Alzheimer’s disease (AD) is marked by amyloid beta accumulation, tau pathology, and cognitive decline. Sleep disturbances in AD are linked to amyloid beta, yet the influence of tau pathology on sleep remains unexplored. Using Drosophila melanogaster, we investigated adult-onset tau expression effects on sleep, addressing the knowledge gap in tauopathy's impact on sleep-related changes in AD progression. Pan-neuronal expression of wild-type tau and pseudo-phosphorylated tau E14 in Drosophila was induced in adult flies by RU 486 and activity and sleep were monitored in an automated Drosophila Activity Monitor. Results revealed that tau-expressing flies had a shorter lifespan. An unexpected, heightened activity observed in gene-switch controls creating confounding effects in analysis of locomotor activity. Despite this, neither genetic controls nor the RU inducer affected sleep phenotypes, enabling the investigation of sleep disruptions due to tau expression. Female, not male, flies expressing tau showed increased sleep bouts during the daytime, with pseudo-phosphorylated E14 tau exacerbating the phenotype compared to wild-type tau. Immunohistochemistry revealed vacuoles in tau-expressing flies, suggesting neurodegeneration likely caused the observed sleep changes. Our findings suggest that pathological tau expression in Drosophila causes neurodegeneration and increased sleep in females, potentially contributing to sleep disruption in humans, offering a new model system to understand tau's role in neurodegeneration.