Vladimir Mlynarik1,
Lili Sun-Reimer1,
1Laboratory of Functional
& Metabolic Imaging, Ecole Polytechnique Fdrale de Lausanne, Lausanne,
Switzerland; 2Brain Mind Institute, Ecole Polytechnique Fdrale
de Lausanne, Lausanne, Switzerland; 3Departments of Radiology,
Universities of Lausanne & Geneva, Switzerland
A new transgenic mouse model of Alzheimer's disease was studied by in vivo by proton and phosphorus MR spectroscopy. This model developed changes in the neurochemical profile, which are characteristic for the human form of this disease (an increase in myo-inositol and a decrease in N-acetylaspartate), as early as in the 40th week of age. In addition, a significant decrease of GABA was observed in the transgenic mice compared with controls. The pseudo-first-order rate constant of the creatine kinase reaction as well as relative concentrations of phosphorus-containing metabolites were not changed significantly in the 36-week old transgenic mice. These results suggest that mitochondrial activity in the 5xFAD mice at this age is sufficient.