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Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS) that is characterized by a severe and progressive demyelinating process. It is considered a neurodegenerative autoimmune disorder driven by immune cell infiltration, overproduction of cytokines and reactive oxygen species (ROS) accumulation that leads to axonal and neuronal injury. Experimental autoimmune encephalomyelitis (EAE) is the most commonly used pre-clinical model of multiple sclerosis (MS), since it resembles many aspects of the human disease. EAE can be induced in a variety of species and strains (rodents and monkeys), providing models of acute monophasic, relapsing-remitting and chronic progressive CNS inflammation. Thus, the pathology of the lesions varies according to the animal model used. We herein describe in detail a protocol for induction of EAE in C57BL/6 mice by immunization with MOG in CFA, which induces a monophasic, chronic and sustained form of EAE. In addition, we also describe approaches to evaluate disease induction and a technique for pathological examination of CNS tissues to assess ROS accumulation. This animal model could be useful for acute and chronic studies and to assess the effectiveness of different treatments.
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http://dx.doi.org/10.1016/bs.mcb.2025.03.024 | DOI Listing |
Mult Scler
September 2025
Department of Neurology with Friedrich Baur Institute, LMU University Hospital, LMU Munich, Munich, Germany.
Description of a patient with multiple sclerosis (MS) who underwent immunotherapy with ocrelizumab and suffered a severe course of tick-borne encephalitis (TBE): A 33-year-old man presented with acute cerebellitis with tonsillar herniation. The initial suspected diagnosis of TBE was confirmed after a significant diagnostic delay, likely caused by negative serological testing due to B-cell depletion from ocrelizumab treatment for underlying MS. TBE diagnosis was made using polymerase chain reaction (PCR) and oligo-hybrid capture metagenomic next-generation sequencing (mNGS) of cerebral spinal fluid and brain biopsy samples which yielded a near-full length TBE Virus (TBEV) genome.
View Article and Find Full Text PDFMult Scler
September 2025
Department of Neurology, Medical University of Vienna, Vienna, Austria; Comprehensive Center for Clinical Neurosciences and Mental Health, Medical University of Vienna, Vienna, Austria.
Neuroinflammation has emerged as a central and dynamic component of the pathophysiology underlying a wide range of neurodegenerative disorders, including Alzheimer's disease, Parkinson's disease, amyotrophic lateral sclerosis, Huntington's disease, and multiple sclerosis. Far from being a secondary consequence of neuronal damage, inflammatory processes (mediated by microglia, astrocytes, peripheral immune cells, and associated molecular mediators) actively shape disease onset, progression, and symptomatology. This review synthesizes current knowledge on the cellular and molecular mechanisms that govern neuroinflammatory responses, emphasizing both shared and disease-specific pathways.
View Article and Find Full Text PDFCell Death Differ
September 2025
Department of Neurology, China National Clinical Research Center for Neurological Diseases, Beijing Tiantan Hospital, Capital Medical University, Beijing, China.