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Cerebral iron accumulation in multiple sclerosis: Pathophysiology and therapeutic implications.
Autoimmun Rev
January 2025
Department of Chemical, Physical, Mathematical and Natural Sciences, University of Sassari, Italy.
Multiple sclerosis (MS) is a chronic autoimmune disorder of the central nervous system characterized by demyelination, neuroinflammation, and neurodegeneration. Recent studies highlight the role of cerebral iron (Fe) accumulation in exacerbating MS pathophysiology. Fe, essential for neural function, contributes to oxidative stress and inflammation when dysregulated, particularly in the brain's gray matter and demyelinated lesions.
View Article and Find Full Text PDFNuclear receptor PPARγ targets GPNMB to promote oligodendrocyte development and remyelination.
Brain
January 2025
Key Laboratory of Medicinal Resources and Natural Pharmaceutical Chemistry (Shaanxi Normal University), The Ministry of Education; College of Life Sciences, Shaanxi Normal University, Xi'an 710119, China.
Myelin injury occurs in brain ageing and in several neurological diseases. Failure of spontaneous remyelination is attributable to insufficient differentiation of oligodendrocyte precursor cells (OPCs) into mature myelin-forming oligodendrocytes in CNS demyelinated lesions. Emerging evidence suggests that peroxisome proliferator-activated receptor γ (PPARγ) is the master gatekeeper of CNS injury and repair and plays an important regulatory role in various neurodegenerative diseases.
View Article and Find Full Text PDFAberrant Complement Activation Is Associated With Structural Brain Damage in Multiple Sclerosis.
Neurol Neuroimmunol Neuroinflamm
March 2025
Department of Neurology with Institute of Translational Neurology, University Hospital 4 Münster, Germany.
Article Synopsis
- Elevated levels of activated complement proteins in cerebrospinal fluid (CSF) are linked to increased severity of multiple sclerosis (MS) and correlate with brain imaging and disease biomarkers.
- A study involving 239 patients analyzed various complement components and liquid biomarkers in CSF, finding specific proteins like C4a, Ba, and C3a strongly associated with accelerated brain atrophy and lesion formation.
- Results indicate that higher levels of these complement proteins are predictive of greater brain volume loss and increased development of lesions, suggesting their potential role as biomarkers for disease progression in MS.
Optical Assay of the Functional Impact of Cuprizone-Induced Demyelination and Remyelination on Interhemispheric Neural Communication in the Anterior Cingulate Cortex via the Corpus Callosum.
eNeuro
January 2025
Graduate School of Pharmaceutical Science, Tokushima Bunri University, Sanuki 769-2193, Japan
Cuprizone (CPZ) is a widely used toxin that induces demyelinating diseases in animal models, producing multiple sclerosis (MS)-like pathology in rodents. CPZ is one of the few toxins that triggers demyelination and subsequent remyelination following the cessation of its application. This study examines the functional consequences of CPZ-induced demyelination and the subsequent recovery of neural communication within the anterior cingulate cortex (ACC), with a particular focus on interhemispheric connectivity via the corpus callosum (CC).
View Article and Find Full Text PDFBrain organoid methodologies to explore mechanisms of disease in progressive multiple sclerosis.
Front Cell Neurosci
December 2024
Department of Clinical Neurosciences and NIHR Biomedical Research Centre, University of Cambridge, Cambridge, United Kingdom.
Multiple sclerosis (MS), a debilitating autoimmune disorder targeting the central nervous system (CNS), is marked by relentless demyelination and inflammation. Clinically, it presents in three distinct forms: relapsing-remitting MS (RRMS), primary progressive MS (PPMS), and secondary progressive MS (SPMS). While disease-modifying therapies (DMTs) offer some relief to people with RRMS, treatment options for progressive MS (pMS) remain frustratingly inadequate.
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