Obstructive Sleep Apnea and Aging: A Narrative Review

Article information

Sleep Med Res. 2025;16(3):139-150

Publication date (electronic) : 2025 September 29

doi : https://doi.org/10.17241/smr.2025.02964

David Brower, BA ¹, Eric Pan, BS ¹, William Goss, BS ¹, Younghoon Kwon, MD ², William J. Healy, MD ¹

¹Division of Pulmonary, Critical Care, and Sleep Medicine, Wellstar Medical College of Georgia, Augusta, GA, USA

²Division of Cardiology, University of Washington, Seattle, WA, USA

Corresponding Author: William J. Healy, MD, Medical College of Georgia, Augusta University, 1120 15th St, Augusta, GA 30912, USA, Tel +1-706-721-1477, E-mail wihealy@augusta.edu

Received 2025 July 8; Revised 2025 August 12; Accepted 2025 August 18.

Abstract

Obstructive sleep apnea (OSA) is one of the most common sleep disorders. It can greatly increase patient sleepiness, and is associated with cardiovascular and neurological disease. As people age, they are more likely to develop the disease, so with an aging population, understanding how OSA affects the elderly is increasingly important. This review summarizes sleep medicine’s understanding of the disease in older people. It discusses the epidemiology of OSA in this population and then examines differences in risk factors relevant in the elderly, including the effects of menopause. Next, we review the symptomology, with special attention paid to comorbid insomnia, before examining challenges in diagnosing OSA in older people. We examine the pathophysiology of OSA in the elderly with particular focus on changes in anatomy and sleep architecture, as well as positional OSA. We then discuss the intricacies and effectiveness of various treatments including continuous positive airway pressure and surgically implanted devices. We finish by exploring OSA’s implications in cognitive decline and Alzheimer’s disease. OSA is a very common disease in the elderly, with the potential to significantly reduce the patient’s quality of life. This review should serve as a resource for sleep medicine physicians to further educate themselves on this topic.

Keywords: Obstructive sleep apnea; Continuous positive airway pressure; Aging

INTRODUCTION

Obstructive sleep apnea (OSA) is a respiratory disorder characterized by intermittent breathing disruption or cessation during sleep secondary to obstruction of the airway. The cause of this obstruction is often multi-factorial, with common contributing factors including obesity, dysfunction of pharyngeal muscles leading to inadequate airway dilation, and impaired respiratory drive responsiveness resulting in unstable breathing patterns and airway narrowing [1]. More common in males than females, OSA affects approximately 13% of men and 6% of women in the United States, with prevalence increasing with age across both sexes [2]. Other identified risk factors of OSA include body mass index (BMI) greater than 30 kg/m² and ethnic groups impacted by increased frequency of craniofacial structural abnormalities (e.g., East Asians) or obesity (e.g., Black and Hispanic populations) [3]. Patients with OSA are often characterized by loud, habitual snoring and experience symptoms such as morning grogginess and persistent daytime fatigue due to disrupted and non-restorative sleep. The compensatory increased sympathetic tone from recurrent episodes of hypoxemia may contribute to the development of multiple cardiovascular conditions, including resistant hypertension (HTN), atrial fibrillation, heart failure (HF), coronary artery disease, and stroke [4]. Diagnosing OSA involves measuring the apnea-hypopnea index (AHI), or the number of apneas and hypopneas per hour of sleep. Common diagnostic methods include in-laboratory polysomnography (PSG) and home sleep apnea testing (HSAT) [5].

As lifespans increase, the burden of OSA grows at the system and individual level. Recent studies estimate that the financial burden of untreated OSA ranges from $34 billion to $69 billion annually in the United States, equating to an additional $1,950 to $3,899 in healthcare costs per affected individual [6]. Patients over 65 years old are at increased risk of suffering from undiagnosed OSA [7]. Diagnosis in this population is further complicated by atypical clinical presentations, including lower reported rates of daytime sleepiness, witnessed apneas, and obesity, alongside a higher prevalence of insomnia [8]. Diagnosing OSA in older adults is complicated by common age-related conditions such as cognitive impairment, nocturia, and nonspecific fatigue, which can obscure its presentation. Ongoing research continues to explore the disease’s role in increasing the risk of comorbidities such as cardiovascular disease, cognitive decline, and mortality; however, interventions such as continuous positive airway pressure (CPAP) have consistently demonstrated improved outcomes for elderly OSA patients [9].

This manuscript offers a focused review of OSA in the aging, emphasizing age-specific causes, variations in presentation and diagnosis, and the variable efficacy of treatment options. It also examines the relationship between OSA and associated complications drawing on recent findings to provide updated insights that support informed management in older adults.

EPIDEMIOLOGY

Higher Prevalence as People Age

The stereotypical picture of an OSA patient is that of an overweight, middle-aged man; however, the disease may also be present in thinner individuals, women, and the elderly. In particular, OSA is common amongst older populations—globally, a comparatively high prevalence of OSA in elderly patients as compared to younger populations has been demonstrated in multiple countries including Brazil [10], South Korea [11], and Switzerland [12]. Heinzer et al. [12] further go on to estimate that up to 49% of patients aged 60–85 years old in Switzerland have the disease. This challenges the current paradigm and popularly held belief that OSA is a pathology primarily of the young and middle-aged and may in fact be more common in elderly populations. Furthermore, despite OSA’s high prevalence amongst the elderly population, few patients are adequately tested—within the USA, a study of Medicare beneficiaries found over half were high risk, but only 8% of said individuals had been previously tested [7]. These studies demonstrate that it is likely more common than in the younger population, so increased screening should be considered.

Risk Factor Differences in Older Adults

Risk factors for the presence of OSA and its severity in middle-aged and older populations overlap significantly—typical risk factors in middle-aged patients like obesity, snoring, episodes of daily sleepiness (EDS) and HTN were found to positively predict OSA in elderly populations [13]. The use of sleep medications negatively predicted OSA in the older but not younger populations [13]. Interestingly, neck circumference (NC), a common screening measurement for OSA, may not be as useful a predictor in the elderly. In a retrospective study in Seoul, NC ceased to correlate with AHI in the >70-year age group, even though NC correlated with severity for patients in their 60s [14]. Increased age itself may predict increased OSA in elderly populations— in patients aged 65 years or older, increased age was associated with increased AHI but not in those under 65 years [15]. These differences suggest that OSA in the elderly may have a different etiology than in younger populations and may warrant further investigation into mechanisms underlying OSA in the elderly.

Menopause and OSA

While OSA is widely known to be more common in men, it remains highly prevalent in elderly women. One study found that 50.9% of women (mean age, 68 years) in the general population had an AHI ≥15 [16]. Typically, women with OSA have a lower AHI and Apnea Index (AI) than men of similar ages [17]. This trend is observed within the elderly [16]. OSA is common in older women, but is less prevalent and severe than in men. It is possible that the observed high prevalence of OSA in elderly women may be driven by post-menopausal changes, as the prevalence of OSA nearly doubles in women after menopause [18], independent of both age and BMI [19]. Notably, the prevalence of OSA in postmenopausal women without hormone replacement therapy (HRT) was almost 4 times higher than in those receiving HRT, 2.7% versus 0.6% [20]. HRT has been considered as a potential therapy for OSA in elderly women, even emerging as a possible treatment option to reduce AHI in multiple smaller studies [21]. However, HRT as a treatment for OSA in post-menopausal women is not well-characterized and must be balanced with the well-characterized risk for all-cause mortality and myocardial infarction in those taking long-term HRT [22], and represents an important area of further study. Menopausal status and HRT use certainly are important for a physician to consider when evaluating for OSA; however, as of now, it is not considered a viable intervention for the disease.

Though current evidence strongly suggests that menopause may increase the risk of OSA in women, underlying physiological changes driving this phenomenon remain poorly characterized. Excessive arousal is not a likely explanation, post-menopausal women are less arousable than pre- and peri-menopausal women [23], which should protect against OSA. Progesterone has also been shown to correlate with upper airway muscle responsiveness [24], which might explain some of the increased prevalence in this population. Still, more evidence is needed to determine precisely what accounts for the increased risk of OSA in post-menopausal women.

