Sleep quality is a complex construct that can be measured both objectively and subjectively, and includes quantitative aspects of sleep, such as duration and latency, but also qualitative aspects, such as how restored someone feels after sleeping (Buysse et al., 1989; Nelson et al., 2022). Sleep–wake cycle disruptions are frequent during the course of dementia and the prodromic phases of neurodegeneration (Lyketsos et al., 2002; Moran et al., 2005; Zhao et al., 2016). The relationship between sleep and dementia is bidirectional; while physiological and neuropathological aspects of dementia reduce the quality of sleep, poor sleep quality may also increase the risk of neurodegenerative diseases and dementia (McCoy and Strecker, 2011; Lim et al., 2014; Borges et al., 2019). Sleep and nighttime behavior disturbances are among the most important symptoms of dementia, leading to a need for long-term care, institutionalization, and caregiver burden in various populations (Hope et al., 1998; Moran et al., 2005; Fonseca et al., 2021), with attendant costs to individuals and society.

Poor sleep quality and short sleep duration during midlife have been associated with increased amyloid-beta deposition and the acceleration of regional brain hypometabolism (Choe et al., 2019), respectively. A study in young adults also showed that certain sleep disturbance patterns (such as elevated slow waves and daytime sleepiness) were associated with genetic liability for Alzheimer’s Disease (AD) before the appearance of other AD biomarkers (Muto et al., 2020). Disturbed sleep may also impact negatively on sleep-dependent consolidation of memory and on cerebral spinal fluid mediated clearance of metabolic residues from the brain, which are linked processes (Fultz et al., 2019) also known to be correlated with amyloidosis and AD (Bateman et al., 2007).

Sleep plays an important role in cognitive performance (Walker, 2009; Tsapanou et al., 2020), and the importance of sleep for the codification and consolidation of memory as well as for the retrieval of new declarative memories (Walker, 2009) is well established. Without adequate sleep, hippocampal function is disrupted and, consequently, so is the ability to record new experiences (Eichenbaum, 2004). Good sleep quality has been shown to correlate with better cognitive function in children (El-Sheikh et al., 2019) and has an impact on cognitive function during the waking period in adolescence, contributing to learning (Tarokh et al., 2016). In 141 middle-aged participants on the Sleep Heart Health Study, more severe oxygen saturation was associated with worse motor speed and processing speed performance after 9–40 months (Quan et al., 2006). A 25-year follow-up study including 7,959 participants demonstrated that persistent short sleep duration (<6 h) at ages 50, 60 and 70 was associated with a 30% increase in the risk of dementia compared with 6–8 h of sleep duration (Sabia et al., 2021). Correlations between sleep disorders and cognitive measures in healthy individuals (Walker, 2009; Tsapanou et al., 2016) and those with AD (Bonanni et al., 2005; Shin et al., 2014) have been found, with poorer nighttime sleep quality being associated with worse performance on praxis, immediate recall, and global cognition in AD patients (Shin et al., 2014). Furthermore, daytime sleepiness has been associated with cognitive performance deficits in both cross-sectional and longitudinal studies (Foley et al., 2001; Ohayon and Vecchierini, 2002; Bonanni et al., 2005; Merlino et al., 2010; Elwood et al., 2011; Tsapanou et al., 2016; Muto et al., 2020), as well as with incident dementia in many longitudinal studies (Foley et al., 2001; Elwood et al., 2011; Schlosser Covell et al., 2012). Some studies have also found sleep-disordered breathing to be associated with generally impaired cognitive function (Cohen-Zion et al., 2001; Spira et al., 2008), particularly impaired executive function (Ju et al., 2012) and memory (Aloia et al., 2003; Ju et al., 2012).

There is a growing body of evidence showing that there are racial/ethnic disparities related to sleep quality (Kalliny and McKenzie, 2017; Pandi-Perumal et al., 2017; Prasad et al., 2018; Denney et al., 2023). Sleep quality is influenced by various social, cultural, and genetic factors (Kalliny and McKenzie, 2017; Prasad et al., 2018). It is believed that the racial differences found in sleep disorders are due to several environmental stressors in personal health, such as socioeconomic inequalities, acculturation, and racism (Ruiter et al., 2011; Egan et al., 2017; Prasad et al., 2018; Liu et al., 2021). Sleep-related disorders, such as obstructive sleep apnea, and excessive daytime sleepiness have been linked to poor health outcomes, including cardiovascular disease (Ruiter et al., 2010; Drager et al., 2017; Egan et al., 2017). Also, there is evidence that both sleep disorders (Ruiter et al., 2010; Chen et al., 2015) and cardiovascular diseases (Egan et al., 2017; Zuma et al., 2021) are influenced by race/ethnicity. Furthermore, sleep-related disorders as well as vascular factors that can be associated with sleep deficiencies, such as arterial hypertension, diabetes, and hypercholesterolemia, are known risk factors for cognitive impairment and AD and related dementias. American Indians have a high prevalence of cerebral vascular disease (Hutchinson and Shin, 2014; Suchy-Dicey et al., 2017), stroke (Harris et al., 2015) and type 2 diabetes (Centers for Disease Control and Prevention, 2003; Cholerton et al., 2019), along with the presence of other health disparities (Hutchinson and Shin, 2014), but the impact of sleep-related disorders and their relationships with dementia are understudied in this population.

