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Multiple sclerosis is characterized by inflammatory processes occurring within the central nervous system. In multiple sclerosis, inflammation could be either a physiological response secondary to the immune system activation or a phenomenon triggered by primary cytodegeneration of neurons and/or oligodendrocytes without the involvement of immune cells. The arachidonic acid metabolism is activated via cyclooxygenases (COXs) and lipoxygenases (LOXs) in postmortem brain samples and in the cerebrospinal fluid of multiple sclerosis patients. It has been hypothesized that the arachidonic acid–mediated neuroinflammation could play a role in the pathogenic mechanisms triggering demyelination, oligodendrocyte loss, axonal pathology and, ultimately, motor dysfunctions, which are hallmarks of multiple sclerosis. COX-2 and 5-LOX selective inhibitors efficiently inhibit each of the hallmarks mentioned above in different animal models of multiple sclerosis. Thus, it is suggested that the arachidonic acid pathway represents a potential pharmacological target to ameliorate multiple sclerosis pathology and symptoms.
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