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

Abstract : Sir, Garden et al. (2009) 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 Alzheimer's disease and already at the stage of amnestic mild cognitive impairment (Minoshima et al., 1997, Chételat et al., 2003a, b). The study by Garden et al. (2009) is therefore important for the understanding of the pathophysiology of the memory impairment that characterizes early Alzheimer's disease as the proposed underlying synaptic mechanism could be amenable to specific pharmacological modulation.
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Brain - A Journal of Neurology , Oxford University Press (OUP), 2009, 132 (Pt 12), e133; author reply e134. 〈10.1093/brain/awp253〉
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Gaël Chételat, Nicolas Villain, Béatrice Desgranges, Francis Eustache, Jean-Claude Baron. Posterior cingulate hypometabolism in early Alzheimer's disease: what is the contribution of local atrophy versus disconnection?. Brain - A Journal of Neurology , Oxford University Press (OUP), 2009, 132 (Pt 12), e133; author reply e134. 〈10.1093/brain/awp253〉. 〈inserm-00538450〉

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