ArticleMetabolic brain disease2020
Nrf2 deficiency increases oligodendrocyte loss, demyelination, neuroinflammation and axonal damage in an MS animal model.
Article in Metabolic brain disease, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 53 citations in OpenAlex.
- Targeting neuroinflammation in neurodegenerative disorders: the emerging potential of semaglutide.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Synergistic Modulation of Microglial Polarization by Acteoside and Ferulic Acid via Dual Targeting of Nrf2 and RORγt to Alleviate Depression-Associated Neuroinflammation.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- The Role of Oligodendrocyte Lineage Cells in the Pathogenesis of Alzheimer's Disease.Neurochemical research · 2025Review
- The transcriptional and cellular landscape of cognitive resilience to Alzheimer's disease.Frontiers in molecular neuroscience · 2025Review
- Multitarget Effects of Nrf2 Signalling in the Brain: Common and Specific Functions in Different Cell Types.Antioxidants (Basel, Switzerland) · 2024Review
- Microglial Neuroinflammation-Independent Reversal of Demyelination of Corpus Callosum by Arsenic in a Cuprizone-Induced Demyelinating Mouse Model.Molecular neurobiology · 2024Article
- The Antioxidant Drug Edaravone Binds to the Aryl Hydrocarbon Receptor (AHR) and Promotes the Downstream Signaling Pathway Activation.Biomolecules · 2024Article
- Neuroprotective effects of rutin against cuprizone-induced multiple sclerosis in mice.Inflammopharmacology · 2024Article
- The cell-specific roles of Nrf2 in acute and chronic phases of ischemic stroke.CNS neuroscience & therapeutics · 2024Review
- Mechanisms Governing Oligodendrocyte Viability in Multiple Sclerosis and Its Animal Models.Cells · 2024Review
- Bifidobacterium breve Probiotic Compared to Lactobacillus casei Causes a Better Reduction in Demyelination and Oxidative Stress in Cuprizone-Induced Demyelination Model of Rat.Molecular neurobiology · 2024Article
- The Potential Association Between microRNA 135-5P and p62 and Their Effect on NRF2 Pathway in Multiple Sclerosis.Reports of biochemistry & molecular biology · 2024Article
- The untapped potential of targeting NRF2 in neurodegenerative disease.Frontiers in aging · 2023Article
- Article
- Exogenous Antioxidants in Remyelination and Skeletal Muscle Recovery.Biomedicines · 2022Review
- Dysfunction of the oligodendrocytes in amyotrophic lateral sclerosis.Journal of biomedical research · 2022Article
- Neurodegeneration in Multiple Sclerosis: The Role of Nrf2-Dependent Pathways.Antioxidants (Basel, Switzerland) · 2022Review
- Paeonol Ameliorates Cuprizone-Induced Hippocampal Demyelination and Cognitive Deficits through Inhibition of Oxidative and Inflammatory Events.Journal of molecular neuroscience : MN · 2022Article
- Fetal Zone Steroids Show Discrete Effects on Hyperoxia-Induced Attenuation of Migration in Cultured Oligodendrocyte Progenitor Cells.Oxidative medicine and cellular longevity · 2022Article
- Glial Purinergic Signaling-Mediated Oxidative Stress (GPOS) in Neuropsychiatric Disorders.Oxidative medicine and cellular longevity · 2022Review
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Oxidative stress is a pathophysiological hallmark of many CNS diseases, among multiple sclerosis (MS). Accordingly, boosting the astrocytic transcription factor nuclear factor E2-related factor 2 (Nrf2) system in an MS mouse model efficiently ameliorates oligodendrocyte loss, neuroinflammation and axonal damage. Moreover, Dimethylfumarate, an efficient activator of Nrf2, has recently been approved as therapeutic option in MS treatment. Here, we use the cuprizone mouse model of MS to induce oxidative stress, selective oligodendrocyte loss, microglia and astrocyte activation as well as axonal damage in both wild type and Nrf2-deficient mice. We found increased oligodendrocyte apoptosis and loss, pronounced neuroinflammation and higher levels of axonal damage in cuprizone-fed Nrf2-deficient animals when compared to wild type controls. In addition, Nrf2-deficient animals showed a higher susceptibility towards cuprizone within the commissura anterior white matter tract, a structure that is relatively insensitive to cuprizone in wild type animals. Our data highlight the cuprizone model as a suitable tool to study the complex interplay of oxidative stress, neuroinflammation and axonal damage. Further studies will have to show whether distinct expression patterns of Nrf2 are involved in the variable susceptibility towards cuprizone in the mouse.
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