Motor units with less synaptic plasticity exhibit early susceptibility to loss in motor neurone degenerative disease, and in the SOD1 mouse model of ALS, a progressive impairment of stimulus-induced synaptic sprouting was observed over the course of the disease, suggesting that the absence of synaptic plasticity, and disease-induced synaptic loss are mechanistically linked [109,110]. The gene discussed is SOD1; the disease is neurodegenerative disease.