Abstract #2939

Association of multiple sclerosis central fatigue with inhibitory and excitatory neurotransmitters

Jameen ARM^1,2, Georg Oeltzschner^3,4, Oun Al-Iedani^1,2, Rodney Lea^5,6, Jeannette Lechner-Scott^5,7,8, and Sadallah Ramadan^1,5

¹School of Health Sciences, University of Newcastle, Newcastle, Australia, ²Imaging centre, Hunter Medical Research Institute, Newcastle, Australia, ³The Russell H. Morgan Department of Radiology and Radiological Science, Johns Hopkins University School of Medicine, Baltimore, MD, United States, ⁴F. M. Kirby Research Center for Functional Brain Imaging, Kennedy Krieger Institute, Baltimore, MD, United States, ⁵HMRI Imaging centre, Hunter Medical Research Institute, Newcastle, Australia, ⁶School of Biomedical Sciences, Queensland University of Technology, Brisbane, Australia, ⁷Faculty of Health and Medicine, University of Newcastle, Newcastle, Australia, ⁸Department of Neurology, John Hunter Hospital, Newcastle, Australia

Despite neuro metabolic and morphological alterations linked to central fatigue in multiple sclerosis (MS), the pathophysiology of this symptom is not fully understood. Dysfunction of the GABAergic/Glutamatergic pathways involving inhibitory and excitatory neurotransmitters such as γ-aminobutyric acid (GABA) and glutamine+glutamate pools (Glx) have been implicated in several neurological disorders, including MS. In this study, we evaluated if GABA and Glx levels are associated with central fatigue in MS. Our results showed significant correlations of GABA and Glx levels with fatigue scores which suggest dysregulation of GABAergic/glutamatergic neurotransmission is possibly implicated in the mechanisms of mediating central fatigue in MS

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