Furthermore, researchers found that in neuromuscular junctions of Drosophila, transcription and translation of the MAP1B homologue, Futsch, was reduced in the context of TDP-43-induced proteinopathy, and associated with mitochondrial transport impairment, leading to progressive neurodegenerative changes (Bettencourt da Cruz et al., 2005; Coyne et al., 2014). The gene discussed is MAP1B; the disease is proteostasis deficiencies.