In addition, aging has been linked to deleterious physiological alterations. Hence, their degeneration would inevitably compromise motor function. These sensory neurons detect changes in the amount and rate of muscle contraction, and utilize this information to coordinate and modulate the activity of α-motor neurons. For example, we recently showed that IA/II proprioceptive sensory neuron soma and nerve ending at muscle spindles degenerate with increasing age and progression of amyotrophic lateral sclerosis (ALS) in mice (Vaughan, Kemp, Hatzipetros, Vieira & Valdez, 2015 Vaughan, Stanley & Valdez, 2016). Age- and disease-related motor deficits occur because of deleterious changes in neuronal and non-neuronal components of the somatic nervous system (Bennett et al., 1996 Boillée et al., 2006 Dentel et al., 2013 Fiatarone & Evans, 1993). Aging compromises gait speed, balance, and the command of fine motor skills (Fried, Ferrucci, Darer, Williamson & Anderson, 2004 Sorond et al., 2015), increasing the risk of injury due to falls and age-associated diseases (Ambrose, Paul & Hausdorff, 2013 Bennett et al., 1996 Camicioli, Moore, Sexton, Howieson & Kaye, 1999 Martin, 2011 Richards, Stern & Mayeux, 1993 Soriano, DeCherrie & Thomas, 2007 Verghese, Wang, Lipton, Holtzer & Xue, 2007). Motor function progressively erodes as individuals transition from adulthood into old age. These findings broaden our understanding of the degeneration of the somatic motor system that precipitates motor dysfunction with advancing age. Thus, the loss of synaptic inputs may contribute to age-related dysfunction of α-motor neurons. However, in aged rhesus monkeys and mice, there were fewer cholinergic and glutamatergic synaptic inputs directly abutting α-motor neurons, evidence that aging causes α-motor neurons to shed synaptic inputs. Moreover, the transcripts and proteins associated with α-motor neurons do not decrease in the spinal cord of old mice. In fact, there is no difference in the number of motor axons populating ventral roots in old mice compared to adult mice. Although the rate of aging varies, α-motor neurons do not atrophy in old age. ![]() ![]() Interestingly, the lipofuscin profile varied considerably, indicating that α-motor neurons age at different rates. We found that, in both species, α-motor neurons retain their soma size despite an accumulation of large amounts of cellular waste or lipofuscin. In this study, we examined the soma of α-motor neurons and innervating synaptic inputs in the spinal cord of aged rhesus monkeys and mice, two species with vastly different lifespans. While it is well established that skeletal muscles and neuromuscular junctions (NMJs) degenerate with increasing age, the effect of aging on α-motor neurons and their innervating synaptic inputs remains largely unknown. Motor function deteriorates with advancing age, increasing the risk of adverse health outcomes.
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