How Obstructive Sleep Apnea May Influence Parkinson Disease Risk

Emerging evidence suggests obstructive sleep apnea may play a meaningful—and modifiable—role in Parkinson disease (PD) risk.

In this interview, Oregon Health and Science University faculty Lee Neilson, MD, assistant professor of neurology, and Gregory Scott, MD, PhD, assistant professor of pathology, unpack their large Veterans Administration database study showing increased Parkinson disease incidence in patients with obstructive sleep apnea (OSA), and a striking 30% risk reduction with early continuous positive airway pressure (CPAP) use.

Drs Neilson and Scott provide practical insights into risk interpretation, potential mechanisms, and how sleep apnea screening may become an essential component of brain-health–focused care.

Those interested in reading the study, “Obstructive sleep apnea, positive airway pressure, and implications of early treatment in Parkinson disease,” published in JAMA Neurology in November 2025, can access it here.

Neurology Learning Network (NLN): What motivated your team to examine the relationship between obstructive sleep apnea (OSA) and Parkinson disease (PD)? Given prior conflicting epidemiologic studies, what gap in understanding were you primarily trying to fill?

Lee Neilson, MD, and Gregory Scott, MD, PhD: Scott: It all starts in a patient-centered manner. The first observation in clinic was that it seemed a high proportion of people with Parkinson disease had sleep apnea. Then we turned to think about, is there some biological plausibility for this association? It made some sense that hypoxia, sleep fragmentation, and accelerated cerebrovascular disease—all potential downstream consequences of sleep apnea—are deleterious to brain health in general. So it may be that provides one ‘hit’ along the pathway to neurodegeneration.

Then we reviewed the literature. We saw a few studies out there with mixed results. Furthermore, their methodologies were not as rigorous as one would hope. In these large-scale studies it is important to know when we are examining exposures—like sleep apnea—and examining outcomes—like Parkinson disease—that we have confidence in those measures. So, we thought we could apply our own algorithm to this question and be meticulous about examining this potential association.

But we couldn’t stop there. It all comes back to the patient. What is the meaning for them? We knew we had to examine the next step: What are the implications of treatment, in this case continuous positive airway pressure (CPAP), on Parkinson disease? A positive result there could be exciting.

NLN: Please briefly describe the study method and your most significant finding(s). 

Drs Neilson and Scott: We tapped into the large nationwide database of medical records housed within the Department of Veterans Affairs. This is a system that goes back decades and allows you to look at changes in health over a long period of time. We compared all those people who had sleep apnea to those who did not have sleep apnea, and showed that the risk of developing PD in those with OSA was significantly higher.

We then tried to see if there were some alternative explanations for this. We made sure to adjust for key variables like age, smoking, and body mass index, and still found the same strong link. We also showed that those who got treated within 2 years of their OSA diagnosis with CPAP had a 30% reduction in their risk of PD. Finally, since this is not an entirely preventive measure, we wanted to examine in the cases of those with sleep apnea who did get PD, did their trajectory change at all depending on whether or not they used CPAP? It turns out the CPAP users may have had a more benign course. We showed they had fewer fractures, fewer falls, and lower mortality.

NLN: Your results reported an excess of 1.61 additional PD cases per 1,000 individuals at 6 years among veterans with OSA compared with those without. How should clinicians interpret this magnitude of increased risk—is this clinically meaningful, and how does it compare to other known midlife risk factors for PD?

Drs Neilson and Scott: We try to report both relative and absolute risks. The former can help convey the strength of the association and the latter can convey the real-world impact.  Since we expect about 1% of this population to develop PD (or 10 cases out of a sample of 1000), then making that 11 to 12 cases instead is notable. Most other risk factors report only relative risks, but we previously published on the association of hearing loss and Parkinson disease. I wouldn’t necessarily directly compare these studies, but this absolute risk is on par or higher than what we showed for hearing loss.

NLN: Your findings raise the possibility that OSA may accelerate or unmask prodromal PD in susceptible individuals. Do you see OSA as a causal risk factor, an early marker of neurodegenerative vulnerability, or a disease-modifying comorbidity? What evidence do we still need to distinguish between these possibilities?

Drs Neilson and Scott: We performed an observational study, so we cannot draw conclusions on causality. However, the evidence showing that an intervention—CPAP—attenuates the risk of PD does suggest that OSA may be not merely a prodromal symptom but a causal player in at least some subset of people who get PD. We looked through the lens of Parkinson disease, but it absolutely could be something that contributes to other neurodegenerative pathology. A prospective study examining the effect of CPAP on PD incidence or on a marker of disease progression, would be helpful in distinguishing these phenomena.

NLN: If OSA truly contributes to PD risk, what biomarkers—sleep-based, imaging-based, inflammatory, or genetic—might help identify individuals most likely to benefit from early OSA treatment?

Drs Neilson and Scott: Great question. We were not set up to answer this question with our study, so I would just be speculating. Since this is a public health intervention it’d be great if we had a simple decision tool that can be applied broadly, too. Perhaps that’s a blood test looking at alpha-synuclein? Or perhaps it is a respiratory measure already captured in the polysomnography. It’d be interesting to look at those sleep studies and find if there were 1 or 2 factors we could point to that suggested ‘CPAP responsiveness’.

NLN: Given the potential modifiability of OSA, do you see CPAP treatment as a candidate for disease-modifying intervention trials in prodromal PD or high-risk populations? What trial design would you consider most informative?

Drs Neilson and Scott: There is ample evidence already that treating sleep apnea is good for health. It reduces stroke risk, it lowers mortality, it improves cognition. This is yet another reason we should be encouraging sleep apnea screening and CPAP usage. Therefore, I think it’d be unethical to perform a clinical trial and withhold CPAP from people who are diagnosed with OSA. We would need to understand the putative mechanism better before trying this in someone without OSA. So, at this stage, in my clinical practice when I see people who are worried about PD but are relieved to hear they don’t have it, I would add sleep apnea screening to the list of the recommendations.

NLN: What is the most significant takeaway from this study that you’d like to emphasize for our audience?

Drs Neilson and Scott: The biggest takeaway is that early CPAP usage following the diagnosis of sleep apnea reduces one’s risk of developing Parkinson disease by about 30%. I don’t believe PD is entirely preventable, but I hope people consider sleep apnea screening and treatment as part of their prescription for brain health.

 Lee Neilson, MD, is an assistant professor of neurology who specializes in all aspects of movement disorders including Parkinson’s disease, deep brain stimulation, and botulinum toxin injections. A graduate of Case Western Reserve University school of medicine and the Portland VA Medical Center advanced fellowship in movement disorders, he recently joined the University of Iowa to continue his research focused on risk factor identification, biomarker development, and metabolism in Parkinson’s disease and prodromal disorders.

Gregory Scott, MD, PhD, is an assistant professor of pathology who studies Parkinson’s disease, dementia, and related neurodegenerative diseases.  He trained in pathology at Stanford University and returned to the Portland VA and Oregon Health and Science University to continue research and practice surgical pathology. 

© 2026 HMP Global. All Rights Reserved.

Any views and opinions expressed above are those of the author(s) and do not necessarily reflect the views, policy, or position of the Psych Congress Network or HMP Global, their employees, and affiliates.