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Brain Advance Access originally published online on October 10, 2007
Brain 2007 130(11):2837-2844; doi:10.1093/brain/awm238
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© 2007 The Author(s)
This is an Open Access article distributed under the terms of the Creative Commons Attribution Non-Commercial License (http://creativecommons.org/licenses/by-nc/2.0/uk/) which permits unrestricted non-commercial use, distribution, and reproduction in any medium, provided the original work is properly cited

ß-amyloid imaging and memory in non-demented individuals: evidence for preclinical Alzheimer's disease

Kerryn E. Pike1, Greg Savage1,8, Victor L. Villemagne2,3,4, Steven Ng2, Simon A. Moss1, Paul Maruff3,4,5, Chester A. Mathis6, William E. Klunk6, Colin L. Masters3,4 and Christopher C. Rowe2,7

1School of Psychology, Psychiatry and Psychological Medicine, Monash University, Melbourne, 2Department of Nuclear Medicine, Centre for PET, Austin Health, Heidelberg, 3Centre for Neurosciences, University of Melbourne, 4The Mental Health Research Institute, Parkville, 5Cogstate Pty Ltd, Melbourne, Victoria, Australia, 6Departments of Radiology and Psychiatry, University of Pittsburgh, PA, USA and 7Department of Medicine, Austin Health, University of Melbourne, Victoria, Australia

Correspondence to: Christopher Rowe, Department of Nuclear Medicine, Centre for PET, Austin Health, Studley Road, Heidelberg, Victoria 3084, Australia E-mail: christopher.rowe{at}austin.org.au

ß-amyloid (Aß) deposition is pathognomic for Alzheimer's disease (AD), but may occur in normal elderly people without apparent cognitive effect. Episodic memory impairment is an early and prominent sign of AD, but its relationship with Aß burden in non-demented persons and in AD patients is unclear. We examined this relationship using 11C-PIB-PET as a quantitative marker of Aß burden in vivo in healthy ageing (HA), mild cognitive impairment (MCI) and AD. Thirty-one AD, 33 MCI and 32 HA participants completed neuropsychological assessment and a 11C-PIB-PET brain scan. Multiple linear regression analyses were conducted relating episodic memory performance and other cognitive functions to Aß burden. Ninety-seven percent of AD, 61% of MCI and 22% of HA cases had increased cortical PIB binding, indicating the presence of Aß plaques. There was a strong relationship between impaired episodic memory performance and PIB binding, both in MCI and HA. This relationship was weaker in AD and less robust for non-memory cognitive domains. Aß deposition in the asymptomatic elderly is associated with episodic memory impairment. This finding, together with the strong relationship between PIB binding and the severity of memory impairment in MCI, suggests that individuals with increased cortical PIB binding are on the path to Alzheimer's disease. The data also suggests that early intervention trials for AD targeted to non-demented individuals with cerebral Aß deposition are warranted.

Key Words: memory performance; Alzheimer's disease; mild cognitive impairment; beta-amyloid; PET imaging

Abbreviations: AD, Alzheimer's disease; MCI, mild cognitive impairment; SUV, standardized uptake value

.

Received June 29, 2007. Revised August 14, 2007. Accepted September 5, 2007.

8Present address: Macquarie Centre for Cognitive Science (MACCS), Macquarie University, Sydney, NSW, Australia


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