title: Evidence for dying-back axonal degeneration in age-associated skeletal muscle decline.
abstract: Age-associated muscle strength decline is a major contributing factor to increased late-life functional decline and comorbidity, and is strongly associated with early mortality. Although all parts of the neuromuscular system seem to be affected by aging, dying-back of motor axons likely plays a major role.
  
  
  
  We compared the degeneration in ventral roots and neuromuscular junction denervation in young and aged mice and correlated the findings with strength and electrophysiological measures.
  
  
  
  With normal aging, there is little decline in motor axon numbers in the ventral roots, but the neuromuscular junctions show marked partial denervation that is associated with increased jitter on stimulated single fiber electromyography and a decrease in muscle strength.
  
  
  
  These findings suggest that dying-back axonal degeneration may be partially responsible for the electrophysiological and strength changes observed with aging. Muscle Nerve 55: 894-901, 2017.
authors.affiliation: Department of Physical Medicine and Rehabilitation, Johns Hopkins School of Medicine, Baltimore, Maryland, USA.
authors.forename: Tae
authors.initials: T
authors.lastname: Chung
authors.affiliation: Department of Neurology, Johns Hopkins School of Medicine, Baltimore, Maryland, 21205, USA.|Department of Physical Education, Kongju National University, Gongju, Republic of Korea.
authors.forename: Jae Sung
authors.initials: JS
authors.lastname: Park
authors.affiliation: Department of Neurology, Johns Hopkins School of Medicine, Baltimore, Maryland, 21205, USA.
authors.forename: Sangri
authors.initials: S
authors.lastname: Kim
authors.affiliation: Department of Physical Medicine and Rehabilitation, VA Caribbean Healthcare System, San Juan, Puerto Rico.
authors.forename: Nataly
authors.initials: N
authors.lastname: Montes
authors.affiliation: Department of Medicine, Johns Hopkins, Baltimore, Maryland, USA.
authors.forename: Jeremy
authors.initials: J
authors.lastname: Walston
authors.affiliation: Department of Neurology, Johns Hopkins School of Medicine, Baltimore, Maryland, 21205, USA.
authors.forename: Ahmet
authors.initials: A
authors.lastname: Höke
mesh_terms: D000375:Aging; D000818:Animals; D001369:Axons / Q000473:pathology*; D004576:Electromyography; D051379:Mice; D008810:Mice, Inbred C57BL; D009045:Motor Endplate / Q000473:pathology; D009121:Muscle Denervation; D053580:Muscle Strength / Q000502:physiology*; D018482:Muscle, Skeletal / Q000503:physiopathology*; D009410:Nerve Degeneration / Q000473:pathology* / Q000503:physiopathology*; D009469:Neuromuscular Junction / Q000378:metabolism / Q000473:pathology; D017729:Presynaptic Terminals / Q000473:pathology; D013126:Spinal Nerve Roots / Q000473:pathology; D014404:Tubulin / Q000378:metabolism
chemical_list: D014404:Tubulin; C462941:beta3 tubulin, mouse
keywords: SFEMG; denervation; distal axon; dying-back axonopathy; frailty; neuromuscular junction