Having Both Insomnia and Sleep Apnea May Raise Neurodegenerative Disease Risk
Comorbid insomnia and sleep apnea (COMISA) may be a distinct and underrecognized risk factor for neurodegeneration, beyond either condition alone.
Summary
Most sleep research treats insomnia and sleep apnea as separate conditions, but many people suffer from both simultaneously — a syndrome called COMISA. This editorial in Sleep Journal argues that COMISA may represent a unique and compounded threat to brain health that goes beyond what either disorder causes alone. The combination of fragmented sleep, oxygen deprivation, and heightened physiological stress may accelerate the accumulation of neurotoxic waste products like amyloid beta, promote neuroinflammation, and impair the glymphatic system's nightly brain-cleaning function. The author calls for COMISA to be recognized and studied as an independent risk factor for conditions such as Alzheimer's disease and other neurodegenerative disorders, urging clinicians to screen patients for both conditions together rather than treating them in isolation.
Detailed Summary
Sleep disorders have long been linked to cognitive decline and dementia, but most research has focused on insomnia and obstructive sleep apnea as separate entities. An emerging body of evidence suggests that when both conditions co-occur — a phenomenon termed COMISA (comorbid insomnia and sleep apnea) — the resulting biological insult to the brain may be qualitatively different and potentially more dangerous than either condition in isolation.
This commentary, authored by Galit Levi Dunietz of the University of Michigan's Division of Sleep Medicine, raises the question of whether COMISA should be classified as an independent risk factor for neurodegenerative disease. The argument centers on the idea that the two disorders interact in ways that compound neurobiological harm: sleep apnea causes repeated nocturnal hypoxia and sleep fragmentation, while insomnia prevents adequate restorative sleep even when apnea events are controlled.
From a mechanistic standpoint, this combination may severely impair the glymphatic system — the brain's waste-clearance network that operates primarily during deep, uninterrupted sleep. When glymphatic function is compromised, toxic proteins such as amyloid beta and tau accumulate. COMISA may also drive chronic neuroinflammation and dysregulate the hypothalamic-pituitary-adrenal axis, creating sustained cortisol elevations that are independently neurotoxic.
The clinical implication is significant: patients with COMISA are often underdiagnosed because treating apnea with CPAP therapy does not resolve insomnia, and vice versa. This bidirectional treatment challenge means patients may go years without adequate sleep restoration, silently accumulating neurological damage.
The commentary calls for dedicated longitudinal studies examining COMISA as a distinct phenotype and its association with biomarkers of neurodegeneration such as cerebrospinal fluid amyloid, tau PET imaging, and cognitive trajectories. Clinicians are urged to screen for both disorders simultaneously and consider combination therapies.
Important caveats apply: this paper is a commentary or editorial rather than an original research study, and the full text was not available for review. Conclusions about causation cannot yet be drawn.
Key Findings
- COMISA (co-occurring insomnia and sleep apnea) may pose a greater neurodegenerative risk than either condition alone.
- Glymphatic brain-waste clearance is likely impaired by the combined sleep disruption and hypoxia of COMISA.
- CPAP therapy for apnea does not resolve insomnia, leaving many COMISA patients chronically underprotected.
- Chronic cortisol dysregulation from COMISA may independently accelerate neuronal damage over time.
- Authors call for COMISA to be recognized and studied as a distinct neurodegenerative risk phenotype.
Methodology
This is a commentary or editorial piece published in Sleep Journal, authored by a single University of Michigan sleep neurologist. It synthesizes existing evidence to argue for a new conceptual framework around COMISA as a neurodegenerative risk factor. No original data or clinical trial results are presented.
Study Limitations
This summary is based on the abstract only, as the full text is not open access. The paper is a commentary rather than an original research study, so no new clinical data are presented and causal relationships cannot be established. The proposed neurodegenerative risk of COMISA remains a hypothesis requiring longitudinal epidemiological and biomarker-based confirmation.
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