This notion may be supported by a report that Atlastin-1 modulates seizure activity and neuronal excitability [59] and the observation that Drosophila atlastin decreases evoked transmitter release at the neuromuscular junction and causes age-dependent decline in adult locomotion [57,60], even though both works surmise that interference with BMP trafficking could also be a potential source of these phenotypes, conceivably suggesting that perturbation of trafficking could underlie HSP-disease. Here, ATL1 is linked to hereditary spastic paraplegia.