Indeed, in other contexts exercise has been shown to be neuroprotective.34 In animal models of ALS it has been shown that activation of mTOR signalling via metabotropic cholinergic receptor activation at the neuromuscular junction (NMJ) protects MN from the development of ALS via changes in neuronal excitability.13 This provides a mechanism whereby exercise—leading to NMJ activity—could be neuroprotective if mTOR signalling is functioning normally (Fig. 5F, top panel). Here, MTOR is linked to amyotrophic lateral sclerosis.