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Brain Advance Access published online on October 25, 2009
Brain, doi:10.1093/brain/awp253
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© The Author (2009). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org

Posterior cingulate hypometabolism in early Alzheimer's disease: what is the contribution of local atrophy versus disconnection?

Gaël Chételat1, Nicolas Villain1, Béatrice Desgranges1, Francis Eustache1 and Jean-Claude Baron2

1 Inserm-EPHE-Université de Caen/Basse-Normandie, Unité U923, GIP Cyceron, CHU Côte de Nacre, Caen, France 2 Department of Clinical Neurosciences, Neurology Unit, University of Cambridge, Cambridge, UK

Correspondence to: Gaël Chételat, Inserm-EPHE-Université de Caen/Basse-Normandie, Unité U923, GIP Cyceron, Bd H. Becquerel, BP 5229, 14074 Caen Cedex, France E-mail: chetelat@cyceron.fr

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Sir, Garden et al. (2009Go) reported an important experimental study highlighting a potential mechanism for neuronal dysfunction distant from the site of damage, specifically a loss of synaptic plasticity in the retrosplenial/posterior cingulate cortex (PCC) after anterior thalamic lesion in the rat. In the discussion section of their article, they make the assumption that this phenomenon plays a role in the early episodic memory impairment characterizing Alzheimer's disease: the PCC would be disconnected from the anterior thalamic nucleus—affected by early neuronal/synaptic loss—through disruption of the cingulum bundle. This would in turn lead to PCC hypometabolism, which occurs very early in . . . [Full Text of this Article]


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