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. 2022 Jan 4;44(3):1199–1213. doi: 10.1007/s11357-021-00510-2

Table 1.

Effect of aging on key neuromuscular junction (NMJ) mediators and the possible outcomes in the NMJ that may contribute to sarcopenia

Mediator Effect of aging Possible outcomes in NMJ References
Presynaptic signaling
P/Q-type VGCC • ↓ P/Q-type VGCC activity [48]
• ↓ Calcium influx
Bassoon • ↓ Signal transmission [40, 42, 48]
• ↓ Muscle contraction
ACh • NMJ fragmentation [58]
• Denervation
• Axon sprouting
Agrin • NMJ fragmentation [77]
• Nerve terminal branching
• Denervation
• Smaller AChRs clusters
LRP4 • ↓ Agrin-LRP4-MuSK signaling [68]
p-MuSK
BDNF (serum) • Denervation (?) [8991]
• ↓ ACh release (?)
• ↓ Synapse maintenance (?)
BDNF (mRNA) = • ——————— [67]
GDNF (mRNA) • ↓ ACh release (?) [95]
GDNF =/↓ • ↓ Postsynaptic maintenance (?)
Postsynaptic signaling
CGRP • ↓ Reinnervation (?) [77]
GAP-43 [77, 113]

ACh, acetylcholine; AChRs, acetylcholine receptors; BDNF, brain-derived neurotrophic factor; CGRP, calcitonin gene–related protein; GAP-43, growth-associated protein; GDNF, glial-cell-line-derived neurotrophic factor; LRP4, low-density lipoprotein receptor–related protein 4; p-MuSK, phosphorylated muscle-specific kinase; VGCC, voltage-gated calcium channel