The locus coeruleus (LC) is a predominant nucleus of the brainstem involved in the modulation of sleep, wakefulness and stress response. Tau pathology develops in the LC decades before Alzheimer's disease (AD) symptoms manifest in humans, and widespread LC degeneration occurs as the disease progresses. While LC degeneration has been characterised by total neuron death in AD, little research has explored the effect of tau pathology on the electrophysiological properties of LC neurons. The intrinsic electrical properties of LC neurons were investigated in the PS19 and rTg4510 tau transgenic murine models of AD. LC neuronal properties were not significantly different from wildtype littermates in both strains at 9 months of age, which represents a stage where AD symptoms persist and tau pathology is present in the LC. However, the resting potential of LC neurons was significantly depolarised in 9 mo PS19 transgenic mice, compared to 5 mo PS19 transgenic mice. Since the LC densely expresses orexin 1 receptors (OX1Rs), we then aimed to identify whether antagonising the OX1R, which is involved in modulation of stress and motivated behaviour, would alter cognitive symptoms in aged PS19 mice. Interestingly, the OX1R antagonist 1-SORA-51 exacerbated REM sleep deficits in male transgenic mice while, contrastingly, rescuing anxiety-like behaviours. These results suggest that tau pathology may act to 'accelerate' aging, contributing to hyperactivity of the LC and consequent sleep disruption in AD patients, and that modulation of the OX1R can produce divisive effects on sleep architecture while ameliorating anxiety symptoms.