Abstract #2901

GluCEST imaging of spinal cord in a mouse model of Friedreich ataxia

Jérémy Pépin^1,2, Françoise Piguet^3,4,5,6, Hélène Puccio^3,4,5,6, and Julien Flament^1,7

¹CEA/DSV/I2BM/MIRCen, Fontenay-aux-Roses, France, ²CNRS Université Paris-Saclay UMR 9199, Fontenay-aux-Roses, France, ³Department of Translational Medecine and Neurogenetics, Institut de Génétique et de Biologie Moléculaire et Cellulaire, Illkirch, France, ⁴INSERM U596, Illkirch, France, ⁵CNRS UMR7104, Illkirch, France, ⁶Université de Strasbourg, Strasbourg, France, ⁷INSERM UMS 27, Fontenay-aux-Roses, France

Friedreich Ataxia (FA) is the most common form of recessive inherited ataxia which induces severe neurological disabilities and reduced life expectancy. As glutamate has been shown to be a potential biomarker of neurodegenerative diseases, we used Chemical Exchange Saturation Transfer imaging of glutamate (gluCEST) in order to characterize our mouse model of FA and to monitor glutamate alterations in the spinal cord. GluCEST images revealed decrease of glutamate level in FA mouse model compared to control littermates, especially in the lumbar part. These results demonstrate the potential of gluCEST in providing innovative and relevant biomarkers of FA.

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