Multiple sclerosis (MS) is a neurological disease characterized by chronic inflammation of the central nervous system and demyelination of the white matter. While the etiology of the disease remains unclear, inflammation and demyelination in MS stand out as the most important pathophysiological conditions. Various clinical symptoms are observed in MS as a result of the apoptosis of oligodendrocytes and the loss of myelin structure. Clinical symptoms of the disease include fatigue, muscle weakness, blindness, loss of sensation, anxiety, depression, and cognitive disorders. Although there is no definitive cure for MS disease, various treatment agents are used to improve the symptoms of the disease. The safety and effectiveness of the agents used for treatment need to be improved. In this context, various animal models are used to elucidate the pathophysiology and treatment of MS disease. In this research, two of the most widely used experimental animal modeling methods were evaluated. The first model is the Experimental Autoimmune/Allergic Encephalomyelitis Model (DOE). The administration of this model antigens to animals creates a chronic MS disease picture characterized by central inflammation, demyelination, and axonal damage. This model is created by injecting an adjuvant (Freund's adjuvant) containing Mycobacterium tuberculosis fragments subcutaneously (s.c). Thanks to the encephalomyelitis model, we can learn more about the pathogenesis of MS and better explain the relationship between demyelination and the immune system. The second model is cuprizone-induced demyelination, which has started to be used more in experimental research in recent years. Cuprizone (CPZ) is a copper chelator with neurotoxic properties. CPZ, when administered mixed with diets, causes demyelination in the corpus callosum in the central nervous system. It induces apoptosis in oligodendrocytes resulting in spontaneous remyelination in CPZ-fed animals. With Multiple sclerosis clinical scoring, created using modeling techniques, disease severity is evaluated using a scale ranging from 0 to 10. The pathophysiology of the disease is quite complex and involves different cell types, antigens, genetic predisposition, and environmental factors. In animal modeling of MS disease, there are no experimental models that cover all the clinical, pathological, and immune features of the disease. Additional models and new approaches are needed to increase the diversity of experimental modeling to cover the specific features of MS disease. ORCID NO: 0000-0002-7293-0974
Anahtar Kelimeler: Multiple sclerosis, animal models, pathophysiology
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