A recent study of self-reported sleep duration and mortality risk in different racial and ethnic groups found elevated risks of all-cause mortality for those who reported sleeping less than 5 h or more than 9 h per day, with variation by racial and ethnic identification (Denney et al., 2023). This study found that relative to White individuals, a significantly higher proportion of American Indians reported sleeping less than 5 h or more than 9 h. However, the authors acknowledged that the study was underpowered to estimate the association between sleep duration and mortality for this specific population.

To our knowledge, there are no studies investigating sleep-related disorders and their cognitive consequences focused specifically on American Indians. Data are needed in this population to identify possible opportunities for primary and secondary prevention of cognitive decline. The aim of this study is to characterize, for the first-time, sleep characteristics and their relationships with cognitive performance and classification of cognitive impairment approximately 10 years later in a sample of American Indians. Based on data showing that prevalent health and racial/ethnic disparities may contribute to sleep disorders (Kalliny and McKenzie, 2017; Pandi-Perumal et al., 2017; Prasad et al., 2018), that sleep disorders are frequently linked to cognitive decline (Foley et al., 2001; Merlino et al., 2010; Tsapanou et al., 2016), and that older American Indians are at greater risk for cognitive decline and dementia (Centers for Disease Control and Prevention, 2003; Hutchinson and Shin, 2014; Suchy-Dicey et al., 2017), we hypothesize that poor sleep quality will be associated with worse cognitive performance 10 years later.

This study characterized, for the first-time, associations between sleep characteristics and cognitive performance in a sample of aging American Indians. We found that sleep characteristics derived from polysomnography predicted cognitive performance assessed 10 years later. Aspects of sleep were correlated with cognitive performance in nearly all domains investigated by the neuropsychological tests – episodic verbal learning, short-delay and long-delay free recall, processing speed, verbal phonemic fluency, and 3MSE general cognition (Table 4). Furthermore, after adjustment for age, BMI, sex, study site, years of education, CESD depressive symptoms score, and presence of the APOE e4 allele, longer sleep latency was associated with increased likelihood of cognitive impairment later in life.

Sleep-related disorders have previously been associated with cognitive decline (Suh et al., 2018; Mei et al., 2023), dementia (Robbins et al., 2021a,b), and neurodegeneration (Mullins et al., 2020). Our findings support our initial hypothesis that sleep characteristics are correlated with subsequent cognitive performance in American Indians, such that future cognitive deficits may be predictable from polysomnographically recorded sleep. Longer sleep latency in particular was associated with worse cognitive outcomes, which is consistent with findings in the general population (Suh et al., 2018; Robbins et al., 2021a). Notably, in a nationally representative longitudinal study with 2,812 Medicare beneficiaries in the United States, more than 30 min of sleep latency as well as very short sleep duration (≤5 h) were associated with incident dementia after 5 years (Robbins et al., 2021a). And in a study comprising 2,238 individuals with normal cognition and 655 individuals with mild cognitive impairment in Korea, more than 30 min of sleep latency was associated with increased risk of cognitive decline at 4-year follow-up (Suh et al., 2018). In our study, 23.7% of the sample had more than 30 min of sleep latency. Longer sleep latency was associated with poorer cognitive scores on the COWA test of verbal phonemic fluency – and, importantly, with increased likelihood of cognitive impairment, as defined by more than 1.5 standard deviations below the mean on the 3MSE.