SYMPTOMS IN THE ELDERLY

Symptomatic presentation of OSA also differs in the elderly population. It has long been established that elderly patients with OSA experience less snoring [25] and daytime sleepiness [26] than younger populations—when compared to the young with similar AHI, patients older than 65 years experienced less daytime sleepiness [27]. Older patients with OSA are far less likely to be sleepy than their younger counterparts.

Nocturia is another OSA symptom worth focused discussion, as from an elderly patient’s perspective, nocturia can make OSA much worse. Having to remove a CPAP mask, walk to the bathroom and back, and put the mask back on is trivial for younger patients, but for weaker, elderly people it is a considerable challenge. OSA is associated with increased risk of experiencing nocturia within the general population [28]. However, this association is not as well characterized in the elderly population, and evidence is mixed regarding the association of nocturia with OSA in this specific population—studies have shown no association between nocturia and OSA [29], while others have observed such an association [30]. Nocturia itself is highly common in the elderly, with some studies observing rates of nocturia over 60% in patients over 70 years [31]. Combined with the high prevalence of OSA within the elderly population, it is difficult to discern if OSA is associated with increased risk of nocturia.

Comorbid Insomnia and OSA

As the prevalence of insomnia also increases with age [27], particularly in the elderly, a key area of focus has been comorbid insomnia and sleep apnea (COMISA). COMISA has previously been shown to show no association with age—a recent meta-analysis including data from over 34,000 patients found no association between age and comorbid insomnia. However, the mean age range of the aforementioned study ranged from 44.50 to 64.79 years and may not adequately represent the elderly population [32]. Further, a large cohort from China showed association with age and COMISA in those over 70 years but not in younger age groups [33]. COMISA is a serious manifestation of OSA, so it is necessary to screen for when managing OSA in the older population. Thus, the relationship between COMISA and age, particularly in the elderly, remains ill-defined and warrants further investigation.

DIAGNOSTIC CHALLENGES

Although OSA is a well-studied and common disease, diagnosis can be challenging, namely due to the requirement of PSG to confirm the diagnosis, traditionally a service with variable accessibility. Furthermore, patients had to stay overnight for sleep study. For patients with limited transportation and reduced mobility, like many elderly, this may posit insurmountable difficulty. Access in the United States improved in 2008 when portable monitoring to diagnose OSA and prescribe CPAP was allowed under Medicare coverage [34]. Since then, at-home PSG for the elderly has been validated repeatedly, with multiple studies finding no difference in AHI when compared to in-laboratory PSG [35], particularly if combined with other clinical data such as NC, symptoms, age, and sex [36]. However, while at home, sleep studies are designed to be executed easily, many older patients may struggle to use newer technology and thus may struggle to execute the study properly. It is important to provide thorough instructions prior to the home study to ensure proper execution.

Screening may also require modification in elderly populations with suspected OSA. The STOP BANG questionnaire (SBQ) is the gold standard for screening. In a study of patients over 65 years in Brazil, the traditional STOP BANG had high sensitivity 0.96, but low specificity 0.13, for predicting AHI >15 [37]. Despite this reassuring data, the SBQ is a questionnaire that is only as reliable as the patient it is performed on. One study from a memory clinic with an average age of 65 years and new onset cognitive or mood issues underwent STOP-BANG then PSG and reported a sensitivity and specificity of 52% and 62%, respectively, for moderate-severe OSA and a sensitivity and specificity of 18% and 87% for severe OSA [38]. Even though the SBQ has been validated in the elderly cognitive impairment is more common in the population, and thus the SBQ may have reduced utility in clinical practice.

PATHOPHYSIOLOGY AND AGE-RELATED CONSIDERATIONS

As discussed previously, OSA often presents differently in older and younger populations—this difference is further reflected in differences observed on PSG between populations. The AHI, the traditional scale used to quantify OSA, is typically higher in older patients [12]. Other measurements of OSA severity also suggest that OSA is more severe in elderly people. Older patients have more time under 90% O₂, and reduced SaO₂ regardless of AHI, indicating increased risk for hypoxemia [39]. Furthermore, increased age is correlated with longer apnea and hypopnea events [40]. By the common measurements, OSA is worse in older people. What physiological differences contribute to the increased severity is under much study.

Anatomical and Physiological Changes with Increased Age

Age-related upper airway changes are likely responsible for the increased prevalence and severity of OSA in the elderly. Soft palate length, pharyngeal length, and anterior tubercle volume increase with age, all of which increase the risk of OSA [41]. As previously discussed, the classic risk factor of increased NC is not associated with OSA [14]; however, pharyngeal fat deposition increases with age regardless of BMI [42]. This may explain why patients over 65 years with OSA were observed to have a lower BMI compared to younger age groups [43]. Further comparative anatomy analysis from Japan found that patients with OSA over 60 years had a wider retroglossal space and a lower soft palate than patients under 40 years [44]. Furthermore, the same study found that increased tonsil size was positively correlated with AHI in multiple age groups under 60 years but not in those over 60 years, suggesting changes in the dynamics of the elderly airway [44]. These changes in anatomy with age likely predispose older patients to OSA.

Upper airway tone and responsiveness decrease with age, which may predispose a patient to upper airway collapse [45]. Notably, the genioglossus, responsible for protruding and depressing the tongue and thus maintaining airway patency in sleep, has reduced responsiveness to low O₂ with increased age [46]. This may explain why the Pcrit, the critical pressure at which the airway collapses, increases with greater age, raising the risk for OSA [47]. A study found that older adults had a more collapsable airway but a lower respiratory drive that triggered arousal and lower loop gain, which suggests that an increased tendency for collapsibility plays a more important role in OSA in the elderly than a dysfunctional ventilatory control system [48]. This has been confirmed on direct visualization with drug induced sleep endoscopy (DISE) studies. Older age groups have a higher rate of vellum collapse and less lateral wall collapse during DISE as compared to younger populations [49]. Changes in muscular tone and responsiveness with age explain the increased airway collapsibility in the elderly, and likely why they are more likely to develop to OSA.

Positional Sleep Apnea

Positional sleep apnea, defined as OSA dependent on the patient’s sleep position, is an important further consideration for OSA treatment in the elderly. Based on the differences in physiology with age suggested earlier, there is particular concern for sleep apnea in the supine position in the elderly due to the elderly population’s predilection for anterior-posterior axis collapse [50]. Supine AHI, as compared to non-supine AHI, has been observed to be nearly double in the older population [51]. Lateral positional sleep apnea is quite rare, with only 4.1% of patients having that phenotype [52]. Data from Korea suggests that 80%–90% of OSA patients have positional sleep apnea [53]. The use of devices to prevent supine sleep has been shown to improve AHI in younger populations, but more research is needed in elderly populations [54]. Positional OSA should be considered for all elderly people presenting with concern for OSA.

Alterations in Sleep Architecture

Sleep architecture changes have also been noted with age. Elderly patients tend to have reduced rapid eye movement (REM) sleep, slow wave sleep [55], and sleep spindles [56], accompanied by an increase in lighter sleep stages [57]. In middle age, OSA is associated with sleep fragmentation and decreases in slow wave and REM sleep [58]. Specific sleep phase changes seen in older OSA patients include increased N1 sleep and decreased N3 sleep, as well as decreased average SpO₂ sleep efficiency [59]. Another study of patients in Egypt being evaluated for OSA found that the older than 65-year group had longer sleep latency and higher sleep latency, and lower sleep efficiency, and N3% than the 18–50-year age group [60]. Older patients with OSA have different sleep architecture than younger patients, which may explain their different presentations.

