Circadian-Modulated Thresholds for Sleep Patterns in Aging and Narcolepsy

In the two-process model of sleep-wake regulation, circadian-modulated thresholds time every sleep onset and awakening, yet they remain free parameters rather than quantities derived from neuronal dynamics. This limitation leaves the framework unable to predict how sleep patterns change when neuromodulatory drive is altered, as in aging and narcolepsy. Here we close that gap by deriving closed-form, circadian-modulated threshold expressions from the Phillips-Robinson model with explicit orexinergic excitation of the wake-promoting population. Within this single threshold geometry, aging and narcolepsy appear as opposite deformations along the orexinergic axis: age-related hyperexcitability of orexin neurons elevates the sleep-onset boundary and creates a fragility regime in which minor nocturnal disturbances trigger premature awakenings, whereas orexin loss depresses the same boundary toward the wake-onset threshold and produces the rapid state fragmentation of narcolepsy. Concurrently, reduced circadian amplitude compresses the inter-threshold corridor, advancing sleep onset and shortening sleep duration. These results convert the classical two-process thresholds from descriptive conveniences into mechanistic organizers of sleep-wake dynamics across healthy aging and orexin deficiency.