were declining but remained in the normal range for age on cognitive tests. Seven of the 9 declining subjects and 3 of the 24 stable subjects, had cortical PIB binding. Aß burden correlated with memory impairment in the declining group (SUVR vs CVLT II delayed recall: r = -0.69, p < 0.0001) and with the rate of decline (r = -0.57, p = 0.0004). Conclusions: Declining subjects are much more likely to show cortical PIB retention than stable subjects. Aß burden as assessed by PIB PET correlates with memory impairment and the rate of memory decline in the ageing population. These observations suggest that Aß deposition is not part of normal ageing and is likely to represent preclinical AD. Further longitudinal observation is required to confirm this hypothesis.
Research Support (if any): Austin Hospital Medical Research Foundation, Neurosciences Victoria, and the University of Melbourne
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