Muscle weakness and neuromuscular junctions in aging and disease.

A critical issue in today's super-aging society is the need to reduce the burden of family care while continuing to make our medical institutions supportive. A rapidly emerging, major health concern is the debilitating effect of muscle weakness and atrophy from aging, termed sarcopenia; however, the molecular basis of this condition is not well understood. Our research aim is to elucidate the molecular mechanisms of age-related muscle atrophy and to devise new measures for preventing and treating this disability. A promising treatment for muscle atrophy is the promotion of muscle regeneration by recruiting stem cells into the targeted region. The first requirement is to understand how the motor system, which consists of muscles and motoneurons, is maintained to accomplish that goal. Recent studies in the field of neuroscience have focused on neuromuscular junctions (NMJ), which play important roles in the maintenance of both motor nerves and muscle fibers. Signaling between muscles and motoneurons at NMJ supports interactions within the motor system. To understand the mechanisms involved, we focus our research on the pathogenic processes underlying neuromuscular diseases. The well-known autoimmune disease, myasthenia gravis (MG), serves as a model not only for tracking the pathogenesis and treatment outcomes of all autoimmune diseases, but also for understanding synaptic functions in maintaining the motor system. Here, we describe recent insights into the molecular mechanisms required for the maintenance of NMJ and the related causes of muscle atrophy.