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Comprehensive Autopsy Program for Individuals with Multiple Sclerosis
Published on: July 19, 2019
NAD(P)H:quinone oxidoreductase 1 expression in multiple sclerosis lesions
Jack van Horssen1, Gerty Schreibelt, Lars Bö
1Department of Molecular Cell Biology and Immunology, VU University Medical Center Amsterdam, P.O. Box 7057, 1007 MB Amsterdam, The Netherlands. j.vanhorssen@vumc.nl
Free Radical Biology & Medicine
|July 4, 2006
Summary
Multiple sclerosis (MS) involves central nervous system inflammation. This study found NAD(P)H:quinone oxidoreductase 1 (NQO1) is upregulated in MS lesions, suggesting a defense against oxidative stress.
Area of Science:
- Neuroimmunology
- Cellular Biology
- Biochemistry
Background:
- Multiple sclerosis (MS) is a chronic CNS inflammatory disease.
- Macrophages infiltrate the brain parenchyma in MS, releasing reactive oxygen species (ROS).
- ROS contribute to MS pathology, including myelin degradation and axonal damage.
Purpose of the Study:
- To investigate the expression and cellular distribution of NAD(P)H:quinone oxidoreductase 1 (NQO1) in MS lesions.
- To determine if NQO1 expression serves as an indicator of oxidative stress in MS.
Main Methods:
- Analysis of NQO1 expression in well-characterized MS lesions.
- Immunohistochemical examination of NQO1 cellular localization.
Main Results:
- NQO1 is significantly upregulated in active and chronic active MS lesions.
- High NQO1 expression was observed in hypertrophic astrocytes and myelin-laden macrophages.
- This upregulation suggests a cellular response to ROS-mediated toxicity.
Conclusions:
- NQO1 upregulation in MS lesions indicates an endogenous antioxidant defense mechanism.
- Targeting pathways that induce antioxidant enzymes like NQO1 may offer new therapeutic strategies for MS.
