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Sleep disturbances increase the risk of dementia: A systematic review and meta-analysis

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... Insufficient sleep also means a higher risk of falls and other accidents. Poor sleep also intensifies and contributes to the progression of dementia (Brewster et al., 2015;Phelan et al., 2010;Sagayadevan et al., 2017;Shi et al., 2018;Wennberg et al., 2013). The health problems connected with inadequate sleep, whether they are secondary or primary, also influence older people's psychosocial and social capabilities with more limited enthusiasm for social interaction. ...
... This is highlighted in previous studies where meaningfulness and experiences of autonomy are essential for the experience of healthy ageing (Karpinnen et al., 201 2016). Cognitive impairment and accelerated brain ageing are effects of longterm sleep deprivation (Brewster et al., 2015;Carvalho et al., 2017;Shi et al., 2018) In addition, accelerated brain ageing associated with sleep deprivation can lead to the development of Alzheimer's disease and vascular dementia (Carvalho et al., 2017;Shi et al., 2018). The improvements that occurred in the residents in the present study are easier to understand based on long-term sleep deprivation on cognitive ability. ...
... This is highlighted in previous studies where meaningfulness and experiences of autonomy are essential for the experience of healthy ageing (Karpinnen et al., 201 2016). Cognitive impairment and accelerated brain ageing are effects of longterm sleep deprivation (Brewster et al., 2015;Carvalho et al., 2017;Shi et al., 2018) In addition, accelerated brain ageing associated with sleep deprivation can lead to the development of Alzheimer's disease and vascular dementia (Carvalho et al., 2017;Shi et al., 2018). The improvements that occurred in the residents in the present study are easier to understand based on long-term sleep deprivation on cognitive ability. ...
Article
Purpose The most common treatment for resident’s health problems is pharmacological. Little research has been done on how an intervention with a non-pharmacological method, such as a weighted blanket, Through the nursing staff view, we can learn how weighted blankets influence resident’s health in nursing homes. The aim of this study was to explore nursing staff’s experiences of how an intervention with weighted blankets influenced resident’s expressions of health. Methods The study had a descriptive qualitative design with semi-structured interviews with 20 nursing staff working in nursing homes, and an inductive content analysis was applied. Results The nursing staff expressed that the weighted blanket positively influenced resident’s health in the areas of sleep, physical activity, and psychological behaviour. The weighted blanket made them fall asleep faster, sleep was uninterrupted andthey felt more rested in the morning. The nursing staff observed an increased level of activity as the resident became more energetic . The nursing staff also experienced reduced negative psychological behaviours like anxiety and worrying.
... times higher risk of preclinical AD [7]. It has been suggested that sleep disturbances contribute to cognitive decline and increase the risk of AD by increasing the brain's Aβ burden [8][9][10]. Indeed, accumulating evidence indicates that over 45% of AD patients have sleep disturbances [9,11]. ...
... Our systematic review showed that sleep continuity and architecture (decreased TST, SWS, and REM sleep) are disturbed in AD patients. Accumulating evidence shows that sleep disturbance contributes to cognitive decline and may increase the risk of AD dementia [8,10,[60][61][62]. A meta-analysis of 18 longitudinal studies revealed that sleep disturbances predict the development of AD dementia [10]. ...
... Accumulating evidence shows that sleep disturbance contributes to cognitive decline and may increase the risk of AD dementia [8,10,[60][61][62]. A meta-analysis of 18 longitudinal studies revealed that sleep disturbances predict the development of AD dementia [10]. Supporting this hypothesis are reports that similar alterations in PSG measured sleep parameters including increased N1 sleep, WASO, SL, REML, and decreased TST, SE, and REM sleep are found in individuals with mild cognitive impairment, a prodromal stage of AD [63]. ...
Article
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Polysomnography (PSG) studies of sleep changes in Alzheimer's disease (AD) have reported but not fully established the relationship between sleep disturbances and AD. To better detail this relationship, we conducted a systematic review and meta-analysis of reported PSG differences between AD patients and healthy controls. An electronic literature search was conducted in EMBASE, MEDLINE, All EBM databases, CINAHL, and PsycINFO inception to Mar 2021. Twenty-eight studies were identified for systematic review, 24 of which were used for meta-analysis. Meta-analyses revealed significant reductions in total sleep time, sleep efficiency, and percentage of slow-wave sleep (SWS) and rapid eye movement (REM) sleep, and increases in sleep latency, wake time after sleep onset, number of awakenings, and REM latency in AD compared to controls. Importantly, both decreased SWS and REM were significantly associated with the severity of cognitive impairment in AD patients. Alterations in electroencephalogram (EEG) frequency components and sleep spindles were also observed in AD, although the supporting evidence for these changes was limited. Sleep in AD is compromised with increased measures of wake and decreased TST, SWS, and REM sleep relative to controls. AD-related reductions in SWS and REM sleep correlate with the degree of cognitive impairment. Alterations in sleep EEG frequency components such as sleep spindles may be possible biomarkers with relevance for diagnosing AD although their sensitivity and specificity remain to be clearly delineated. AD-related sleep changes are potential targets for early therapeutic intervention aimed at improving sleep and slowing cognitive decline.
