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Article type: Research Article
Authors: Jessen, Franka; b; * | Lewczuk, Piotrc | Gür, Okand | Block, Wolfgange | Ende, Gabrielef | Frölich, Lutzf | Hammen, Thilog | Arlt, Sönkeh | Kornhuber, Johannesc | Kucinski, Thomasi | Popp, Juliusj | Peters, Oliverk | Maier, Wolfganga; b | Träber, Franke | Wiltfang, Jensl
Affiliations: [a] Department of Psychiatry, University of Bonn, Bonn, Germany | [b] German Centre for Neurodegenerative Diseases, Bonn, Germany | [c] Department of Psychiatry, University of Erlangen, Erlangen, Germany | [d] Department of Nuclear Medicine, University of Bonn, Bonn, Germany | [e] Department of Radiology, University of Bonn, Bonn, Germany | [f] Central Institute of Mental Health, Mannheim, Germany | [g] Center for Epilepsy, Department of Neurology, University of Erlangen, Erlangen, Germany | [h] Department of Psychiatry, University of Hamburg, Hamburg, Germany | [i] Department of Neuroradiology, Karolinska University Hospital, and Department of Clinical Neuroscience, Karolinska Institute, Stockholm, Sweden | [j] Department of Psychiatry – SUPAA, Lausanne University Hospital, Lausanne, Switzerland | [k] Department of Psychiatry, Charité-University Medicine Berlin, Berlin, Germany | [l] Department of Psychiatry, University Essen, Essen, Germany
Correspondence: [*] Correspondence to: Frank Jessen, MD, Department of Psychiatry, University of Bonn, Sigmund-Freud-Str. 25, 53105 Bonn, Germany. Tel.: +49 228 287 11109; Fax: +49 228 287 16097; E-mail: Frank.Jessen@ukb.uni-bonn.de.
Abstract: The interplay of amyloid and mitochondrial function is considered crucial in the pathophysiology of Alzheimer's disease (AD). We tested the association of the putative marker of mitochondrial function N-acetylaspartate (NAA) as measured by proton magnetic resonance spectroscopy within the medial temporal lobe and cerebrospinal fluid amyoid-β42 (Aβ42), total Tau and pTau181. 109 patients were recruited in a multicenter study (40 mild AD patients, 14 non-AD dementia patients, 29 mild cognitive impairment (MCI) AD-type patients, 26 MCI of non-AD type patients). NAA correlated with Aβ42 within the AD group. Since the NAA concentration is coupled to neuronal mitochondrial function, the correlation between NAA and Aβ42 may reflect the interaction between disrupted mitochondrial pathways and amyloid production.
Keywords: Alzheimer's disease, amyloid-β42, N-acetylaspartate, medial temporal lobe, mitochondria, proton MR spectrocopy
DOI: 10.3233/JAD-2011-110398
Journal: Journal of Alzheimer's Disease, vol. 27, no. 2, pp. 393-399, 2011
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