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Alliance"],"accepted":{"date-parts":[[2024,11,25]]},"published-print":{"date-parts":[[2025,2]]},"abstract":"<jats:p>\n                    A G4C2 hexanucleotide repeat expansion in\n                    <jats:italic>C9orf72<\/jats:italic>\n                    is the most common cause of amyotrophic lateral sclerosis and frontotemporal dementia (C9ALS\/FTD). Bidirectional transcription and subsequent repeat-associated non-AUG (RAN) translation of sense and antisense transcripts leads to the formation of five dipeptide repeat (DPR) proteins. These DPRs are toxic in a wide range of cell and animal models. Therefore, decreasing RAN-DPRs may be of therapeutic benefit in the context of C9ALS\/FTD. In this study, we found that C9ALS\/FTD patients have reduced expression of the AAA+ family members RuvBL1 and RuvBL2, which have both been implicated in aggregate clearance. We report that overexpression of RuvBL1, but to a greater extent RuvBL2, reduced C9orf72-associated DPRs in a range of in vitro systems including cell lines, primary neurons from the C9-500 transgenic mouse model, and patient-derived iPSC motor neurons. In vivo, we further demonstrated that RuvBL2 overexpression and consequent DPR reduction in our\n                    <jats:italic>Drosophila<\/jats:italic>\n                    model was sufficient to rescue a number of DPR-related motor phenotypes. 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