Are you sleeping well?
I have spent time and energy over the past few weeks working through ideas and options to better understand what is happening when one is “feeling off”. Everyone in the Parkinson’s community knows what this means and has their own unique definition of what it means to be “off”. In general, this discussion seems to start from the assumption that your dopamine levels are too low, but in reality, the symptoms may be the same if they are too high, making it both a guessing game and a balancing act. You may also be tired due to poor or not enough sleep or fragmented and disrupted sleep. You may be dehydrated. You may need electrolytes, not just water. You may need an electrolyte drink plus a salty snack. You get the idea. The list goes on and on. It is complicated. It is different for everyone, and it changes.
With all that in mind, I landed on sleep.
I thought I would share some information from my recent dive into obstructive sleep apnea (OSA). After what I learned, I feel that every Parkinson’s patient should be aware of these issues and discuss them with your doctor.
Consider seeking information early in the Parkinson’s journey about whether a sleep study is appropriate. I was not aware of the strong links between OSA, Parkinson’s and overall physical and cognitive decline. There are benefits to starting Continuous Positive Airway Pressure (CPAP) sooner rather than later, if it is appropriate for you.
I looked into obstructive sleep apnea and Parkinson’s and found a rich line of research. It appears that the relationship between obstructive sleep apnea and Parkinson’s runs both directions. OSA is a significant risk factor for developing Parkinson’s (Neilson et al., 2026) and OSA is more prevalent among PD patients than the general public ( 50 – 70% of PD patients have obstructive sleep apnea, depending on the study cited).
There is a lot going on, and the impacts and influences move back and forth. It is hard to determine what comes first and what the cycle of influence is. It can feel a bit like the chicken or the egg example.
Clinical studies show that OSA is more prevalent among PD patients than in the general population. This suggests that hypoxia (oxygen deprivation) and fragmented sleep may be factors that contribute to a Parkinson’s diagnosis. These factors are also related to motor and cognitive PD symptoms. This translates into OSA being a contributing factor to a Parkinson’s diagnosis.
On the other side of the equation, PD-associated issues (autonomic nervous system impairment and cognitive impairment) negatively impact respiratory control and may be linked to OSA. The complexity is increased because systems and symptoms overlap. Sleep disturbances, cognitive decline, and autonomic dysfunction make for a complicated, deeply connected system.
I found several studies that explain how OSA may drive PD symptoms, expression, and pathology. I don’t want to get into the weeds here, but I think information is important, and I will do my best to explain this.
Clinical studies suggest that hypoxia (low levels of oxygen within body tissues) and sleep fragmentation may be key factors that contribute to worsening motor and cognitive symptoms.
The studies in this space focus on the interactions among three factors: the brain’s lack of oxygen due to obstructive sleep apnea, its impact on neuroinflammation, and alpha-synuclein.
It is easy to understand that lack of oxygen to the brain is bad, and that neuroinflammation is bad. The question is what in the world is alpha-synuclein?
Alpha-synuclein is a normal protein found in the human brain. There is a lot of it, and it is heavily involved in neurotransmitter release. This protein is at the heart of Parkinson’s.
Neurotransmitters are the body’s chemical messengers. They carry signals from a neuron (nerve cell) across a microscopic gap called a synapse to a target cell. The target cell can be another nerve cell, a muscle cell, or a gland. Neurotransmitters are essential for regulating everything. They regulate movement, breathing, and heart rate, as well as mood, sleep, digestion, brain function, and everything in between.
In Parkinson’s disease, the protein alpha-synuclein misfolds and malfunctions, disrupting normal cellular function and leading to the death of dopamine-producing neurons.
In healthy neurons, alpha-synuclein enables brain cells to communicate. In Parkinson’s disease, this process goes awry.
What this research points to is a substantial relationship between obstructive sleep apnea and accelerated progression of Parkinson’s symptoms due to the lack of oxygen to the brain and its impact on neuroinflammation and alpha-synuclein.
Research in the area continues to increase. We all need to know about this and have conversations with our medical providers. We can ask questions and request sleep studies.
Continuous Positive Airway Pressure (CPAP) therapy produces significant clinical benefits. It appears to significantly slow PD progression and cognitive decline.
I include seven references that are at the end of this article, and five are from 2025 and 2026. The recent work in this area is exciting and hopeful. I continue to be amazed and deeply grateful for the doctors and scientists who devote their professional lives to better understanding this disease. May we all use their information to make better choices that improve our outcomes.
Here’s to a good night’s sleep!
Cheers to all.
Lauren
References
1. Guo M, Ji X and Liu J (2022) Hypoxia and Alpha-Synuclein: Inextricable Link Underlying the Pathologic Progression of Parkinson’s Disease. Front. Aging Neurosci. 14:919343. doi: 10.3389/fnagi.2022.919343
2. Gao Y, Zhang J, Tang T, Liu Z. Hypoxia Pathways in Parkinson’s Disease: From Pathogenesis to Therapeutic Targets. Int J Mol Sci. 2024 Sep 29;25(19):10484. doi: 10.3390/ijms251910484. PMID: 39408813; PMCID: PMC11477385.
3. Li J, Zhang N, Zhang Z, Fu J, Ren W, Sun Y, Song S, Liu X, Liu J, Wang J, Sun Y, Zhang K, Guo R, Lv C, Pan L, Qu G, Han F, Yu Y. Molecular mechanisms of α-syn abnormal phase separation in cognitive impairment induced by chronic intermittent hypoxia and the neuroprotective effects of Danshensu methyl ester. Mol Med. 2025 Oct 29;31(1):320. doi: 10.1186/s10020-025-01366-4. Erratum in: Mol Med. 2026 Jun 8;32(1):87. doi: 10.1186/s10020-026-01519-z. PMID: 41162854; PMCID: PMC12570643.
4. Neilson LE, Montaño I, May JL, et al. Obstructive Sleep Apnea, Positive Airway Pressure, and Implications of Early Treatment in Parkinson Disease. JAMA Neurol. 2026;83(1):68–75. doi:10.1001/jamaneurol.2025.4691
5. Shasha Zhu, Di An, Xiaoxi Liu,Obstructive sleep apnea, biomarker profiles, and clinical progression in Parkinson’s disease: Longitudinal effects of CPAP therapy, Sleep Medicine,Volume 139,2026,108766,ISSN 1389-9457, https://doi.org/10.1016/j.sleep.2026.108766.
6. Wang JDJ, Chua NYM, Chan LL, Tan EK. Obstructive Sleep Apnea and Parkinson’s Disease: Bidirectional Clinical and Pathophysiologic Links. Int J Mol Sci. 2025 Apr 16;26(8):3762. doi: 10.3390/ijms26083762. PMID: 40332389; PMCID: PMC12028076.
7. Zhai MR, Pan J, Wu ZH, He YY, Zhang KR, Ren L, Wang YR, Li YB, Gao J, Xiao L, Liu YH. Chronic intermittent hypoxia increases Parkinson’s disease susceptibility via PPARα-mediated lipid droplet-mitochondrial dysfunction. Theranostics. 2026 Jan 1;16(5):2466-2487. doi: 10.7150/thno.122944. PMID: 41424864; PMCID: PMC12712921.