Abstract
The neuromuscular junction (NMJ) is the synapse joining the motor neuron with the myofiber(s) that are innervated by an excitatory neuron, enabling the proper function of the neuromuscular system. Since sarcopenia is currently defined mainly by age-related declines in muscle function, rather than mass, the importance of understanding age-related degeneration of the NMJ has grown in importance. Morphological and physiological disruptions of the NMJ significantly contribute to, and are at the core of, age-related decrements in muscle strength and power, and thus, the larger phenomenon of sarcopenia. Opposing explanations of “dying forward” and “dying back” have been proposed to explain the beginning and progression of sarcopenia. Likely, both play roles, but in distinct components of the neuromuscular system. Here, we examine the effects of age-related deterioration of the NMJ on muscle function, and thus sarcopenia, an increasingly common malady that imposes severe health and financial burdens on societies throughout the world.
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