Table of Contents
International Journal of Molecular Imaging
Volume 2013 (2013), Article ID 205045, 6 pages
Research Article

Cholinergic Depletion in Alzheimer’s Disease Shown by [18F]FEOBV Autoradiography

1Translational Neuroimaging Laboratory, McGill Centre for Studies in Aging, Douglas Mental Health University Institute, Montreal, Canada H4H 1R3
2Département de Psychologie, Université du Québec à Montreal (UQAM), Montreal, Canada H3C 3P8
3Department of Psychiatry, McGill University, Douglas Mental Health University Institute, Montreal, Canada H4H 1R2
4Montreal Neurological Institute (MNI), Montreal, Canada H3A 2B4

Received 5 June 2013; Revised 21 September 2013; Accepted 23 September 2013

Academic Editor: Guy Bormans

Copyright © 2013 Maxime J. Parent et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.


Rationale. Alzheimer’s Disease (AD) is a neurodegenerative condition characterized in part by deficits in cholinergic basalocortical and septohippocampal pathways. [18F]Fluoroethoxybenzovesamicol ([18F]FEOBV), a Positron Emission Tomography ligand for the vesicular acetylcholine transporter (VAChT), is a potential molecular agent to investigate brain diseases associated with presynaptic cholinergic losses. Purpose. To demonstrate this potential, we carried out an [18F]FEOBV autoradiography study to compare postmortem brain tissues from AD patients to those of age-matched controls. Methods. [18F]FEOBV autoradiography binding, defined as the ratio between regional grey and white matter, was estimated in the hippocampus (13 controls, 8 AD) and prefrontal cortex (13 controls, 11 AD). Results. [18F]FEOBV binding was decreased by 33% in prefrontal cortex, 25% in CA3, and 20% in CA1. No changes were detected in the dentate gyrus of the hippocampus, possibly because of sprouting or upregulation toward the resilient glutamatergic neurons of the dentate gyrus. Conclusion. This is the first demonstration of [18F]FEOBV focal binding changes in cholinergic projections to the cortex and hippocampus in AD. Such cholinergic synaptic (and more specifically VAChT) alterations, in line with the selective basalocortical and septohippocampal cholinergic losses documented in AD, indicate that [18F]FEOBV is indeed a promising ligand to explore cholinergic abnormalities in vivo.