title: Degeneration of neuromuscular junction in age and dystrophy.
abstract: Functional denervation is a hallmark of aging sarcopenia as well as of muscular dystrophy. It is thought to be a major factor reducing skeletal muscle mass, particularly in the case of sarcopenia. Neuromuscular junctions (NMJs) serve as the interface between the nervous and skeletal muscular systems, and thus they may receive pathophysiological input of both pre- and post-synaptic origin. Consequently, NMJs are good indicators of motor health on a systemic level. Indeed, upon sarcopenia and dystrophy, NMJs morphologically deteriorate and exhibit altered characteristics of primary signaling molecules, such as nicotinic acetylcholine receptor and agrin. Since a remarkable reversibility of these changes can be observed by exercise, there is significant interest in understanding the molecular mechanisms underlying synaptic deterioration upon aging and dystrophy and how synapses are reset by the aforementioned treatments. Here, we review the literature that describes the phenomena observed at the NMJ in sarcopenic and dystrophic muscle as well as to how these alterations can be reversed and to what extent. In a second part, the current information about molecular machineries underlying these processes is reported.
authors.affiliation: Institute of Molecular and Cell Biology, University of Applied Sciences Mannheim , Mannheim , Germany ; Institute of Medical Technology, University of Heidelberg and University of Applied Sciences Mannheim , Mannheim , Germany ; Institute of Toxicology and Genetics, Karlsruhe Institute of Technology , Eggenstein-Leopoldshafen , Germany.
authors.forename: Rüdiger
authors.initials: R
authors.lastname: Rudolf
authors.affiliation: Institute of Molecular and Cell Biology, University of Applied Sciences Mannheim , Mannheim , Germany ; Institute of Toxicology and Genetics, Karlsruhe Institute of Technology , Eggenstein-Leopoldshafen , Germany.
authors.forename: Muzamil Majid
authors.initials: MM
authors.lastname: Khan
authors.affiliation: Institute of Integrative Pathophysiology, University Medical Centre Mannheim , Mannheim , Germany.
authors.forename: Siegfried
authors.initials: S
authors.lastname: Labeit
authors.affiliation: Department of Kinesiology and Health Sciences, The College of William and Mary , Williamsburg, VA , USA.
authors.forename: Michael R
authors.initials: MR
authors.lastname: Deschenes
keywords: aging; dystrophy; exercise therapy; neuromuscular junction; sarcopenia