Abstract

Multiple sclerosis (MS) is a neurological condition with a complicated autoimmune component that mainly affects women in their forties and fifties. The disorder appears in several forms, ranging from episodic somatosensory impairment to progressive and irreversible central nervous system (CNS) injury. The fundamental cause of this disorder is lack of serotonin (5HT), a neurotransmitter with numerous immune effects. Decreased 5-HT levels or synthesis have also been related to increased proinflammatory cytokines in the CNS. Among several other proinflammatory cytokines, two prototypic pro-inflammatory cytokines, interleukin-1 (IL-1β) and tumor necrosis factor (TNF-α) have been identified as primary effectors of neuroinflammation's functional effects on neurodegeneration.TNF-α is a pleiotropic cytokine that regulates homeostasis, immunity, and inflammation and IL-1β is also a cytokine with neuroimmunological and neurophysiological functions. MS patients are usually on drugs that change the serotonergic system, because of increased clinical comorbidities and proven serotonin deficits. Several studies have shown that higher 5-HT levels have anti-inflammatory and immune-modulating properties, which could help to delay the progression of the disease.

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