Relaxium Sleep Irregular sleep are associated with cognitive decline in older
According to a study, irregular sleep patterns are associated with cognitive decline in older adults.
A recent study examining the relationship between sleep patterns and age-related cognitive changes in older adults was published in the journal JAMA Network Open.
Context
Cognitive decline is preceded by amyloid deposition, which manifests ≥15 years prior to cognitive impairment. Targeting pathogenic mechanisms at an early stage of the disease’s progression may prove to be the most effective treatment strategy. Decades before dementia manifests, therapy and prevention efforts can be directed toward identifying the factors that precede cognitive and functional decline.
Dementia has been linked to sleep disturbances, but it is unclear how long-term changes in sleep impact the development of cognitive impairments.
Amyloid plaques do not cause Alzheimer’s
Reduced sleep duration and low quality of sleep are linked to an increased pathological load of Alzheimer’s disease. illness. Research showing a connection between a diagnosis of dementia and persistent sleep disturbance are limited by simple sleep metrics.
Concerning the study
In the current study, researchers looked into the possibility of a relationship between older adults’ cognitive impairment and self-reported sleep duration patterns over time.
The group conducted a longitudinal analysis of data from the Seattle Longitudinal Study (SLS), which evaluated older adults’ self-reported sleep durations from 1993 to 2012 and their cognitive function from 1997 to 2020. From 1956 to 2020, the team enrolled SLS participants from the Group Health Cooperative (GHC) of Puget Sound and the Health Maintenance Organization (HMO) of Washington.
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Only those who submitted comprehensive demographic information, underwent neuropsychologic testing, and completed the Health Behavior Questionnaire (HBQ) were included in the study.
Apolipoprotein E ε4 (APOE*E4) allele carrier status, race, ethnicity, sex (male or female), and educational attainment were among the demographic variables that subjects self-reported.
From 1993 to 2012, the participants completed the HBQ five times, and from 1997 to 2019, they had neuropsychological evaluations every five to seven years.
Metabolic syndrome and related disorders journal
The study’s conclusion was cognitive impairment, as indicated by results on the Mini-Mental State Examination (MMSE, scores below 26) and the Mattis Dementia Rating Scale (DRS, scores below 129) that fell below thresholds. Additionally, the Center for Epidemiologic Studies-Depression Scale (CES-D) was a component of the SLS neuropsychological battery.
The median amount of sleep each night over the previous week was self-reported, and it was assessed longitudinally at multiple intervals. The sleep phenotypes were assessed by the researchers:
short sleep (less than seven hours], medium sleep (seven hours), long sleep (more than seven hours), changes in the median amount of sleep, and variability in the amount of sleep. They analyzed the data between September 2020 and May 2023 and calculated the hazard ratios (HRs) using Cox proportional-type hazard regression modeling.
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Outcomes
Of the SLS participants who were initially enrolled, 278 were excluded due to insufficient demographic information, particularly regarding APOE genotype;
only 1,104 who completed neuropsychological assessments and the HBQ were included in the study. Thus, the study population consisted of 826 people [mean age = 76 years; 57% (n = 468) women; 26% (n = 217) APOE*E4 carriers].
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Greater variability in sleep patterns (HR, 3.1) and short sleeper status (HR, 3.7) were found to be significantly correlated with cognitive impairment, according to Cox proportional regression modeling (concordance, 0.8). The team found that as people aged, there was a greater cognitive decline.
At the final assessment, 44 out of 614 individuals (or 7% of the total) had a cognitive decline; older individuals had a greater cognitive decline.
The presence of ≥1.0 APOE*E4 copies (HR, 2.1) and educational attainment (HR, 1.2) were found to be significantly associated with cognitive impairment.
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The results of modeling with the impact of depression revealed a significant relationship between the risk of cognitive decline and the APOE*E4 carrier status (HR, 2.1) and educational attainment (HR, 1.1).
The association between age-associated cognitive decline and short sleepers (HR, 2.8) and rising variability in sleep patterns (HR, 2.2) was significant.
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When longitudinal sleep assessment parameters were added to the models, it was found that a number of variables, such as educational attainment (HR, 1.3), APOE*E4 carrier status (HR, 2.7), short-sleep phenotypes (HR, 3.7), and greater sleep pattern variability (HR, 3.1), were significantly associated with the risk of cognitive impairment. Age and educational attainment were found to be significantly correlated in the study, with older people having lower educational attainment.
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The researchers did not discover any appreciable variations in APOE*E4 allele status according to age. According to global CES-D scores, people between the ages of 65 and 84 reported less depression than people between the ages of 56 and 85.
Chronic ischemic heart disease acute coronary syndrome
The length of sleep was also significantly influenced by age, with older people sleeping for longer periods of time and having fewer short- and medium-sleepers. In all longitudinal tests of sleep duration, age was linked to decreased sleep variability.
Overall, the study’s conclusions demonstrated a link between poor cognitive function and short sleep duration and significant sleep variability.
Chronic sleep disturbance increases the risk of depression, diabetes, metabolic syndrome, stroke, cardiovascular disease, and cognitive deterioration.
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Lack of sleep is linked to higher levels of amyloid plaque and faster ventricular enlargement, which exacerbates the neurodegeneration linked to Alzheimer’s disease. Glymphatic activity of the sleep-active typeenhances the clearance of tau, α-synuclein, and amyloid, while acute sleep deprivation reduces it.
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