... Aβ and tau protein aggregations on sleepregulating centers such as the ventrolateral preoptic area and periaqueductal gray matter possibly contribute to sleep disturbances in AD patients [17,[19][20][21]. At the same time, disturbed sleep is associated with increased levels of Aβ and tau protein in both human and animal studies [22][23][24][25][26]. Accordingly, sleep disturbances such as insomnia, sleep fragmentation, and sleep-disordered breathing are associated with an increased risk of developing AD [27,28]. In addition, such disturbances are related to a higher rate of cognitive decline in cognitively unimpaired individuals [29]. ...
... In the current study, we demonstrated that the cognitive decline of patients with mild-moderate AD is different among those with distinct sleep profiles. Accordingly, patients that Several studies demonstrated an association between sleep disturbances and increased risk of AD and other dementias [27]. Sindi and collaborators (2018) showed that midlife insomnia and late-life terminal insomnia increased the risk of dementia after assessing three population-based studies with cognitively unimpaired individuals [28]. ...
... Sindi and collaborators (2018) showed that midlife insomnia and late-life terminal insomnia increased the risk of dementia after assessing three population-based studies with cognitively unimpaired individuals [28]. Similarly, community-dwelling older adults without dementia who had fragmented sleep presented an increased risk of developing AD during a 6-year follow-up [27]. In fact, sleep disturbances such as sleep fragmentation, increased sleep latency, and long sleep duration are associated with a higher rate of cognitive decline in cognitively unimpaired individuals [27,29]. ...
Article
To investigate the association between sleep and the cognitive evolution of mild‐moderate Alzheimer’s disease patients. Observational, prospective, single‐center study, including consecutive patients diagnosed with mild‐moderate Alzheimer’s disease (NCT02814045). The individuals were submitted to overnight polysomnography, followed by neuropsychological evaluations at baseline and after 12 months of follow‐up. Principal component analysis characterized the sleep architecture of the cohort into two main types: individuals with a propensity to deepen their sleep (deep sleepers) and individuals who spent most of the time in the lighter sleep stage (light sleepers). The cohort included 125 subjects with a median [IQR] of 75.0 [72.0;80.0] years. The mean difference (95% CI) in the Mini‐mental state examination score at 12 months between deep and light sleepers was ‐1.51 (95% CI: ‐2.47 to ‐0.54; p‐value = 0.002). Accordingly, sleep depth and cognitive evolution presented a dose‐response relationship (p‐for‐trend = 0.02). Regarding the specific cognitive subdomains, we observed differences related to the processing speed, demonstrated by the Stroop words test (‐1.48; 95% CI: ‐2.58 to ‐0.38; p‐value = 0.009), and to the executive function, demonstrated by the Verbal fluency test (‐1.70; 95% CI: ‐2.85 to ‐0.55; p‐value = 0.004). Considering that light sleepers presented an increased cognitive decline, the sleep profile may have a predictive role in the cognitive evolution of mild‐moderate Alzheimer’s disease patients. The modifiable nature of sleep sets this behavior as a possible useful intervention for the improvement of cognitive evolution.
... Additionally, it has been proposed [12] that ADHD might lead to development of cumulative health-compromising factors along the lifespan, which in turn present risk factors for developing MCI and dementia in later life. Low educational attainment, common metabolic disorders or metabolic syndrome (i.e., hypertension, type 2 diabetes [T2D] and obesity), sleep disorders, head injuries, and psychiatric disorders (i.e., depression, anxiety, substance use disorder [SUD], and bipolar disorder), are associated with ADHD [1,2], and well-established risk factors for dementia [13][14][15][16]. Unfortunately, only a few studies have explored the potential impact of these factors on the association between ADHD and dementia, with inconsistent findings. ...
... The following variables, associated with ADHD and/or dementia in previous research, were addressed as covariate sets: (a) sex [1,11] and birth year [11]; (b) educational attainment (highest level of education by age 50 with categories: compulsory education ≤9 years/upper secondary/postsecondary/postgraduate) [1,13]; (c) metabolic disorders: hypertension, T2D, and obesity [2,13]; (d) sleep disorders (organic and nonorganic) [2,15]; (e) head injuries [2,16]; (f) psychiatric disorders: depression, anxiety, SUD, and bipolar disorder; [1,2,13,14] (g) other developmental disorders (i.e., autism spectrum disorder, intellectual disability, motor disorders, and learning disorders) [17]. We extracted a first diagnosis of included disorders and head injuries, coded according to the ICD-8/9/10 from the NPR (Supplementary Table S1) and acquired at any age. ...
