The onset of Alzheimer disease (AD) and of abnormal sleep patterns are both signaled by initially minute but ultimately disastrous physiological malfunctions of the brain. Among these, the Locus Coeruleus (LC) belongs to the primary brain areas that show such malfunctions in the early stages of AD. The LC generates large noradrenaline (NA) signals that are key for the architecture of sleep in mice. In contrast, how LC malfunctions relate to sleep disturbances in AD remains unknown.We explore the real-time functionality of the noradrenergic system during AD’s prodromal phase in an established AD mouse model using dual fiber photometric measurements in freely behaving animals that express biosensors for free NA in thalamus and for neuronal Ca2+ fluctuations in LC neurons. In combination with polysomnography (EEG/EMG), we record local field potential (LFP) activity in somatosensory cortex (S1) and in the hippocampus (CA1) to assess vigilance states in mice aged 2-9 months.We currently investigate sleep architecture parameters such as the time spent in each vigilance state and bout duration, with a focus on excessive fragmentation in both light and dark phases. We track how Ca2+ activity in the LC and its NA output in thalamus relate to sleep properties. Preliminary data indicate that the Novel Object Location test is a useful measure for evaluating the animals’ cognitive abilities.Decoding the patterns of LC’s dysfunction during the prodromal phase of AD and its consequences on sleep could prove essential to early diagnosis of AD and for potential interventions.