Abstract #3200

Longitudinal 9.4 Tesla 1H MRS in the thalamus of the Theiler’s encephalomyelitis virus (TMEV) mouse model of multiple sclerosis

Poonam Choudhary^1,2, Suyog Pol², Marilena Preda³, Michele Sveinsson², Robert Zivadinov^2,3, and Ferdinand Schweser^2,3

¹Department of Medical Physics, University at Buffalo, The State University of New York, Buffalo, NY, United States, ²Buffalo Neuroimaging Analysis Center, Department of Neurology, Jacobs School of Medicine and Biomedical Sciences, University at Buffalo, The State University of New York, Buffalo, NY, United States, ³Center for Biomedical Imaging at the Clinical and Translational Science Institute, University at Buffalo, The State University of New York, Buffalo, NY, United States

This study investigated thalamic metabolic alterations related to acute and chronic inflammation in mice infected with TMEV, a model of MS. TMEV-inoculation causes a biphasic neurological disease starting with an early acute inflammation of the subcortical gray matter (<1 month) and progressing into a late chronic demyelinating phase associated with oligodendroglial damage that develops into a neurodegenerative phase (>4 months).

Our hypothesis was that the influx of immune cells will result in increased glutamate and myoinositol in the acute phase, and that glutamate will further increase in the chronic phase whereas gamma-aminobutyric acid, N-acetylaspartate, and choline will decrease.

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