Neuromuscular sarcopenia: what do we know?

Sarcopenia is a common and relevant health problem in the treatment of geriatric patients. After many years of dealing with the definition of this phenomenon, the focus in the future must be on underlying and treatable pathomechanisms.

The article describes the initial state with regard to the definition of sarcopenia and derives from this the focus on subgroups of sarcopenia with treatable pathomechanisms. One subgroup of neuromuscular sarcopenia, which focuses on the degeneration of the neuromuscular junction, is discussed. In this context, the proteoglycan agrin with its ability to cluster acetylcholine receptors in the postsynaptic membrane of the muscle plays a role. Inactivation of agrin leads to destabilization of the neuromuscular junction and thus to sarcopenia. The resulting neuronal 22 kDa C-terminal agrin fragment should serve as a biomarker of neuromuscular sarcopenia.

The neuronal C-terminal agrin fragment must be established as a biomarker for neuromuscular sarcopenia, taking renal function into account as the fragment accumulates in renal insufficient patients. On this basis, treatment with agrin could be a therapeutic option for this subgroup of sarcopenia.