We also found that higher oxygen saturation at baseline was associated with worse total learning, short-delay free recall, and long-delay free recall performance, as measured by the CVLT-SF as well as the WAIS-IV digit symbol coding test at follow-up. These findings were unexpected and inconsistent with what many general population studies have found (Cohen-Zion et al., 2001; Aloia et al., 2003; Spira et al., 2008; Yamout et al., 2012). In our study, surprisingly, associations for all variables related to oxygen saturation and cognitive performance indicated that greater severity of oxygen desaturation was associated with better cognitive performance. We have some hypotheses for these findings. It is possible that participation in the SHHS stimulated awareness of sleep disruptions, particularly in participants meeting criteria for sleep treatment. Thus, those with worse rates of oxygen saturation at baseline may have sought sleep treatment during the approximately 10-year interval between the SHHS and the CDCAI study and, with treatment, improved their cognitive performance. It is also possible that those who had low average oxygen saturation during the SHHS study did not survive to follow up or were too debilitated to participate in the CDCAI study, causing a bias in the results and leaving those who had good average oxygen saturation in the CDCAI study to be relatively more cognitively impaired. However, it is also important to note that the associations between oxygen saturation and cognition in our sample are not statistically robust and may not generalize to other samples. Moreover, since the literature on sleep and cognition in indigenous population is scarce, we used a discovery-based approach with a non-conservative correction for multiple comparisons (FDR), and therefore, we need to consider potential type 1 error. Future studies with larger samples of American Indians that are focused on cognitive disruptions related to sleep are needed to clarify this.

Our study found an influence of study site on associations of sleep with cognitive impairment, even when considering differences in time interval among participants. This raises questions regarding geographical location and its environmental impact or the possibility of inconsistency among sites. All sites included in the study for both the SHHS and CDCAI studies underwent the same training and certification to administer the cognitive tests and perform home polysomnography. The quality of polysomnograms was monitored through central scoring and quality assurance procedures, with no differences observed among study sites (Redline et al., 1998). Nevertheless, future studies should ensure methodological rigidity and consistency of the collected measurements to investigate whether the geographic region of different tribes and communities may have a substantive impact on the associations between sleep quality and cognitive performance.

Our findings highlight the importance of considering subjective and objective measures of sleep in research on sleep and cognition. Different ethnic and racial populations may subjectively experience sleep quality in different ways. In the present study, quantitative measures using polysomnography were better at capturing cognitive performance 10 years later in this population. Given that many determinants of sleep health are modifiable and that sleep is an important population-wide health indicator, public interventions in sleep health can have an impact on mitigating health disparities (Hale et al., 2020). Sleep disorders may be a modifiable risk factor for physical and mental health concerns later in life, including dementia (van Straten et al., 2018; Blackman et al., 2021). As a population facing significant health disparities (Hutchinson and Shin, 2014; Manson and Buchwald, 2021), American Indians have been shown to be at risk for vascular disease (Suchy-Dicey et al., 2017) and cognitive decline (de Souza-Talarico et al., 2016; Cholerton et al., 2019), but studies investigating sleep in this population have been lacking. The current study helps to fill this gap. Documenting sleep characteristics in aging American Indians and determining their relationship with cognitive outcomes provides direction for testing more specific hypotheses in this population, such as whether there is a predictive relationship between mid-life sleep latency and subsequent neurodegeneration, whether sleep treatments would be beneficial for long-term cognitive performance, and whether any deleterious effects of racial and ethnic sleep health disparities are involved.

This is the first study to analyze relationships between sleep and cognitive measures in an aging sample of American Indians. We reported novel findings regarding the associations between sleep characteristics, derived from polysomnography and questionnaires, and cognitive performance assessed approximately 10 years later. We found that polysomnography-derived sleep characteristics, but not self-reported sleep measures, collected in mid-life were associated with deficits in cognitive performance in this population later in life. In particular, longer sleep latency was associated with cognitive impairment approximately 10 years later. If further research indicates that sleep latency may serve as a biomarker of cognitive decline with advanced aging, it could provide a straightforward and important tool for early intervention. As American Indians have increased risk for AD and other age-related disorders (Centers for Disease Control and Prevention, 2006; Hutchinson and Shin, 2014; Suchy-Dicey et al., 2017), understanding how poor sleep affects American Indians health across the lifespan is paramount. Sleep and sleep disorders are possible modifiable risk factors for cognitive impairment and dementia, and therefore, are suitable candidates for interventions aimed at preventing neurodegenerative disease development and progression.

The data supporting the findings of this study are the intellectual property of the sovereign tribes and communities from whom they were collected and are not directly shareable without the express permission and consent of those entities. Researchers interested in using the data may follow standard Strong Heart Study procedures, per tribal data use agreements. Further inquiries can be directed to the corresponding author.

Ethical review and approval were granted for the Strong Heart Study and its ancillary studies. Written informed consent was obtained from all participants. Study procedures for this specific analysis of deidentified data were approved by the appropriate Institutional Research Boards, Tribal Research Review Boards, or Tribal Councils.

LF: Writing – review & editing, Writing – original draft, Software, Methodology, Investigation, Formal analysis, Conceptualization. MF: Writing – review & editing. NC: Writing – review & editing. NM: Writing – review & editing. DB: Writing – review & editing. HVD: Writing – review & editing. SQ: Writing – review & editing, Supervision. AS-D: Writing – review & editing, Supervision.