ArticleFrontiers in molecular neuroscience2025
Impaired peroxisomal beta-oxidation in microglia triggers oxidative stress and impacts neurons and oligodendrocytes.
Article in Frontiers in molecular neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed.
- Oxidative memory in microglia: persistent OSI-driven polarization and ıts modulation by mitochondrial dynamics (Mdivi-1).Experimental brain research · 2026Article
- Ganoderma lucidum mediates microglial polarization and ameliorates experimental autoimmune encephalomyelitis by reducing oxidative stress and inhibiting NF-κB/STAT3 pathway.Chinese medicine · 2026Article
- Lipid metabolism reprogramming: key mechanism of breast cancer endocrine therapy resistance.Frontiers in oncology · 2026Review
- Dysregulated lipid metabolism and hypomyelination in postnatal peroxisome-deficientFrontiers in molecular neuroscience · 2026Article
- Peroxisomes and the nervous system: progress and challenges in neuroinflammation and cell-specific functions.Frontiers in molecular neuroscience · 2026Article
- Lipid signature in X-ALD: a comparison between phenotypes.Frontiers in molecular biosciences · 2026Article
- Peroxisomes in Alzheimer's disease: emerging mechanistic insights and therapeutic opportunities.Frontiers in aging neuroscience · 2026Review
- Review
- Combined Maternal Immune Activation and Prenatal Intermittent Hypoxic Stress Lead to Developmental Motor Deficits in Rats: a Two-hit Animal Model for Cerebral Palsy Across Different Age Trajectories.Molecular neurobiology · 2025Article
- ZEB1 and Neural Stem Cells: Insights into Microglia-Conditioned Medium-Driven Neuroinflammation.Cells · 2025Article
- Histological and Functional Breakdown of the Blood-Brain Barrier in Alzheimer's Disease: A Multifactorial Intersection.Neurology international · 2025Review
- Review
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Abstract
Microglia, the immune cells of the central nervous system, activate neuroinflammatory pathways in response to homeostatic disturbances, a process implicated in the pathogenesis of various neurodegenerative diseases. Emerging evidence identifies abnormal microglial activation as a causal factor at the onset of peroxisomal leukodystrophies, including X-linked adrenoleukodystrophy (X-ALD). This study investigates how primary peroxisomal deficiencies influence oxidative properties of microglia and examines the subsequent impact on neurons and oligodendrocytes. Using BV-2 microglial cells lacking ABCD1, ABCD2, or ACOX1, peroxisomal proteins that play key roles in the very-long-chain fatty acid beta-oxidation, we analyzed their response under basal condition and after stimulation by lipopolysaccharide (LPS). Transcriptomic analysis of the mutant microglial cells revealed numerous differentially expressed genes, particularly in redox-related pathways following LPS exposure. These changes are consistent with the increased production of reactive oxygen species (ROS) and nitric oxide (NO). Conditioned media (CM) from the mutant cells were then applied to cultures of neuron and oligodendrocyte cell lines. Exposure to CM from LPS-stimulated mutant microglial cells significantly increased apoptosis in both cell types. Furthermore, treated neurons exhibited a reduction in cell complexity and an increased ability to secrete neuropeptides. These findings demonstrate that peroxisomal impairments in microglia exacerbate inflammatory response and ROS/NO production, affecting the survival of neurons and oligodendrocytes, as well as neuronal morphology and function. This dysfunction might contribute to the early neurodegenerative events in X-ALD by triggering and sustaining neuroinflammatory cascades. Therapeutic strategies that target microglial activation and secretion profiles could hold promise in managing peroxisomal disorders such as X-ALD.
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