Circadian disruption, notably sleep disturbances, serves as an early indicator of Alzheimer’s disease (AD), preceding symptoms like memory loss. The suprachiasmatic nucleus (SCN) governs biological rhythms and receives direct retinal input via melanopsin-expressing retinal ganglion cells (mRGCs) to synchronize with environmental light cycles. The anatomical and functional basis for circadian disruption in AD remains unclear. Here, we explore the relationships between non-visual photoreception, SCN connectome evolution, and sleep regulation in the APP/PS1 mouse model.We measured mRGCs' light-induced electrical responses in 3 to 8-month-old APP/PS1 mice on a multielectrode array and obtained SCN image volumes via serial block-face scanning electron microscopy at matching ages. Simultaneously, we recorded electroencephalograms, electromyograms, temperature, and locomotor activity of 8-month-old WT and APP/PS1 mice to assess their sleep patterns.At 3 months, we observed an increased discharge ratio in response to light, associated with increased sensitivity of mRGCs of APP/PS1 mice. Contrastingly, at 8 months, mRGCs in AD mice exhibited reduced discharge rates compared to WT mice. We noted serval modifications in SCN connectomics, including a dendro-dendritic chemical synapse network reduction, crucial for synchronicity between SCN neurons, and a reduction of axonal boutons volume. Additionally, APP/PS1 mice displayed significantly reduced rapid-eye-movement sleep, associated with a reduced daily temperature amplitude and locomotor hyperactivity.These preliminary results suggest considerable changes in non-visual light response and the SCN connectivity that may be responsible for circadian disruption in those with AD. Further investigation will evaluate the use of non-pharmacological approaches to mitigate the observed circadian disruption.