Untreated Sleep Apnea Nearly Doubles Parkinson’s Risk: Study Reveals Critical Role of Early Treatment

Sarah Johnson
December 3, 2025
Brief
New research reveals untreated sleep apnea nearly doubles Parkinson’s risk, with early CPAP treatment cutting that risk by 30%. This analysis explores implications for prevention and neurological health.
Opening Analysis
A groundbreaking study linking untreated obstructive sleep apnea (OSA) with a significantly increased risk of developing Parkinson’s disease (PD) challenges our understanding of neurological disease etiology and prevention strategies. More than just a correlation, the research suggests that early intervention with continuous positive airway pressure (CPAP) therapy may mitigate this risk and improve patient outcomes. This insight highlights the intricate ties between sleep health and neurodegeneration, underscoring an urgent need for integrated approaches to neurological disease prevention.
The Bigger Picture
Parkinson’s disease, a progressive neurodegenerative disorder marked by motor dysfunction and non-motor symptoms, affects millions worldwide. While genetic factors contribute, the majority of cases are sporadic, with environmental and lifestyle influences playing prominent roles. Sleep disturbances have long been observed as both prodromal symptoms and co-morbidities of Parkinson’s, but the directionality and causality have remained unclear.
Obstructive sleep apnea is a prevalent condition affecting roughly 9% to 38% of the adult population, characterized by repeated airway collapse during sleep causing intermittent hypoxia (oxygen drops) and sleep fragmentation. Prior research has linked OSA with cardiovascular disease, cognitive impairment, and mood disorders, but its connection to neurodegeneration is an emergent area of study.
The Oregon Health and Science University team’s large-scale veteran cohort study, spanning over two decades and more than 11 million individuals, provides unprecedented statistical power to detect associations beyond small clinical samples. Their findings build upon a growing body of evidence suggesting that chronic nocturnal hypoxia and disrupted sleep architecture may contribute to neuronal vulnerability.
What This Really Means
This study goes beyond recognizing sleep apnea as a mere health nuisance—it positions OSA, particularly when untreated, as a modifiable risk factor for a debilitating neurodegenerative disease. Veterans with untreated sleep apnea were almost twice as likely to develop Parkinson’s over approximately five years, translating into 1 to 2 additional cases per 1000 individuals.
More strikingly, initiating CPAP therapy within two years of diagnosis reduced the risk by about 30%, corresponding to roughly 2.3 fewer Parkinson’s cases per 1000 people. This suggests that early detection and treatment of OSA could delay or even prevent disease onset in a meaningful subset of the population.
Mechanistically, repetitive drops in oxygen saturations during apnea episodes may lead to neuronal damage through oxidative stress, neuroinflammation, and impaired clearance of toxic proteins like alpha-synuclein — a hallmark of Parkinson’s pathology. The brain’s glymphatic system, responsible for waste clearance during sleep, may be disrupted by fragmented, non-restorative sleep, allowing pathological proteins to accumulate and trigger neurodegeneration.
Furthermore, CPAP improves oxygenation and sleep continuity, potentially stabilizing neuronal microenvironments and reducing cumulative damage over time. The observed reduction in falls, fractures, and mortality among CPAP users with Parkinson’s further underscores its holistic benefits beyond simple respiratory support.
However, the study’s observational design means causation cannot be definitively established. Residual confounding and reverse causality remain concerns—early Parkinson’s symptoms may predispose patients to sleep apnea diagnoses, complicating interpretations.
Expert Perspectives
Dr. Lee Neilson, OHSU neurologist and lead author: "If you stop breathing several times an hour and your oxygen levels are dropping… you’re essentially stunning those brain cells every time that is happening. This repetitive stress may set the stage for neurodegeneration."
Dr. Greg Scott, OHSU pathologist and co-author: "People who still got Parkinson’s but had been on CPAP had fewer fractures, fewer falls and lower mortality. We tested this rigorously and the result kept happening. Prevention and early intervention are crucial."
Dr. Ronald Petersen, Director, Mayo Clinic Alzheimer’s Disease Research Center (not part of the study): "This research aligns with growing evidence that vascular and sleep-related factors play a vital role in neurodegenerative disease progression. It highlights a potentially modifiable risk factor that deserves further clinical trial assessment."
Data & Evidence
- Study cohort: >11 million U.S. veterans aged 40+, followed between 1999 and 2022
- Parkinson’s incidence: nearly doubled in untreated OSA versus non-OSA
- CPAP early therapy: ~30% risk reduction in developing Parkinson’s
- Estimated NNT (number needed to treat) with CPAP to prevent one case: 439 over 5 years
- Adjusted for confounders: age, sex, race, smoking, other health conditions
- Limitations: mostly older men, observational design, no granular CPAP adherence data
Looking Ahead
This study paves the way for deeper mechanistic research and randomized clinical trials to test whether treating sleep apnea can causally prevent Parkinson’s or slow its progression. Better phenotyping of at-risk individuals and biomarkers for early neurodegeneration could allow personalized interventions.
Clinically, these findings argue for more routine screening of sleep disorders in populations at risk for neurodegenerative diseases, including older adults and veterans. Sleep medicine and neurology fields may need to collaborate more intensively in prevention strategies.
Public health initiatives targeting sleep health awareness, increasing CPAP accessibility, and adherence support could tangibly reduce Parkinson’s disease burden. Additionally, this connection warrants exploration of other neurodegenerative diseases like Alzheimer’s, given shared pathological features.
Future research will need to clarify causality, understand gender and racial differences beyond veteran populations, and evaluate other sleep disorder treatments. Longitudinal data on CPAP adherence and mechanistic studies on oxygen deprivation and protein aggregation pathways will be crucial.
The Bottom Line
The link between untreated obstructive sleep apnea and increased Parkinson’s disease risk offers a critical new vantage point on neurodegenerative disease origins and prevention. Early CPAP therapy emerges as a promising intervention to reduce incidence and improve outcomes, highlighting sleep health as a vital frontier in brain protection. While causality remains to be firmly established, this evidence should prompt heightened clinical awareness, further research, and public health action to harness sleep disorder treatment in combating Parkinson’s.
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Editor's Comments
This extensive study linking sleep apnea and Parkinson’s disease risk offers a paradigm shift in our understanding of neurodegeneration. It elevates sleep health from a secondary symptom to a potentially modifiable risk factor, emphasizing prevention over treatment after onset. However, the observational nature requires cautious interpretation—reverse causality and confounding cannot be fully excluded. For example, early-stage Parkinson’s often causes REM sleep behavior disorder and disrupted breathing, possibly inflating sleep apnea diagnoses prior to full disease development. Ultimately, these findings highlight the necessity of integrating sleep medicine with neurology in both clinical practice and research, paving the path for novel preventative strategies. Going forward, randomized controlled trials with diverse populations will be critical to establish definitive causality and inform public health policies. This study also underscores the value of large-scale veteran health databases in uncovering subtle but impactful associations in complex diseases.
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