سامانه همایش های دانشگاه آزاد اسلامی واحد نجف آباد

صفحه اصلی / اولین همایش بین المللی تحول خدمات سلامت: تلفیق مراقبت، درمان، بازتوانی و امیدبخشی

Myelin protection and remyelination in cuprizone animal model of multiple sclerosis

نویسندگان :

Sahar Ghosouri¹

1- دانشگاه آزاد اسلامی واحد نجف آباد

کلمات کلیدی :

مولتیپل اسکلروزیس،بیماری التهابی،سمی،عصبی،بهبود

چکیده :

Background: Multiple sclerosis (MS) is a chronic inflammatory disease characterized by myelin destruction in central nervous system. One of the main causes of neurological disability in MS is demyelination (1). Although immunomodulatory treatments decrease relapse rates, but these pharmacological compounds cannot stop demyelination and MS progression. The cuprizone model has gained popularity among research and industrial groups due to its high reproducibility and ease of use (2). Therefore, in the present study, toxic animal model for improvement of re-myelination in MS was investigated. Method: A literature search was conducted in PubMed, Google Scholar, Scopus and Web of Science to identify articles published on treatment of MS. Finding: Cuprizone-induced demyelination occurs through two distinct yet overlapping mechanisms: intrinsic cell damage originating within oligodendrocytes and extrinsic cellular damage exerted by inflammatory molecules and resident glial cells. Evidence indicated that the application of neurotrophic factors on the cuprizone animal model could upregulated Olig2 and MBP genes expression and can decrease oligodendrocyte death (3). Following cessation of cuprizone intoxication, endogenous remyelination proceeds through a well-characterized sequence: activation of oligodendrocyte progenitor cells (OPCs), their proliferation and migration to demyelinated areas, and finally differentiation into mature myelinating oligodendrocytes (4.5). The cuprizone model has also illuminated gut-brain axis involvement in demyelination and remyelination. Conclusion: The cuprizone model continues to provide crucial insights into the mechanisms of myelin protection and repair, enabling evaluation of diverse therapeutic strategies from targeted receptor agonism and non-invasive neuromodulation to metabolic interventions.