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The prevalence of myasthenia gravis (MG) in people over 50 years of age is increasing, mainly because of the increase in the percentage of people aged 65 years and over in society. The clinical symptoms are the same as in early onset, but may be more difficult to detect in the elderly. Most MG patients with symptom onset after 50 years of age have thymic atrophy. Approximately 10–15% of all patients with MG have a thymoma. Antibodies to non-acetylcholine receptors, such as titin and the ryanodine receptor, are common in early-onset MG thymoma, and more than 40% of patients with late-onset MG have such antibodies. The outcome after thymectomy in MG is generally less favorable in patients over 45 years of age. Standard nonsurgical therapy for late-onset MG follows a similar pattern as for early onset.

Of sera of patients with myasthenia gravis (MG), 30% contains titin and ryanodine receptor (RyR) antibodies. In early-onset MG (i.e., before 50 years of age), the presence of titin antibodies strongly suggests a thymoma. Late-onset MG comprises one MG group, characterized by a broad antimuscle immune response, including both titin and the acetylcholine receptor (AChR). Another group is preferentially associated with the HLA-A3, B7 and DRw2 antigens, representing a delayed early-onset of the disease that has a selective AChR immune response. The presence of titin and RyR antibodies is associated with more severe disease. Titin antibodies may, in some patients with rippling muscle disease, affect the contractile machinery of myofibers, thereby affecting their mechanical sensitivity. It is not known whether this occurs in MG. RyR antibodies may impair excitation–contraction coupling and contribute to muscle weakness in MG patients. Titin antibodies may serve as tumor markers in early-onset MG patients.