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. 2021 Apr 1;12(2):494–514. doi: 10.14336/AD.2020.0708

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copyright: © 2021 Fuertes-Alvarez et al.

this is an open access article distributed under the terms of the creative commons attribution license, which permits unrestricted use, distribution and reproduction in any medium provided that the original work is properly attributed.

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Figure 2. — Age-associated disruption of signaling pathways at the NMJs. Normal adult (upper panel) and aged (lower panel) neuromuscular junctions are depicted showing major dysregulated pathways. NRG-ErbB -mediated signaling, implicated in NMJ stability and sprouting of tSCs, could also be involved in the migration of tSCs during aging that results in partial coverage of the NMJ. The cell surface glycoprotein CD44 seems to increase tSC plasticity, at least in ALS and aging mouse models. Agrin-MuSK pathway is essential for NMJ maintenance. The dysregulation of agrin levels in tSCs could induce NMJ destabilization during sarcopenia. Intracellular S100 proteins present altered expression in aged tSCs, which in turn affects Ca²⁺-mediated signaling.