Despite the lack of consensus, it should be noted that thermoregulation has been implicated in sleep regulation and function from the earliest days of research in the field and recent studies have established that subsets of neural circuits regulating sleep also overlap with circuits regulating thermoregulation. With this in mind, we propose two novel strategies to elucidate the functional relationship between sleep and temperature regulation. The first approach uses a minimally invasive sleep-fragmentation protocol to disrupt sleep for 1 minute every 15 minutes. Sleep fragmentation modifies temperature preference without affecting sleep homeostasis or causing memory impairments; flies that receive the same number of stimuli but without disrupting sleep do not show changes in temperature preference. Thus, sleep fragmentation can perturb sleep regulatory centers while reducing the confounding or nonspecific effects associated with total sleep loss. The second approach that can be used to elucidate the functional relationship between sleep and temperature regulation harnesses the precision of Drosophila genetics to target specific neural circuits. Techniques such as thermogenetics and optogenetics can modulate neuronal activity. However, it's worth noting that body temperature and sleep are altered in the context of Alzheimer’s disease. Thus, we hypothesize that the targeted expression of Alzheimer's-related genes, such as Aβ-Arctic, will provide a novel, cell-specific approach to modulate the neuronal physiology of neurons that regulate temperature preference and sleep. In contrast to thermogenetics and optogenetics, which may or may not alter one feature of a neuron, neuronal excitability, Aβ-Arctic can modify a broader range of physiological parameters.