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Here, we propose the misfolding of the mutant ATXN3 protein and the subsequent aggregation process, with eventual deposition of insoluble intracellular aggregates, to be the hub of the pathogenic process, and discuss how protein dyshomeostasis impacts key cellular pathways causing dysfunction and disease (Fig

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However, more studies are needed to fully understand the contribution of PARPs to the age-related decline in NAD + levels