MANAGEMENT IN OLDER PATIENTS

In consideration of the less severe symptomatology of OSA in elderly patients despite a relatively higher AHI compared to younger populations, the value of treating OSA in this population is less clear. Given that treatment, namely CPAP, can be uncomfortable and costly, deciding whether to treat OSA should be highly personalized to the individual patient. Current expert consensus from the International Geriatric Sleep Medicine Task Force recommends initiating treatment of OSA in the old and frail [61]. OSA in the elderly has been associated with higher healthcare costs [62]. However, evidence on whether treating OSA in the elderly may improve long-term outcomes remains mixed. Medicare beneficiaries with cardiovascular disease and undiagnosed OSA had an increased risk of hospitalization [63]. Notably, a prospective study of patients without coronary heart disease (CAD) or HF >70 years found that OSA was not a predictor of CAD after being followed for median of 8.7 years [64], even for those with severe OSA [65]. Patients were selected from the general population, not from those with symptoms of OSA [64]. Independent diagnosis rate of moderate to severe OSA in the study population at 5 years after the study significantly differed from the OSA diagnosis rate at the time of study, thus making it unclear if these patients definitively have OSA [64]. Another study of males over 50 years found no greater risk of all-cause mortality [66]. Evidence regarding long-term outcomes in the elderly is inconsistent and remains an important area for further study.

CPAP Compliance

CPAP therapy is the gold standard treatment for OSA [67]. Despite this, it can be challenging to convince the elderly to begin CPAP treatment, with studies estimating that only 21% [68]–31% [69] of older patients begin treatment. Even after starting CPAP, adherence, typically defined as CPAP usage >4 hours a night, can be particularly challenging to older patients. One study found CPAP compliance significantly decreases with age [70]. Patient adherence for CPAP is certainly a challenge in this population.

Even though there is evidence of worse adherence in the elderly, ample data to the contrary exists. A study from Paris found age over 60 years was not associated with decreased compliance of CPAP after correcting for confounders [71]. One study found no difference in adherence between the ≥80 and the 70–80-year age groups [72]. A retrospective study again showed that age was not associated with CPAP adherence [73], and some data even shows that patients older than 60 [74] or 70 years [75] had greater compliance. In patients treated with CPAP for at least 4 months, adherence increased until age 80 years [76]. Older patients have been reported to have high levels of compliance, with one from France of patients with an AHI >15 and at least one major cardiovascular or respiratory comorbidity, or excessive daytime sleepiness were 85.5% compliant at 5 months after diagnosis [77]. This recent data suggests that elderly people may be more compliant with CPAP than the younger population. Certainly, concerns about compliance should not be based solely on age.

CPAPs Effects on Sleep and Quality of Life

Another important symptom of OSA is sleepiness. Although, as discussed previously, elderly people with OSA are less sleepy than their younger counterparts, many randomized control trials (RCTs) have demonstrated CPAP’s ability to reduce daytime sleepiness. Studies have shown that CPAP reduces sleepiness per scores on Epworth Sleepiness Scale (ESS) [78], and additionally, that it may improve anxiety, depression, and neurocognitive symptoms [79]. Contrary to the previously discussed trials, a study of patients over 80 years with moderate sleep apnea AHI >15 found that although CPAP improved witnessed apneas and AHI, it did not improve ESS, any neurocognitive test, OSA-related symptoms, blood pressure, anxiety, or depression [80]. CPAP seems to improve sleepiness in the elderly; however, there may be a ceiling effect in those over 80 years. CPAP’s ability to improve quality of life in the elderly is unproven; however, we recommend encouraging patients to attempt CPAP therapy. It is a low cost, non-invasive and safe intervention to noticeably improve their quality of life. Thus, it should be trialed in patients on a personalized basis.

CPAP’s Effects on Other Health Outcomes

CPAP is the gold standard treatment for OSA, and there has been ample research into the effectiveness of CPAP in the elderly concerning various health outcomes. Characteristics of key trials are described in Table 1. An area of particular focus is cardiovascular health. One retrospective study of 888,835 Medicare beneficiaries observed that those with evidence of CPAP initiation had significantly lower all-cause mortality risk and fewer major adverse cardiac events [81]. Some observational studies have made use of a non-adherent pseudo-control group to infer CPAPs efficacy. One such study noted significantly higher cardiovascular mortality in those with an AHI >30 than their treated counterparts [82]. Furthermore, over 6-year period, patients with severe OSA who declined CPAP assessed at baseline had an increased risk of stroke [83]. A meta-analysis found that patients who were not treated with CPAP had a higher overall risk of death, improved sleepiness, and lower cardiovascular risk [84]. Furthermore, a Swedish panel of experts recommended CPAP in patients if they are symptomatic or if the AHI is greater 30 and they have a cardio-metabolic comorbidity [85].

Table 1

Characteristics of selected CPAP trials in the elderly

Despite this data supporting CPAP’s cardiovascular benefit, some studies have found that CPAP is ineffective at preventing cardiovascular causes of death, myocardial infarction, stroke, or hospitalization for unstable angina, HF, or transient ischemic attack in patients over 60 years [86]. A study in Spain randomized patients to either CPAP or usual care within after an episode of acute coronary syndrome, and they found no difference between the groups in various cardiovascular endpoints [87]. Additionally, a study of 8 sleep centers in Madrid, Spain of patients over 70 years with moderate OSA between the treated and untreated groups in cardiovascular outcomes [88]. More study is needed to determine if CPAP can improve cardiovascular outcomes in the elderly.

Pharmacological Treatment

Though CPAP remains the gold standard for treatment of OSA, pharmacological options have emerged as a potential avenue for reducing OSA symptoms, including noradrenergics, antimuscarinics, acetylcholinesterase inhibitors, and glucagon like peptide (GLP)-agonists, among others [89]. Notable pathophysiological mechanisms targeted by pharmacological options include increasing upper airway muscle tone, decreasing airway congestion, increasing arousal threshold, increasing respiratory drive, and weight loss [90]. Notably, combined noradrenergic-antimuscarinic therapies, such as atomoxetine-oxybutynin, and GLP-1 agonists seemed to be most effective in improving OSA symptoms [89,91]. However, tirzepatide is currently the only pharmacological treatment approved for the treatment of OSA, specifically in adults with obesity and moderate to severe OSA [92]. Further study is needed for other pharmacologic options in the treatment of OSA, particularly in older populations—there are currently no trials investigating pharmacological treatment specifically in this population. Certain drug classes studied as possible pharmacologic options, such as antimuscarinics and hypnotics, may present with greater risk in elderly populations; thus, their use must be well-studied before they can be deemed safe treatments for the elderly.

Surgical Treatments

Older patients are already at higher risk for surgical complications, and comorbid OSA only increases said risk. In sleep specific procedures, retrospective data of older patients who underwent sleep surgery had higher rates of complication [93]. Still, these surgeries can be effective treatment of OSA in this population. The ADHERE registry of upper airway stimulating devices, such as INSPIRE, consisting of 13 US hospitals and 3 in Germany, found that older adults on average had a greater reduction in AHI and higher usage than the younger population. Surgical times and complications were similar between the two groups [94]. Surgeries are higher risk in this population, but they can be an effective means of controlling OSA.

Dentures

Complete dentures have been considered as a treatment for OSA. They are thought to maintain upper airway structure and prevent collapse. As the rate of denture use is high at baseline in the elderly (as high as 75% in some elderly populations) [95], the effect of dentures on OSA has been explored. Edentulous patients with OSA were found to have worsened OSA with longer edentulous periods [96]. One study of 23 patients found that the group sleeping with dentures had an increased AHI compared to the control group that did not wear dentures [97]. In a crossover study, sleeping without dentures again led to a higher AHI [98]. Another study with crossover yielded the opposite findings, finding that the mean AHI was lower when without dentures [99]. A recent meta-analysis of 3 RCTs concluded there was no association between denture use and AHI [100]. Deciding whether to wear dentures while sleeping depends on individual factors.

