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Abstract #2029

Noradrenaline shortage accelerates metabolic alterations in a transgenic model of Alzheimer´s disease

Takashi Watanabe1, Ana Martinez-Hernandez2, Jens Frahm1, and Thomas Michaelis1

1Biomedizinische NMR Forschungs GmbH, Max-Planck-Institut für biophysikalische Chemie, Göttingen, Germany, 2Abteilung Gene und Verhalten, Max-Planck-Institut für biophysikalische Chemie, Göttingen, Germany

Cerebral MRS of APP/PS1/Ear2(-/-) mice in vivo reveals significant alterations of several metabolites suggesting (i) an impaired cellular respiration compensated for by accelerated anaerobic glycolysis (i.e., elevated lactate), (ii) a loss of neurons (reduced N-acetylaspartate, glutamate, total creatine, and γ-aminobutyric acid) possibly compensated for by osmoregulators (elevated myo-inositol and taurine), (iii) an accumulation of paramagnetic iron (shortened water proton T2) possibly associated with inflammation, and (iv) subsequent gliosis (elevated myo-inositol). More specifically, a 60-75% reduction of noradrenaline is shown to accelerate the reduction of N-acetylaspartate and glutamate in the hippocampus as well as the T2-shortening in the frontal cortex.

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