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Dissociating memory networks in early Alzheimer’s disease and frontotemporal lobar degeneration: A combined study of hypometabolism and atrophy

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Frisch,  Stefan
Department Neurology, MPI for Human Cognitive and Brain Sciences, Max Planck Society;
Department of Neurology, Goethe University, Frankfurt, Germany;

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Dukart,  Jürgen
Department Neurology, MPI for Human Cognitive and Brain Sciences, Max Planck Society;
Laboratoire de Recherche en Neuroimagerie (LREN), Centre hospitalier universitaire vaudois, Lausanne, Switzerland;
Leipzig Research Center for Civilization Diseases (LIFE), University of Leipzig, Germany;

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Vogt,  Barbara
Max Planck Research Group Body and Self, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

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Horstmann,  Annette
Department Neurology, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

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Villringer,  Arno
Department Neurology, MPI for Human Cognitive and Brain Sciences, Max Planck Society;
Leipzig Research Center for Civilization Diseases (LIFE), University of Leipzig, Germany;

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Mueller,  Karsten
Methods and Development Unit Nuclear Magnetic Resonance, MPI for Human Cognitive and Brain Sciences, Max Planck Society;

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Schroeter,  Matthias L.
Department Neurology, MPI for Human Cognitive and Brain Sciences, Max Planck Society;
Leipzig Research Center for Civilization Diseases (LIFE), University of Leipzig, Germany;
German Consortium for Frontotemporal Lobar Degeneration (FTLD), Bonn, Germany;

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Citation

Frisch, S., Dukart, J., Vogt, B., Horstmann, A., Becker, G., Villringer, A., et al. (2013). Dissociating memory networks in early Alzheimer’s disease and frontotemporal lobar degeneration: A combined study of hypometabolism and atrophy. PLoS One, 8(2): e55251. doi:10.1371/journal.pone.0055251.


Cite as: https://hdl.handle.net/11858/00-001M-0000-000E-CA47-7
Abstract
Introduction We aimed at dissociating the neural correlates of memory disorders in Alzheimer’s disease (AD) and frontotemporal lobar degeneration (FTLD). Methods We included patients with AD (n=19, 11 female, mean age 61 years) and FTLD (n=11, 5 female, mean age 61 years) in early stages of their diseases. Memory performance was assessed by means of verbal and visual memory subtests from the Wechsler Memory Scale (WMS-R), including forgetting rates. Brain glucose utilization was measured by [18F]fluorodeoxyglucose positron emission tomography (FDG-PET) and brain atrophy by voxel-based morphometry (VBM) of T1-weighted magnetic resonance imaging (MRI) scans. Using a whole brain approach, correlations between test performance and imaging data were computed separately in each dementia group, including a group of control subjects (n=13, 6 female, mean age 54 years) in both analyses. The three groups did not differ with respect to education and gender. Results Patients in both dementia groups generally performed worse than controls, but AD and FTLD patients did not differ from each other in any of the test parameters. However, memory performance was associated with different brain regions in the patient groups, with respect to both hypometabolism and atrophy: Whereas in AD patients test performance was mainly correlated with changes in the parieto-mesial cortex, performance in FTLD patients was correlated with changes in frontal cortical as well as subcortical regions. There were practically no overlapping regions associated with memory disorders in AD and FTLD as revealed by a conjunction analysis. Conclusion Memory test performance may not distinguish between both dementia syndromes. In clinical practice, this may lead to misdiagnosis of FTLD patients with poor memory performance. Nevertheless, memory problems are associated with almost completely different neural correlates in both dementia syndromes. Obviously, memory functions are carried out by distributed networks which break down in brain degeneration.