OSA AND COGNITIVE DECLINE

As neurocognitive decline is one of the most harmful aspects of aging, understanding its connection to a pathology as common as OSA is clearly important, and some research already shows an association between OSA and neurocognitive decline. To begin, a study following patients over 5 years found that those over 70 years of age with OSA had an increased risk of the development of dementia even when adjusting for HTN, hyperlipidemia, diabetes, stroke, urbanization level, and monthly income [101]. A sub study of the previously discussed aspirin study showed those with OSA had lower Mini-Mental State Examination (MMSE) scores than those without the disease [102], and another study showed AHI ≥20 was associated with greater decline in phonemic efficiency [9]. Interestingly, mean SpO₂ (%) <92.5 was associated with greater cognitive decline measured by MMSE, delayed free recall OR, while AHI was not [9]. Other studies have reiterated the between O₂ (%) and cognitive decline. A multicenter study in the United States discovered that having more than 1% of time spent with SpO₂ <90%, but not increased AHI, had decline on the on the MMSE [103]. Furthermore, a study in France without stroke history found that Pulse rate variability, but not AHI, was associated with increased stroke risk [104]. Lastly, a meta-analysis of 5 cohort studies on elderly patients with average reported ages all over 62 years found that those with sleep disordered breathing (SDB) had increased risk of cognitive decline [105]. There is good evidence to suggest a connection between OSA and neurocognitive decline in the elderly population, although that connection may not be associated with the AHI.

In contrast to the evidence presented above, some quality research suggests that OSA does not predispose an individual with OSA to neurocognitive decline. A study with an average starting age of 61 years demonstrated that there was no difference between the OSA and no OSA group, even when stratified by OSA severity for delayed word recall, word fluency, and digit symbol substitution challenge at 10-year follow-up [106]. Additionally, there is evidence EDS, as opposed to damage from OSA, is the cause of neurocognitive decline [107]. Although the relationship between OSA and cognitive impairment is well established, more research is needed to clarify the relationship between OSA and neurocognitive decline.

Though the association between OSA and neurocognitive decline has been well characterized, the ability of CPAP to alter the trajectory of neurocognitive changes continues to be an area of active study. Evidence so far in this domain has been mixed— a cohort study showed CPAP use delayed onset of mild cognitive impairment (MCI) [108], while a pilot RCT showed no improvement of cognition in patients with MCI and OSA after 12 weeks of CPAP use [109]. Another RCT showed improvement in multiple cognitive domains with CPAP treatment in patients over 65 years with newly-diagnosed severe OSA [110]. However, progression of dementia in those with OSA seems to have no association with CPAP adherence [111]. A double blind, RCT showed no difference between the groups in Pathfinder Number Total Time, Buschke Selective Reminding Test Sum Recall, or Sustained Working Memory Test Overall Mid day Index even among those with AHI >30 [112]; however, the average age was only 52 years in the treated group, so it may not apply to our population. Additionally, a 14-center RCT in the UK found CPAP did not improve cognition compared to only supportive care [113]. The possible effects of CPAP on neurocognitive decline in elderly patients with OSA are not well-characterized and require further investigation.

Alzheimer’s Disease

Alzheimer’s disease (AD) is the most common cause of dementia in the United States and is highly prevalent in the elderly [114]; as such, there is considerable overlap with the elderly OSA population. As expected, CPAP seems effective in improving sleepiness in AD patients with comorbid OSA [115] and improving sleep quality [116]. The impact of CPAP on cognition in this population is less clear than its effect on sleep. One study showed CPAP-treated patients had significantly slower decline on MMSE after 3 years [117]; this is complemented by an older study that showed no improvement in cognition after 3 weeks of CPAP but reduced cognitive decline in a small subset of patients after 6 weeks [118]. OSA may raise the risk of developing AD. A study from Korea found that patients in their 60s and 70s with SDB had an increased risk for developing AD [119]. Furthermore, elevated tau proteins have been found in patients with OSA, thus suggesting possible mechanism for tau protein collection [120]. Additionally, donepezil has been found to improve AHI in a small RCT in OSA-AD comorbid patients [121]. OSA has also been shown to interfere with proper function of the glymphatic system, which is associated with the development of neurodegenerative disorders [122]. Many elderly patients suffer from both AD and OSA, so understanding their interplay plays a significant role in treating OSA in the elderly population at large.

CONCLUSION

The established paradigm of OSA is that of a disease mainly affecting middle-aged, obese men, presenting largely with daytime sleepiness and risk of cardiovascular complication. However, OSA is highly prevalent in the elderly population, who often do not fit this typical OSA picture (Table 2). Recognizing that elderly patients may not present with daytime sleepiness, snoring, or increased NC, among other considerations, is of great importance to adequately screen and diagnose patients of this population— especially given the many comorbid conditions and polypharmacy that may mimic OSA.

Table 2

Summary of key differences between elderly and non-elderly populations with obstructive sleep apnea

Treatment of OSA in elderly patients remains largely oriented towards the use of CPAP—clear benefits are seen with sleep-related symptoms; however, the benefits of CPAP on long-term outcomes, including cardiovascular events and neurocognitive decline, are not well-characterized. The intersection between elderly populations with OSA and other comorbid conditions common amongst the elderly, such as insomnia and AD, needs further investigation. More research is needed in this population— in particular with the pathophysiology underlying these changes, risk factors in this population, and the long-term outcomes of CPAP treatment, particularly in those with comorbid conditions.

Notes

Availability of Data and Material

Data sharing not applicable to this article as no datasets were generated or analyzed during the study.

Author Contributions

Conceptualization: William J. Healy, David Brower. Funding acquisition: Younghoon Kwon. Methodology: David Brower. Project administration: William J. Healy, David Brower. Supervision: William J. Healy, Younghoon Kwon. Visualization: David Brower, Eric Pan. Writing—original draft: David Brower, Eric Pan, William Goss. Writing—review & editing: all authors.

Conflicts of Interest

The authors have no potential conflicts of interest to disclose.

Funding Statement

This work was funded by Dr. Younghoon Kwon’s NIH grants R21HL167126 and R01HL158765.

Acknowledgements

None

References

1. Sanchez-Azofra A, Malhotra A, Owens RL, Healy WJ. Obstructive sleep apnea: pathophysiology and endotypes. ATS Sch 2023;4:567–8.

2. Senaratna CV, Perret JL, Lodge CJ, Lowe AJ, Campbell BE, Matheson MC, et al. Prevalence of obstructive sleep apnea in the general population: a systematic review. Sleep Med Rev 2017;34:70–81.

3. Mukherjee S, Patel SR, Kales SN, Ayas NT, Strohl KP, Gozal D, et al. An official American Thoracic Society statement: the importance of healthy sleep. Recommendations and future priorities. Am J Respir Crit Care Med 2015;191:1450–8.

4. Javaheri S, Javaheri S, Somers VK, Gozal D, Mokhlesi B, Mehra R, et al. Interactions of obstructive sleep apnea with the pathophysiology of cardiovascular disease, part 1: JACC state-of-the-art review. J Am Coll Cardiol 2024;84:1208–23.

5. Gottlieb DJ, Punjabi NM. Diagnosis and management of obstructive sleep apnea: a review. JAMA 2020;323:1389–400.

6. Knauert M, Naik S, Gillespie MB, Kryger M. Clinical consequences and economic costs of untreated obstructive sleep apnea syndrome. World J Otorhinolaryngol Head Neck Surg 2015;1:17–27.

7. Braley TJ, Dunietz GL, Chervin RD, Lisabeth LD, Skolarus LE, Burke JF. Recognition and diagnosis of obstructive sleep apnea in older Americans. J Am Geriatr Soc 2018;66:1296–302.

8. Monti A, Doulazmi M, Nguyen-Michel VH, Pautas E, Mariani J, Kinugawa K. Clinical characteristics of sleep apnea in middle-old and oldest-old inpatients: symptoms and comorbidities. Sleep Med 2021;82:179–85.

9. Marchi NA, Solelhac G, Berger M, Haba-Rubio J, Gosselin N, Vollenweider P, et al. Obstructive sleep apnoea and 5-year cognitive decline in the elderly. Eur Respir J 2023;61:2201621.

