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Irregular sleep patterns linked to cognitive decline in older adults, study shows

In a recent study published within the journal JAMA Network Open, researchers evaluated the association between sleep patterns and age-associated cognitive alterations amongst older adults.



Study: Longitudinal Sleep Patterns and Cognitive Impairment in Older Adults. Image Credit: Tero Vesalainen / Shutterstock

Background

Amyloid deposition, which appears ≥15 years before cognitive impairment, precedes cognitive decline. Essentially the most effective treatment strategy could also be to focus on pathogenic mechanisms early within the disease’s progression. Identifying the aspects that precede cognitive and functional decline can result in therapy and prevention a long time before the event of dementia.

Sleep disturbance has been related to dementia; nevertheless, it’s unknown how longitudinal variations in sleep affect the occurrence of cognitive impairments. Short sleep duration and poor sleep quality are related to the next pathological load of Alzheimer’s disease. Easy sleep metrics restrict studies that display a relationship between chronic sleep disturbance and dementia diagnosis.

In regards to the study

In the current study, researchers investigated whether longitudinal patterns of self-documented sleep duration were related to cognitive impairment amongst older adults.

The team longitudinally analyzed the Seattle Longitudinal Study (SLS) data; the study assessed cognitive function (between 1997 and 2020) and self-documented sleep durations (between 1993 and 2012) amongst older adults. The team enrolled SLS participants from the Health Maintenance Organization (HMO) of Washington and the Group Health Cooperative (GHC) of Puget Sound from 1956 to 2020. The researchers included only individuals who provided complete demographic data and people who were administered the neuropsychologic battery and filled out the Health Behavior Questionnaire (HBQ).

Self-reported demographic data included sex (male or female), ethnicity, race, apolipoprotein E ε4 (APOE*E4) allele carrier status, and academic attainment. The participants filled out the HBQ every three to 5 years, five times from 1993 to 2012, and underwent neuropsychological assessments every five to seven years from 1997 to 2019. Cognitive impairment was the study consequence, as described by performances below thresholds on the Mattis Dementia Rating Scale (DRS, scores below 129) and the Mini-Mental State Examination (MMSE, scores below 26). As well as, the SLS neuropsychological battery included the Center for Epidemiologic Studies-Depression Scale (CES-D).

Sleep duration was self-reported because the median of night sleep over the previous week and evaluated longitudinally at several time points. The researchers evaluated sleep phenotypes [short sleep (less than seven hours), medium sleep (seven hours), long sleep (more than seven hours)], median duration of sleep, sleep duration alterations, and sleep variability. They performed Cox proportional-type hazard regression modeling to find out the hazard ratios (HRs) and data evaluation between September 2020 and May 2023.

Results

Among the many SLS participants enrolled initially, only one,104 who accomplished neuropsychological assessments and the HBQ were included within the study after excluding 278 individuals lacking demographic information, especially the APOE genotype. Because of this, 826 individuals [with a mean age of 76 years; 57% (n=468) women; 26% (n=217) APOE*E4 carriers] comprised the study population.

Cox proportional regression modeling (concordance, 0.8) showed that higher variability in sleep patterns (HR, 3.1) and short sleeper status (HR, 3.7) were significantly related to cognitive impairment. The team observed higher cognitive decline with advancing age. Of 614 individuals, 44 (seven percent) showed a cognitive decline at the ultimate assessment, with the next cognitive decline amongst older individuals.

Educational attainment (HR, 1.2) and possessing ≥1.0 APOE*E4 copies (HR, 2.1) were significantly related to cognitive impairment. Modeling considering the influence of depression showed that APOE*E4 carrier status (HR, 2.1) and academic attainment (HR, 1.1) were significantly related to cognitive decline risk. Short sleepers (HR, 2.8) and increasing variability in sleep patterns (HR, 2.2) were significantly related to age-associated cognitive decay.

Incorporating longitudinal sleep assessment parameters within the models showed that several aspects were significantly related to cognitive impairment risk, including educational attainment (HR, 1.3), APOE*E4 carrier status (HR, 2.7), short-sleep phenotypes (HR, 3.7), and better variability in sleep patterns (HR, 3.1). The study found a major correlation between age and academic attainment, with older individuals being less educated.

Nonetheless, the team found no significant differences in APOE*E4 allele status by age. Global CES-D scores showed that individuals aged 65 to 84 years reported lower depression in comparison with those aged <56 and ≥85 years. Age also significantly influenced sleep duration, with older individuals experiencing longer sleep durations and fewer short- and medium-sleepers. Age was related to lower sleep variability across longitudinal sleep duration assessments.

Overall, the study findings showed that short sleep duration and significant sleep variability were related to poor cognitive function. Chronic sleep disturbance may raise heart problems, metabolic syndrome, stroke, depression, and diabetes risks, which increase cognitive decay risk. Sleep deprivation is related to increased amyloid plaque load in addition to faster ventricular enlargement, aggravating Alzheimer’s disease-associated neurodegeneration. Sleep-active-type glymphatic activity aids amyloid, α-synuclein, and tau clearance, whereas acute sleep deprivation decreases it.

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