Circadian-Modulated Thresholds for Sleep Patterns in Aging and Narcolepsy

The two-process model of sleep-wake regulation posits that circadian-modulated thresholds govern both sleep onset and awakening. However, these thresholds remain as adjustable parameters rather than quantities derived from neuronal dynamics, hindering the model's ability to predict sleep pattern changes due to alterations in neuromodulatory drive, such as those seen in aging and narcolepsy.

By deriving closed-form expressions from the Phillips-Robinson model that incorporate explicit orexinergic excitation of the wake-promoting population, researchers have managed to bridge this gap. In this single threshold geometry, aging and narcolepsy manifest as opposite deformations along the orexinergic axis. In aging, increased orexin neuron excitation raises the sleep-onset boundary, leading to a fragile system where minor nocturnal disturbances can precipitate premature awakenings.

Conversely, a reduction in orexin levels lowers the same boundary towards the wake-onset threshold, resulting in the rapid state fragmentation characteristic of narcolepsy. Additionally, decreased circadian amplitude tightens the inter-threshold corridor, advancing sleep onset and shortening overall sleep duration. By transforming the classical two-process thresholds from mere descriptive tools into mechanistic organizers of sleep-wake dynamics, this study sheds light on how healthy aging and orexin deficiency impact sleep patterns.