10. Tufik S, Santos-Silva R, Taddei JA, Bittencourt LR. Obstructive sleep apnea syndrome in the Sao Paulo Epidemiologic Sleep Study. Sleep Med 2010;11:441–6.

11. Sunwoo JS, Hwangbo Y, Kim WJ, Chu MK, Yun CH, Yang KI. Prevalence, sleep characteristics, and comorbidities in a population at high risk for obstructive sleep apnea: a nationwide questionnaire study in South Korea. PLoS One 2018;13:e0193549.

12. Heinzer R, Vat S, Marques-Vidal P, Marti-Soler H, Andries D, Tobback N, et al. Prevalence of sleep-disordered breathing in the general population: the HypnoLaus study. Lancet Respir Med 2015;3:310–8.

13. Gabbay IE, Lavie P. Age- and gender-related characteristics of obstructive sleep apnea. Sleep Breath 2012;16:453–60.

14. Lee YG, Lee YJ, Jeong DU. Differential effects of obesity on obstructive sleep apnea syndrome according to age. Psychiatry Investig 2017;14:656–61.

15. Hongyo K, Ito N, Yamamoto K, Yasunobe Y, Takeda M, Oguro R, et al. Factors associated with the severity of obstructive sleep apnea in older adults. Geriatr Gerontol Int 2017;17:614–21.

16. Sforza E, Chouchou F, Collet P, Pichot V, Barthélémy JC, Roche F. Sex differences in obstructive sleep apnoea in an elderly French population. Eur Respir J 2011;37:1137–43.

17. Tashkandi Y, Badr MS, Rowley JA. Determinants of the apnea index in a sleep center population. Sleep Breath 2005;9:181–6.

18. Anttalainen U, Saaresranta T, Aittokallio J, Kalleinen N, Vahlberg T, Virtanen I, et al. Impact of menopause on the manifestation and severity of sleep-disordered breathing. Acta Obstet Gynecol Scand 2006;85:1381–8.

19. Young T, Finn L, Austin D, Peterson A. Menopausal status and sleep-disordered breathing in the Wisconsin Sleep Cohort Study. Am J Respir Crit Care Med 2003;167:1181–5.

20. Bixler EO, Vgontzas AN, Lin HM, Ten Have T, Rein J, Vela-Bueno A, et al. Prevalence of sleep-disordered breathing in women: effects of gender. Am J Respir Crit Care Med 2001;163:608–13.

21. Lindberg E, Bonsignore MR, Polo-Kantola P. Role of menopause and hormone replacement therapy in sleep-disordered breathing. Sleep Med Rev 2020;49:101225.

22. Amsterdam EA, Wenger NK, Brindis RG, Casey DE Jr, Ganiats TG, Holmes DR Jr, et al. 2014 AHA/ACC guideline for the management of patients with non-ST-elevation acute coronary syndromes: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol 2014;64:e139–228.

23. Qiu Q, Mateika JH. Pathophysiology of obstructive sleep apnea in aging women. Curr Sleep Med Rep 2021;7:177–85.

24. Popovic RM, White DP. Upper airway muscle activity in normal women: influence of hormonal status. J Appl Physiol (1985) 1998;84:1055–62.

25. Young T, Shahar E, Nieto FJ, Redline S, Newman AB, Gottlieb DJ, et al. Predictors of sleep-disordered breathing in community-dwelling adults: the Sleep Heart Health Study. Arch Intern Med 2002;162:893–900.

26. Johansson P, Alehagen U, Svanborg E, Dahlström U, Broström A. Sleep disordered breathing in an elderly community-living population: relationship to cardiac function, insomnia symptoms and daytime sleepiness. Sleep Med 2009;10:1005–11.

27. Lammintausta A, Anttalainen U, Basoglu ÖK, Bonsignore MR, Gouveris H, Grote L, et al. Clinical characteristics and positive airway pressure adherence among elderly European sleep apnoea patients from the ESADA cohort. ERJ Open Res 2023;9:00506–2022.

28. Zhou J, Xia S, Li T, Liu R. Association between obstructive sleep apnea syndrome and nocturia: a meta-analysis. Sleep Breath 2020;24:1293–8.

29. Bing MH, Jennum P, Moller LA, Mortensen S, Lose G. Obstructive sleep apnea in a Danish population of men and women aged 60–80 years with nocturia. J Clin Sleep Med 2012;8:515–20.

30. Endeshaw YW, Johnson TM, Kutner MH, Ouslander JG, Bliwise DL. Sleep-disordered breathing and nocturia in older adults. J Am Geriatr Soc 2004;52:957–60.

31. Middelkoop HA, Smilde-van den Doel DA, Neven AK, Kamphuisen HA, Springer CP. Subjective sleep characteristics of 1,485 males and females aged 50–93: effects of sex and age, and factors related to self-evaluated quality of sleep. J Gerontol A Biol Sci Med Sci 1996;51:M108–15.

32. Zhang Y, Ren R, Lei F, Zhou J, Zhang J, Wing YK, et al. Worldwide and regional prevalence rates of co-occurrence of insomnia and insomnia symptoms with obstructive sleep apnea: a systematic review and meta-analysis. Sleep Med Rev 2019;45:1–17.

33. Wu M, Xue P, Yan J, Benedict C. Association between age and comorbid insomnia and sleep apnea. Sleep Med 2024;124:659–61.

34. Collop NA. Portable monitoring for the diagnosis of obstructive sleep apnea. Curr Opin Pulm Med 2008;14:525–9.

35. Polese JF, Santos-Silva R, de Oliveira Ferrari PM, Sartori DE, Tufik S, Bittencourt L. Is portable monitoring for diagnosing obstructive sleep apnea syndrome suitable in elderly population? Sleep Breath 2013;17:679–86.

36. Morales CR, Hurley S, Wick LC, Staley B, Pack FM, Gooneratne NS, et al. In-home, self-assembled sleep studies are useful in diagnosing sleep apnea in the elderly. Sleep 2012;35:1491–501.

37. Martins EF, Martinez D, Cortes AL, Nascimento N, Brendler J. Exploring the STOP-BANG questionnaire for obstructive sleep apnea screening in seniors. J Clin Sleep Med 2020;16:199–206.

38. Lam A, D’Rozario AL, Kong S, Ireland C, Mowszowski L, LaMonica HM, et al. Screening for obstructive sleep apnea in the memory clinic: a comparison of questionnaires, pulse oximetry, and polysomnography. J Alzheimers Dis 2025;103:218–29.

39. Soria Robles AI, Aguado Blanco C, Juárez España M, Andrés Pretel F, Massó Núñez ML, Vizcaíno García MS, et al. Obstructive sleep apnea and oxygenation in very old adults: a propensity-score match study. J Am Med Dir Assoc 2024;25:105023.

40. Leppänen T, Töyräs J, Mervaala E, Penzel T, Kulkas A. Severity of individual obstruction events increases with age in patients with obstructive sleep apnea. Sleep Med 2017;37:32–7.

41. Shigeta Y, Enciso R, Ogawa T, Clark GT. Changes in three dimensional simulation models of the airway which are due to increases in age or body mass index. Stud Health Technol Inform 2008;132:460–2.

42. D’Angelo GF, de Mello AAF, Schorr F, Gebrim E, Fernandes M, Lima GF, et al. Muscle and visceral fat infiltration: a potential mechanism to explain the worsening of obstructive sleep apnea with age. Sleep Med 2023;104:42–8.

43. Chung S, Yoon IY, Lee CH, Kim JW. Effects of age on the clinical features of men with obstructive sleep apnea syndrome. Respiration 2009;78:23–9.

44. Tagaya M, Nakata S, Yasuma F, Noda A, Hamajima N, Katayama N, et al. Morphological features of elderly patients with obstructive sleep apnoea syndrome: a prospective controlled, comparative cohort study. Clin Otolaryngol 2011;36:139–46.

