The complex pathology of neurodegenerative diseases presents a challenge to researchers who model the disease, and clinicians who treat patients. The identification of early, perhaps even prodromal, biomarkers is important for developing strategies to ameliorate disease progression. Sleep disturbances are a clinical feature of Huntington's disease (HD) as well as a part of normal aging. Whether sleep dysfunctions in HD patients are epiphenomenal or central to the neurodegenerative disease process is unclear. We show that sleep fragmentation is shared among Drosophila transgenic models that express mutant forms of huntingtin (mHtt), and flies with RNAi-mediated knockdown of the endogenous gene (dhtt). Our data suggest that sleep disturbances in HD may represent loss of function in the endogenous dhtt gene and that sleep perturbations in Drosophila HD models present an opportunity for screening therapeutic interventions.