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.
Multiple sclerosis (MS) is one of the most affecting autoimmune neurodegenerative disease characterized by chronic neuroinflammation, demyelination and impaired neuronal conduction. The oligodendrocytes toxicity by inflammatory cytokines and oxy-radicals are considered to be the most important factor in demyelination of motor neurons. The dysfunction of neuronal A1 adenosine receptor (A1AR) contributes to the demyelination of neurons by triggering the pro-inflammatory cytokines, oxy-radicals and neuroinflammatory cascades. In MS pathogenesis, Antigen presenting cells, MHC protein, CD4+T-cells, GM-CSF along with effector cells enhance the activation of macrophages in adenosinergic declined conditions, where it shows cumulative effects which leads to oligodendrocytes toxicity and demyelination of motor neurons. In general, A1AR is mainly expressed in macrophage lineage cells in central nervous system which could control the macrophage activation upon stimulation by its agonists. In this review, we have mainly emphasized on the pathogenesis of MS and highlighted the importance of adenosinergic system in reversing the molecular events in MS. In addition, we have discussed about the beneficial role of A1AR agonists in MS management.
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