45. Erskine RJ, Murphy PJ, Langton JA, Smith G. Effect of age on the sensitivity of upper airway reflexes. Br J Anaesth 1993;70:574–5.

46. Klawe JJ, Tafil-Klawe M. Age-related response of the genioglossus muscle EMG-activity to hypoxia in humans. J Physiol Pharmacol 2003;54Suppl 1. :14–9.

47. Stanley JJ. Sleep apnea surgery in the elderly. Oper Tech Otolayngol Head Neck Surg 2020;31:260–4.

48. Edwards BA, Wellman A, Sands SA, Owens RL, Eckert DJ, White DP, et al. Obstructive sleep apnea in older adults is a distinctly different physiological phenotype. Sleep 2014;37:1227–36.

49. Zhao C, Viana A Jr, Ma Y, Capasso R. The effect of aging on drug-induced sleep endoscopy findings. Laryngoscope 2018;128:2644–50.

50. Vicini C, De Vito A, Iannella G, Gobbi R, Corso RM, Montevecchi F, et al. The aging effect on upper airways collapse of patients with obstructive sleep apnea syndrome. Eur Arch Otorhinolaryngol 2018;275:2983–90.

51. Ann L, Lee CH, Immen R, Dyken ME, Im K. Older age is associated with positional obstructive sleep apnea. Am J Geriatr Psychiatry 2023;31:943–52.

52. Ben Sason Y, Oksenberg A, Sobel JA, Behar JA. Characteristics of patients with positional OSA according to ethnicity and the identification of a novel phenotype-lateral positional patients: a Multi-Ethnic Study of Atherosclerosis (MESA) study. J Clin Sleep Med 2023;19:529–38.

53. Shin C. Sleep disordered breathing in elderly: current evidence and future directions in clinical practice. Sleep Med Res 2023;14:127–8.

54. van Maanen JP, Richard W, Van Kesteren ER, Ravesloot MJ, Laman DM, Hilgevoord AA, et al. Evaluation of a new simple treatment for positional sleep apnoea patients. J Sleep Res 2012;21:322–9.

55. Espiritu JR. Aging-related sleep changes. Clin Geriatr Med 2008;24:1–14.

56. Peters KR, Ray LB, Fogel S, Smith V, Smith CT. Age differences in the variability and distribution of sleep spindle and rapid eye movement densities. PLoS One 2014;9:e91047.

57. Geisler P, Wehrle R, Yassouridis A, Ultsch A, Wetter TC, Schulz H. Sleep and aging. A polysomnographic follow-up study, some 40 years later. J Sleep Res 2025. Mar. 18. [Epub]. Available from: https://doi.org/10.1111/jsr.70039 .

58. Heinzer R, Gaudreau H, Décary A, Sforza E, Petit D, Morisson F, Montplaisir J. Slow-wave activity in sleep apnea patients before and after continuous positive airway pressure treatment: contribution to daytime sleepiness. Chest 2001;119:1807–13.

59. Shao C, Wang H, He Y, Yu B, Zhao H. Clinical phenotype of obstructive sleep apnea in older adults: a hospital-based retrospective study in China. Ir J Med Sci 2023;192:2305–12.

60. El-Helbawy RH, Kasemy ZA, Eid HA. Effect of obstructive sleep apnea syndrome on sleep architecture: comparative study between geriatrics and middle-aged adult patients. Egypt J Chest Dis Tuberc 2023;72:559–64.

61. Netzer NC, Ancoli-Israel S, Bliwise DL, Fulda S, Roffe C, Almeida F, et al. Principles of practice parameters for the treatment of sleep disordered breathing in the elderly and frail elderly: the consensus of the International Geriatric Sleep Medicine Task Force. Eur Respir J 2016;48:992–1018.

62. Tarasiuk A, Greenberg-Dotan S, Simon-Tuval T, Oksenberg A, Reuveni H. The effect of obstructive sleep apnea on morbidity and health care utilization of middle-aged and older adults. J Am Geriatr Soc 2008;56:247–54.

63. Kirk J, Wickwire EM, Somers VK, Johnson DA, Albrecht JS. Undiagnosed obstructive sleep apnea increases risk of hospitalization among a racially diverse group of older adults with comorbid cardiovascular disease. J Clin Sleep Med 2023;19:1175–81.

64. Gottlieb DJ, Yenokyan G, Newman AB, O’Connor GT, Punjabi NM, Quan SF, et al. Prospective study of obstructive sleep apnea and incident coronary heart disease and heart failure: the sleep heart health study. Circulation 2010;122:352–60.

65. Punjabi NM, Caffo BS, Goodwin JL, Gottlieb DJ, Newman AB, O’Connor GT, et al. Sleep-disordered breathing and mortality: a prospective cohort study. PLoS Med 2009;6:e1000132.

66. Lavie P, Lavie L, Herer P. All-cause mortality in males with sleep apnoea syndrome: declining mortality rates with age. Eur Respir J 2005;25:514–20.

67. Qaseem A, Holty JE, Owens DK, Dallas P, Starkey M, Shekelle P, et al. Management of obstructive sleep apnea in adults: a clinical practice guideline from the American College of Physicians. Ann Intern Med 2013;159:471–83.

68. Ng SS, Chan TO, To KW, Chan KK, Ngai J, Tung A, et al. Prevalence of obstructive sleep apnea syndrome and CPAP adherence in the elderly Chinese population. PLoS One 2015;10:e0119829.

69. Yang MC, Lin CY, Lan CC, Huang CY, Huang YC, Lim CS, et al. Factors affecting CPAP acceptance in elderly patients with obstructive sleep apnea in Taiwan. Respir Care 2013;58:1504–13.

70. Martinez-Garcia MA, Valero-Sánchez I, Reyes-Nuñez N, Oscullo G, Garcia-Ortega A, Gómez-Olivas JD, et al. Continuous positive airway pressure adherence declines with age in elderly obstructive sleep apnoea patients. ERJ Open Res 2019;5:00178–2018.

71. Pelletier-Fleury N, Rakotonanahary D, Fleury B. The age and other factors in the evaluation of compliance with nasal continuous positive airway pressure for obstructive sleep apnea syndrome. A Cox’s proportional hazard analysis. Sleep Med 2001;2:225–32.

72. Lammintausta A, Anttalainen U, Bouloukaki I, Schiza SE, Pataka A, Fanfulla F, et al. Factors influencing the PAP adherence of elderly European sleep apnea patients in the ESADA cohort. Sleep 2025;48:zsae266.

73. Schoch OD, Baty F, Niedermann J, Rüdiger JJ, Brutsche MH. Baseline predictors of adherence to positive airway pressure therapy for sleep apnea: a 10-year single-center observational cohort study. Respiration 2014;87:121–8.

74. Barroso A, Carrondo MC, Moita J. Influence of age on adherence to auto-CPAP: experience from a sleep center in Portugal. Adv Respir Med 2022;90:143–7.

75. Woehrle H, Graml A, Weinreich G. Age- and gender-dependent adherence with continuous positive airway pressure therapy. Sleep Med 2011;12:1034–6.

76. Prigent A, Blanloeil C, Serandour AL, Barlet F, Gagnadoux F, Jaffuel D. A biphasic effect of age on CPAP adherence: a cross-sectional study of 26,343 patients. Respir Res 2023;24:234.

77. Onen F, Onen SH, Le Vaillant M, Gagnadoux F, Martin FS, ; AGES Study Group. Adherence to continuous positive airway pressure treatment in a cohort of elderly adults with newly diagnosed obstructive sleep apnea. Sleep Breath 2023;27:1847–55.

78. Ponce S, Pastor E, Orosa B, Oscullo G, Catalán P, Martinez A, et al. The role of CPAP treatment in elderly patients with moderate obstructive sleep apnoea: a multicentre randomised controlled trial. Eur Respir J 2019;54:1900518.

79. Martínez-García MÁ, Chiner E, Hernández L, Cortes JP, Catalán P, Ponce S, et al. Obstructive sleep apnoea in the elderly: role of continuous positive airway pressure treatment. Eur Respir J 2015;46:142–51.

