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Metabolomics approaches in experimental allergic encephalomyelitis
S Battini1, C Bund2, F M Moussallieh3
1ICube, UMR 7357 University of Strasbourg/CNRS, France.
Journal of Neuroimmunology
|December 12, 2017
Summary
This study identifies metabolic biomarkers for inflammation in experimental allergic encephalomyelitis (EAE). Decreased N-acetyl-aspartate (NAA) in the spinal cord correlates with disease severity.
Area of Science:
- Neuroscience
- Immunology
- Biochemistry
Background:
- Experimental allergic encephalomyelitis (EAE) is an autoimmune disease model.
- EAE is induced by myelin basic protein (MBP) and causes spinal cord inflammation and paraplegia.
- Understanding the metabolic changes during EAE is crucial for developing treatments.
Purpose of the Study:
- To identify metabolic biomarkers of inflammation in EAE.
- To pinpoint the location of central nervous system (CNS) inflammation during acute EAE.
- To utilize metabolomics for disease insight.
Main Methods:
- Induction of EAE in a preclinical model.
- Metabolomic analysis of CNS samples.
- Correlation of metabolic profiles with clinical signs.
Main Results:
- EAE samples showed elevated lactate, ascorbate, glucose, and amino acids compared to controls.
- A significant decrease in N-acetyl-aspartate (NAA) was observed in EAE samples.
- Reduced NAA levels were specifically noted in the lumbar spinal cord, correlating with clinical symptoms.
Conclusions:
- Metabolomic profiling can identify biomarkers for EAE inflammation.
- N-acetyl-aspartate (NAA) decrease is a potential biomarker for CNS inflammation in EAE.
- Lumbar spinal cord inflammation is a key feature associated with clinical signs in EAE.

