Alzheimer’s Disease (AD) remains the most prevalent form of dementia with increased occurrence expected in coming years with increasing global life expectancy. Treatment efforts remain unfruitful, warranting investigations targeting quality of life improvements and slowing of disease progression. Circadian rhythms are daily periodic alterations in body physiology, impacting various body systems. Circadian dysfunction has been associated with several disease states, including AD. The nature of the bidirectional relationship between AD progression and circadian dysfunction remains elusive. A Drosophila melanogaster AD model paired with behavioral, molecular, and morphological approaches are used elucidate this relationship’s nature. Behavioral analysis of AD model D. melanogaster was conducted using a Drosophila Activity Monitoring system. Results exhibited AD D. melanogaster depending on external cues for circadian function, with removal of time cues diminishing circadian behavior paired with substantial phase shifting. The molecular function of the core circadian clock in our AD model was assessed using reverse transcription - quantitative polymerase chain reaction analyzing the core clock gene period. The core circadian clock functions normally, indicating potential dysfunction downstream of the core circadian clock. These data suggest circadian function is diminished in our AD model. Neurodegeneration was assessed by quantification of the eye area and brain vacuole size of AD model flies with and without circadian clock function. Data suggests circadian clock dysfunction is associated with accelerated disease progression. Further analysis into mechanism may reveal therapeutic targets to improve quality of life and care for AD patients by correcting their circadian rhythms.