Parkinson's disease (PD), the second most common neurodegenerative disorder, shares some core pathological features with Alzheimer's disease (AD), namely the accumulation of misfolded neurotoxic proteins leading to neuronal dysfunction and death, and both are multifactorial diseases resulting from the combined effects of genetic and non-genetic factors. Among these, non-genetic factors, due to their modifiability, have become key targets for disease prevention and therapeutic strategy development, and sleep is a non-genetic factor of great research value. Sleep disorders are highly prevalent in patients with PD, while in AD it has been demonstrated that sleep disorders have a bidirectional relationship with the disease, acting as both a consequence and a risk factor. However, whether such a relationship exists in PD remains unclear. The prevalence of sleep disorders in PD patients ranges from 60% to 98%, encompassing various types such as insomnia, excessive daytime sleepiness, and rapid eye movement sleep behavior disorder (RBD). Polysomnogram (PSG) shows that PD patients exhibit significantly reduced total sleep duration, sleep efficiency, and proportions of sleep stages, along with prolonged wake time after sleep onset, increased proportions of N1 sleep, and extended rapid eye movement latency. Research on the bidirectional relationship between sleep disorders and PD shows that RBD is often a prodromal symptom of PD, with 40% to 50% of idiopathic RBD patients progressing to PD during a 10-year follow-up, and a higher conversion rate observed in patients with cerebrospinal fluid α-Syn positivity. Chronic insomnia, sleep fragmentation, and reduced slow-wave sleep may increase the risk of PD onset or accelerate disease progression. Some studies suggest that sleep disorders could also be early symptoms of PD. The causal relationships between the two remain to be further clarified, and the underlying mechanisms are complex. In PD patients, degeneration of dopaminergic neurons in the substantia nigra-striatal pathway, involvement of non-dopaminergic systems, accumulation of α-Syn in brain regions regulating sleep, as well as non-motor symptoms and therapeutic drug effects collectively contribute to sleep disorders. Conversely, sleep disturbances may exacerbate the pathological progression of PD by disrupting protein homeostasis, increasing α-Syn secretion and aggregation, impairing glymphatic system clearance function, and inducing neuroinflammation. Based on current research, sleep is emerging as a novel target for PD prevention and treatment. Future studies should employ rigorous prospective cohort studies and randomized controlled trials to establish causal relationships between these two factors, develop specific biomarkers, optimize sleep intervention protocols, and integrate sleep management into the comprehensive PD prevention and treatment system to delay disease progression and improve patient outcomes.