80. Martinez-Garcia MA, Oscullo G, Ponce S, Pastor E, Orosa B, Catalán P, et al. Effect of continuous positive airway pressure in very elderly with moderate-to-severe obstructive sleep apnea pooled results from two multicenter randomized controlled trials. Sleep Med 2022;89:71–7.

81. Mazzotti DR, Waitman LR, Miller J, Sundar KM, Stewart NH, Gozal D, et al. Positive airway pressure, mortality, and cardiovascular risk in older adults with sleep apnea. JAMA Netw Open 2024;7:e2432468.

82. Martínez-García MA, Campos-Rodríguez F, Catalán-Serra P, Soler-Cataluña JJ, Almeida-Gonzalez C, De la Cruz Morón I, et al. Cardiovascular mortality in obstructive sleep apnea in the elderly: role of long-term continuous positive airway pressure treatment: a prospective observational study. Am J Respir Crit Care Med 2012;186:909–16.

83. Munoz R, Duran-Cantolla J, Martínez-Vila E, Gallego J, Rubio R, Aizpuru F, et al. Severe sleep apnea and risk of ischemic stroke in the elderly. Stroke 2006;37:2317–21.

84. Yan B, Jin Y, Hu Y, Li S. Effects of continuous positive airway pressure on elderly patients with obstructive sleep apnea: a meta-analysis. Med Sci (Paris) 2018;34Focus issue F1. :66–73.

85. Grote L, Anderberg CP, Friberg D, Grundström G, Hinz K, Isaksson G, et al. National knowledge-driven management of obstructive sleep apnea-the Swedish approach. Diagnostics (Basel) 2023;13:1179.

86. Peker Y, Glantz H, Eulenburg C, Wegscheider K, Herlitz J, Thunström E. Effect of positive airway pressure on cardiovascular outcomes in coronary artery disease patients with nonsleepy obstructive sleep apnea. The RICCADSA Randomized Controlled Trial. Am J Respir Crit Care Med 2016;194:613–20.

87. Sánchez-de-la-Torre M, Sánchez-de-la-Torre A, Bertran S, Abad J, Duran-Cantolla J, Cabriada V, et al. Effect of obstructive sleep apnoea and its treatment with continuous positive airway pressure on the prevalence of cardiovascular events in patients with acute coronary syndrome (ISAACC study): a randomised controlled trial. Lancet Respir Med 2020;8:359–67.

88. López-Padilla D, Terán-Tinedo J, Cerezo-Lajas A, García LR, Ojeda-Castillejo E, López-Martín S, et al. Moderate obstructive sleep apnea and cardiovascular outcomes in older adults: a propensity scorematched multicenter study (CPAGE-MODE study). J Clin Sleep Med 2022;18:553–61.

89. Jaganathan N, Kwon Y, Healy WJ, Taskar V. The emerging role of pharmacotherapy in obstructive sleep apnea. J Otorhinolaryngol Hear Balanc Med 2024;5:12.

90. Nobre ML, Sarmento ACA, de Oliveira PF, Wanderley FF, Diniz J Júnior, Gonçalves AK. Pharmacological treatment for obstructive sleep apnea: a systematic review and meta-analysis. Clinics (Sao Paulo) 2024;79:100330.

91. Malhotra A, Grunstein RR, Fietze I, Weaver TE, Redline S, Azarbarzin A, et al. Tirzepatide for the treatment of obstructive sleep apnea and obesity. N Engl J Med 2024;391:1193–205.

92. Anderer S. FDA approves tirzepatide as first drug for obstructive sleep apnea. JAMA 2025;333:656.

93. Gouveia CJ, Cramer JD, Liu SY, Capasso R. Sleep surgery in the elderly: lessons from the national surgical quality improvement program. Otolaryngol Head Neck Surg 2017;156:757–64.

94. Withrow K, Evans S, Harwick J, Kezirian E, Strollo P. Upper airway stimulation response in older adults with moderate to severe obstructive sleep apnea. Otolaryngol Head Neck Surg 2019;161:714–9.

95. Su Y, Yuki M, Hirayama K, Sato M, Han T. Denture wearing and malnutrition risk among community-dwelling older adults. Nutrients 2020;12:151.

96. Tripathi A, Gupta A, Rai P, Sharma P, Tripathi S. Correlation between duration of edentulism and severity of obstructive sleep apnea in elderly edentulous patients. Sleep Sci 2022;15(Special 2):300–5.

97. Almeida FR, Furuyama RJ, Chaccur DC, Lowe AA, Chen H, Bittencourt LR, et al. Complete denture wear during sleep in elderly sleep apnea patients--a preliminary study. Sleep Breath 2012;16:855–63.

98. Bucca C, Cicolin A, Brussino L, Arienti A, Graziano A, Erovigni F, et al. Tooth loss and obstructive sleep apnoea. Respir Res 2006;7:8.

99. Arisaka H, Sakuraba S, Tamaki K, Watanabe T, Takeda J, Yoshida K. Effects of wearing complete dentures during sleep on the apnea-hypopnea index. Int J Prosthodont 2009;22:173–7.

100. Jurel SK, Bakrolwala HA, Chand P, Singh RD, Bhujbal RB, Singh BP. Nocturnal wearing of complete dentures and obstructive sleep apnea: a meta-analysis. J Indian Prosthodont Soc 2024;24:311–9.

101. Chang WP, Liu ME, Chang WC, Yang AC, Ku YC, Pai JT, et al. Sleep apnea and the risk of dementia: a population-based 5-year follow-up study in Taiwan. PLoS One 2013;8:e78655.

102. Ward SA, Woods RL, Naughton MT, Wolfe R, Gasevic D, Hamilton GS, et al. Sleep apnoea, cognition and aspirin’s effects in healthy older people: an ASPREE substudy. ERJ Open Res 2025;11:00581–2024.

103. Blackwell T, Yaffe K, Laffan A, Redline S, Ancoli-Israel S, Ensrud KE, et al. Associations between sleep-disordered breathing, nocturnal hypoxemia, and subsequent cognitive decline in older community-dwelling men: the Osteoporotic Fractures in Men Sleep Study. J Am Geriatr Soc 2015;63:453–61.

104. Sabil A, Gervès-Pinquié C, Blanchard M, Feuilloy M, Trzepizur W, Goupil F, et al. Overnight oximetry-derived pulse rate variability predicts stroke risk in patients with obstructive sleep apnea. Am J Respir Crit Care Med 2021;204:106–9.

105. Zhu X, Zhao Y. Sleep-disordered breathing and the risk of cognitive decline: a meta-analysis of 19,940 participants. Sleep Breath 2018;22:165–73.

106. Lutsey PL, Bengtson LG, Punjabi NM, Shahar E, Mosley TH, Gottesman RF, et al. Obstructive sleep apnea and 15-year cognitive decline: the Atherosclerosis Risk in Communities (ARIC) study. Sleep 2016;39:309–16.

107. Zhou J, Camacho M, Tang X, Kushida CA. A review of neurocognitive function and obstructive sleep apnea with or without daytime sleepiness. Sleep Med 2016;23:99–108.

108. Osorio RS, Gumb T, Pirraglia E, Varga AW, Lu SE, Lim J, et al. Sleep-disordered breathing advances cognitive decline in the elderly. Neurology 2015;84:1964–71.

109. Hoyos CM, Cross NE, Terpening Z, D’Rozario AL, Yee BJ, LaMonica H, et al. Continuous positive airway pressure for cognition in sleep apnea and mild cognitive impairment: a pilot randomized crossover clinical trial. Am J Respir Crit Care Med 2022;205:1479–82.

110. Dalmases M, Solé-Padullés C, Torres M, Embid C, Nuñez MD, Martínez-Garcia MÁ, et al. Effect of CPAP on cognition, brain function, and structure among elderly patients with OSA: a randomized pilot study. Chest 2015;148:1214–23.

