1. Background
Myasthenia gravis (MG) is an autoimmune disease caused by autoantibodies attacking components of the postsynaptic membrane at the neuromuscular junction. The most common antigen targets are acetylcholine receptors (AChR), muscle-specific tyrosine kinase (MuSK), or AChR-associated proteins (DOI: 10.1038/s41572-019-0079-y). As a rare neurological disorder, MG can affect extraocular muscles, bulbar muscles, and even systemic skeletal muscles, leading to clinical manifestations such as ptosis, diplopia, dysphagia, and dysarthria. In severe cases, it can cause respiratory muscle weakness, leading to myasthenic crises that significantly impair patients' quality of life and endanger their safety (DOI: 10.1056/NEJMra1602678). Late-onset myasthenia gravis (LOMG) is a subtype of MG, primarily affecting individuals over 50 years old. It is characterized by unique features of immune senescence, such as a reduction in initial CD8⁺ T cells, and a lower incidence of thymoma. The pathogenesis of LOMG is more closely related to peripheral immune homeostasis disorders (DOI: 10.1172/jci.insight.199679) (DOI: 10.1016/j.heliyon.2024.e28893). Epidemiological studies have shown that the global prevalence of MG is 173.3 per million, with an annual incidence of approximately 15.7 per million. Although the incidence is relatively low, the disease burden has been increasing significantly due to population aging and improved diagnostic capabilities (DOI: 10.1159/000539577). Currently, while the use of cholinesterase inhibitors, glucocorticoids, immunosuppressants, and targeted biologics has somewhat improved patient outcomes, these traditional therapies often exhibit limited efficacy, significant side effects, and slow onset of action (DOI: 10.1007/s40259-024-00701-1). Additionally, the etiology of MG remains unclear, and it is currently believed to result from the combined effects of multiple factors, including genetic susceptibility, infections that trigger autoimmune responses, thymus abnormalities, and comorbidities with other autoimmune diseases (DOI: 10.1097/JS9.00000000000000164). However, these factors only explain some cases of the disease and cannot account for recent trends in the incidence of MG or regional variations in its distribution. Furthermore, primary prevention strategies for the general population need to be developed, and there is a lack of systematic exploration of environmental, metabolic, and lifestyle factors that may influence the onset of the disease. Therefore, a deeper understanding of the pathogenesis of MG and the identification of more effective intervention targets are urgent priorities in both clinical and basic research fields.
