Open Access Highly Accessed Research

18F-florbetaben Aβ imaging in mild cognitive impairment

Kevin Ong1, Victor L Villemagne123, Alex Bahar-Fuchs14, Fiona Lamb13, Gaël Chételat1, Parnesh Raniga5, Rachel S Mulligan1, Olivier Salvado5, Barbara Putz6, Katrin Roth6, Colin L Masters3, Cornelia B Reininger6 and Christopher C Rowe12*

Author Affiliations

1 Department of Nuclear Medicine and Centre for PET, Austin Health, 145 Studley Road, Heidelberg, VIC 3084, Australia

2 Department of Medicine, University of Melbourne, Parkville, VIC 3010, Australia

3 Mental Health Research Institute, 155 Oak Street, Parkville, VIC 3052, Australia

4 Centre for Research on Aging, Health, and Wellbeing, 63 Eggleston Road, The Australian National University, Acton, ACT 2600, Australia

5 CSIRO Preventative Health National Research Flagship, The Australian e-Health Research Centre - BioMedIA, Herston, QLD 4029, Australia

6 Bayer Pharma AG, Müllerstraße 178, 13353 Berlin, Germany

For all author emails, please log on.

Alzheimer's Research & Therapy 2013, 5:4  doi:10.1186/alzrt158

Published: 16 January 2013

Abstract

Introduction

18F-florbetaben and positron emission tomography were used to examine the relationships between β-amyloid (Aβ) deposition, cognition, hippocampal volume, and white matter hyperintensities in mild cognitive impairment (MCI).

Methods

Forty-five MCI participants were evaluated. A neocortical standardized uptake value ratio threshold ≥ 1.45 was used to discriminate high from low Aβ burden. Correlations were adjusted for age, gender and years of education.

Results

High Aβ burden was found in 53% of MCI. Regression analyses showed standardized uptake value ratio (r = -0.51, P = 0.0015) and hippocampal volume (r = 0.60, P = 0.024) both contributing to episodic memory impairment in independent fashion. White matter hyperintensities correlated with nonmemory cognition, and this correlation was particularly associated with Aβ burden.

Conclusion

Higher Aβ deposition in MCI is associated with more severe memory impairment and is contributing to early amnestic symptoms independent of hippocampal atrophy.