<p>Disruption of circadian rhythms is a key feature of neurodegenerative diseases and a non-motor feature of Parkinson’s disease, which significantly impairs health-related quality of life; yet, the underlying mechanisms are only partially understood. Preclinical animal models with neuropathological and symptomatic significance might contribute to a better understanding of circadian dysfunction. Here, we investigated light-dark phase-dependent modulation of motor and non-motor behavior as well as suprachiasmatic nucleus integrity in <i>α</i>-synuclein-overexpressing rats and wild-type controls. Behavioral testing in 3-month-old animals revealed robust phase-dependent modulation of exploratory activity, locomotion, sucrose preference, and olfaction-guided feeding in wild-type rats, which was absent in their transgenic littermates. Histological analyses demonstrated reduced overall cell density and pronounced <i>α</i>-synuclein accumulation in the suprachiasmatic nucleus of <i>α</i>-synuclein rats, accompanied by altered cellular composition, including altered neuronal, orexinergic, and microglial markers. <i>α</i>-synuclein load was positively correlated with Orexin A⁺ fibers and Iba1⁺ cell counts, suggesting a link between protein aggregation, neuroinflammation, and altered light-dark phase-dependent behavior. These findings indicate that <i>α</i>-synuclein rats lack phase-dependent behavioral alternations and exhibit suprachiasmatic nucleus pathology already at an early disease stage with very mild motor impairment, providing a translational model to study different aspects of non-motor symptoms in Parkinson’s disease.</p>