111. Skiba V, Novikova M, Suneja A, McLellan B, Schultz L. Use of positive airway pressure in mild cognitive impairment to delay progression to dementia. J Clin Sleep Med 2020;16:863–70.

112. Kushida CA, Nichols DA, Holmes TH, Quan SF, Walsh JK, Gottlieb DJ, et al. Effects of continuous positive airway pressure on neurocognitive function in obstructive sleep apnea patients: The Apnea Positive Pressure Long-term Efficacy Study (APPLES). Sleep 2012;35:1593–602.

113. McMillan A, Bratton DJ, Faria R, Laskawiec-Szkonter M, Griffin S, Davies RJ, et al. Continuous positive airway pressure in older people with obstructive sleep apnoea syndrome (PREDICT): a 12-month, multicentre, randomised trial. Lancet Respir Med 2014;2:804–12.

114. Oh ES. Dementia. Ann Intern Med 2024;177:ITC161–76.

115. Chong MS, Ayalon L, Marler M, Loredo JS, Corey-Bloom J, Palmer BW, et al. Continuous positive airway pressure reduces subjective daytime sleepiness in patients with mild to moderate Alzheimer’s disease with sleep disordered breathing. J Am Geriatr Soc 2006;54:777–81.

116. Cooke JR, Ancoli-Israel S, Liu L, Loredo JS, Natarajan L, Palmer BS, et al. Continuous positive airway pressure deepens sleep in patients with Alzheimer’s disease and obstructive sleep apnea. Sleep Med 2009;10:1101–6.

117. Troussière AC, Charley CM, Salleron J, Richard F, Delbeuck X, Derambure P, et al. Treatment of sleep apnoea syndrome decreases cognitive decline in patients with Alzheimer’s disease. J Neurol Neurosurg Psychiatry 2014;85:1405–8.

118. Ancoli-Israel S, Palmer BW, Cooke JR, Corey-Bloom J, Fiorentino L, Natarajan L, et al. Cognitive effects of treating obstructive sleep apnea in Alzheimer’s disease: a randomized controlled study. J Am Geriatr Soc 2008;56:2076–81.

119. Lee JE, Yang SW, Ju YJ, Ki SK, Chun KH. Sleep-disordered breathing and Alzheimer’s disease: a nationwide cohort study. Psychiatry Res 2019;273:624–30.

120. Motamedi V, Kanefsky R, Matsangas P, Mithani S, Jeromin A, Brock MS, et al. Elevated tau and interleukin-6 concentrations in adults with obstructive sleep apnea. Sleep Med 2018;43:71–6.

121. Moraes W, Poyares D, Sukys-Claudino L, Guilleminault C, Tufik S. Donepezil improves obstructive sleep apnea in Alzheimer disease: a double-blind, placebo-controlled study. Chest 2008;133:677–83.

122. Ghaderi S, Mohammadi S, Fatehi F. Glymphatic pathway dysfunction in severe obstructive sleep apnea: a meta-analysis. Sleep Med 2025;131:106528.

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Study	Year	Country	Sample size	Population	Intervention	Control	Duration	Primary outcomes	Key findings
Martinez-Garcia et al. [80]	2022	Spain	97	Patients 80 years or older with AHI 15 or greater	CPAP	No CPAP	3 months	Sleepiness, quality of life, neurocognitive function, anxiety/depression, blood pressure	Significant improvement was noted in snoring, apneic episodes, and AHI in CPAP group; no improvements were noted in any other domains.
Ponce et al. [78]	2019	Spain	143	Patients over 70 years with AHI greater than 15 and less than 30	CPAP	No CPAP	3 months	Sleepiness, quality of life, neurocognitive function, anxiety/depression, blood pressure	Significant improvement in ESS and quality of life observed in treatment group; no significant differences noted between groups in regard to neurocognitive testing, anxiety/depression, or blood pressure.
Peker et al. [86]	2016	Sweden	244	Patients with coronary artery disease having recently undergone revascularization and AHI 15 or greater without daytime sleepiness; mean age 66.0 years	CPAP	No CPAP	Median duration 57 months	Repeat revascularization events, myocardial infarctions, or mortality from stroke or cardiovascular causes	No significant differences noted between treatment groups with regard to primary outcomes; significant cardiovascular risk reduction in patients who used CPAP for 4 or more hours per night after adjusting for baseline comorbidities.
Dalmases et al. [110]	2015	Spain	33	Patients 65 years or older with severe OSA and ESS 12 or greater	CPAP and conservative care	Conservative care	3 months	Cognitive performance via neuropsychologic evaluation	Significant improvement in episodic and short-term memory, executive function, and mental flexibility in CPAP treatment group, as well as increased connectivity in right middle frontal gyrus and less cortical thinning in CPAP group.
Martinez-Garcia et al. [79]	2015	Spain	224	Patients 70 years or older with AHI 30 or greater	CPAP	No CPAP	3 months	Quality of life, sleep symptoms, neurocognitive function, anxiety/depression, blood pressure	Significant improvement was noted in quality of life as measured by Quebec Sleep Questionnaire, sleep-related symptoms, anxiety/depression, and some neurocognitive domains (working memory and trail making) in CPAP group; no differences in blood pressure.
McMillan et al. [113]	2014	UK	231	Patients 65 years or older with newly diagnosed OSA	CPAP and supportive care	Supportive care	12 months	Sleepiness, cost-effectiveness, quality of life, cardiovascular risk factors	Significant improvement in sleepiness measured by ESS at 3 months and 12 months in CPAP group; improved mobility, total cholesterol, and LDL cholesterol at 3 months but not 12 months; probability that CPAP was cost effective based off National Health Service thresholds was 0.61.
Troussière et al. [117]	2014	France	23	Patients with mild to moderate AD and AHI 30 or greater; mean age 75.0 years	CPAP	No CPAP	3 years	MMSE	Significant decrease in MMSE decline observed in treatment group.
Ancoli-Israel et al. [118]	2008	USA	52	Patients with mild to moderate AD and AHI 10 or greater; mean age 78.2 years	CPAP	Placebo CPAP	21 days	Neuropsychological testing	Significant improvement in composite neuropsychological score in therapeutic CPAP group.
Cooke et al. [116]	2009	USA	52	Patients over 50 years with mild to moderate AD and AHI 10 or greater; mean age 78.2 years	CPAP	Placebo CPAP	3 weeks	Sleep parameters via polysomnographic evaluation	Significantly decreased Stage 1 and increased Stage 2 sleep after 1 day of treatment; decreased Stage 1 sleep, wake after sleep onset, and arousals, with increased Stage 3 sleep after 3 weeks.
Chong et al. [115]	2006	USA	39	Patients with mild to moderate AD and SDB; mean age 77.8 years	CPAP	Sham CPAP	6 weeks	Daytime sleepiness (measured via ESS)	Significant improvement in ESS observed at both 3 weeks and 6 weeks in patients receiving therapeutic CPAP.

	Middle aged	Elderly
Epidemiology	Prevalence: 27%–40% in men, 7%–18% women [2] Risk factors: increased neck circumference, obesity [13] menopause [19]	Prevalence: 60%–65% in men, 25%–35% in women [2] Risk factors: obesity, snoring [13], menopause [19]
Symptoms	More snoring [25] and daytime sleepiness [26], O₂ desaturation, apneic and hypopneic events	Less snoring [25] and daytime sleepiness [26], prolonged O₂ desaturation, higher number of apneic and hypopneic events [40], increased prevalence of COMISA [33]
Diagnosis	Polysomnography in lab or at home, screening questionnaires	Polysomnography, in lab or at home [35], screening questionnaires of limited utility due to poor memory [38]
Pathophysiology	Compressive effects of excess soft tissue surrounding airway [1]	Loss of airway muscle tone and responsiveness to respiratory drive, supine POSA, age-related oropharyngeal structural changes [41], changes in sleep architecture [60]
Management	CPAP, surgery, GLP-1 agonists [92]	CPAP [61], surgery, dentures [98]