Abstract
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Objectives Assess Aβ deposition longitudinally in subjects with Mild Cognitive Impairment (MCI) and explore its relationship with cognition and disease progression.
Methods Clinical and neuropsychological examination, 18F-Florbetaben PET (FBB-PET) and 3D MPRAGE MRI were performed at study entry and 12 and 24 months in 45 subjects with MCI. Hippocampal volume (HV) was assessed with Neuroquant®. The age adjusted 25th percentile was used to define hippocampal atrophy (HA). Aβ burden was quantified using SUVR (cerebellar cortex as reference region). Cut-off for low vs high SUVR was 1.4. Cox Proportional Hazards were used to calculate relative risk (RR) adjusted for age, gender and years of education.
Results At baseline 53% of the MCI participants had high neocortical FBB binding while 76% had hippocampal atrophy. Composite memory scores correlated with both neocortical SUVR (r=-0.60, p<0.0001) and HV (r=0.39, p=0.02). At 24-month follow-up, increase in neocortical SUVR was observed in MCI with high-FBB (+3.1%, p=0.02). Progression to AD occurred in 75% of MCI with high-FBB (RR 10.9 p<0.0001) and 53% of MCI with HA (RR 4.1 p=0.03). HA lost significance in multivariate analysis. Of MCI with both high FBB and HA, 80% progressed to AD. Of the low-FBB MCI, 19% progressed to other dementias. For progression to any dementia, HA had a predictive RR 5.0, p=0.009.
Conclusions High 18F-Florbetaben binding indicates a very high risk of progression from MCI to Alzheimer’s disease within two years (RR 10.9) and was a stronger and more specific risk factor than hippocampal atrophy in this cohort.
Research Support Supported in part by NHMRC grant 509016 and Bayer HealthCare