Article
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Background Previous research has indicated that attention-deficit/hyperactivity disorder (ADHD) is associated with an increased risk for dementia, but studies are scarce and inconclusive. We aimed to investigate the association between ADHD, and dementia and mild cognitive impairment (MCI). Additionally, we aimed to investigate the impact of comorbid conditions, educational attainment, head injuries, other developmental disorders, and sex on the association. Methods The study population consisted of 3,591,689 individuals born between 1932 and 1963, identified from Swedish population-based registers. Cases of ADHD, dementia and MCI were defined according to ICD diagnostic codes and ATC codes for medication prescriptions. A Cox proportional hazards model was used to test the associations between ADHD, and dementia and MCI. Results Individuals with ADHD had an increased risk for dementia and MCI. After adjusting for sex and birth year, a hazard ratio (HR) was 2.92 (95% confidence interval 2.40–3.57) for dementia, and 6.21 (5.25–7.35) for MCI. Additional adjustment for psychiatric disorders (depression, anxiety, substance use disorder, and bipolar disorder) substantially attenuated the associations, HR = 1.62 (1.32–1.98) for dementia, and 2.54 (2.14–3.01) for MCI. Common metabolic disorders (hypertension, type 2 diabetes, and obesity), sleep disorders, head injuries, educational attainment, and other developmental disorders, had a limited impact on the association. The association between ADHD and dementia was stronger in men. Conclusions ADHD is a potential risk factor for dementia and MCI, although the risk significantly attenuates after controlling for psychiatric disorders. Further research is needed to confirm these findings and to explore underlying mechanisms of the associations.
... Studies have reported that patients with OSA are more likely to develop mild cognitive impairment (MCI) and AD at a younger age (93). In the same vein, a recent metaanalysis of longitudinal studies reported that individuals presenting sleep disturbances, such as insomnia, OSA, sleepwake rhythm disorders, have a high risk of developing allcause dementia, AD, and vascular dementia (94). Moreover, insomnia increased the risk of AD but not vascular or all-cause dementia, whilst OSA was associated with an increased risk of all-cause dementia, AD, and vascular dementia (94). ...
... In the same vein, a recent metaanalysis of longitudinal studies reported that individuals presenting sleep disturbances, such as insomnia, OSA, sleepwake rhythm disorders, have a high risk of developing allcause dementia, AD, and vascular dementia (94). Moreover, insomnia increased the risk of AD but not vascular or all-cause dementia, whilst OSA was associated with an increased risk of all-cause dementia, AD, and vascular dementia (94). Shared pathological findings between OSA and AD include sleep architecture disturbances, neurogenic neuroinflammation, changes in multipartite synapse and impaired clearance of toxic Aβ and tau (42). ...
Article
Background: Obstructive sleep apnea (OSA) is a chronic, highly prevalent, multi-system and sleep disorder, which may contribute to cognitive impairment and a variety of structural and neurophysiologic changes. The focus on OSA is warranted given its recognized links with major psychiatric and neurologic disorders, including Alzheimer's disease. Some preliminary studies suggest a dual effect of the inflammatory response in OSA. Neuroinflammation may present with initial, potentially adaptive and homeostatic, and later, a more distinctly maladaptive, precipitating and perpetuating role. Objective: We here propose and argue in favour of the inflammatory process in the brain as a likely binding mechanism behind at least some effects that OSA may have on the brain and its function. Several OSA-triggered molecular and cellular events, that could lead to a neurodegenerative cascade, are similarly discussed. Methods: This perspective reviews the body of literature that investigates potential links between the inflammatory processes in the brain and the OSA. A special emphasis is placed on a potential role for neuroplastin, a novel transmembrane synaptic protein involved in the neuroplasticity and known to be differentially regulated in the OSA. Conclusions: The intricate interplay between neuroinflammation and other mechanistic correlates of OSA add to the evidence that neuroinflammation may be a key target for future therapeutic strategies in a number of comorbid disorders. The future studies will need to answer whether it is sleep fragmentation (SF) or intermittent hypoxia (IH) which may drive any such neuroinflammation.
... Unauthorized reproduction of this article is prohibited The 2020 Lancet Commission on Dementia Prevention, Intervention, and Care has reported 12 modifiable risk factors for ADRD prevention and highlighted the importance of healthy lifestyles. 6 Indeed, the protective role of healthy lifestyles, including non-smoking, 7-10 regular exercise, 7,8,11,12 limited alcohol use, 13,14 adequate sleep, 7,15,16 and high-quality diets, 8,17,18 in ADRD has been widely discussed. Recently, some cohort studies have reported synergistic effects of lifestyle factors, [19][20][21][22] showing promising associations of combined scores with >30% reduced risk of ADRD, even among individuals genetically predisposed to the disease. ...
... Modifiable lifestyle factors have attracted increasing attention to prevent or delay the development of ADRD. Evidence from large cohort studies and meta-analysis has accumulated regarding increased risks of cognitive decline and ADRD due to tobacco smoking, 9,10 excessive alcohol drinking, 14 physical inactivity, 11,12 inadequate/disturbed sleep, 15,16 and unhealthy diets. 17,18 Hence, the Alzheimer's Association and World Health Organization have recommended lifestyle interventions to reduce the risk of ADRD, including smoking cessation, physical activity, healthy diet, moderate alcohol consumption, and management of obesity, diabetes, hypertension, dyslipidemia, and depression. ...
Article
Abstract Objective: While the importance of healthy lifestyles for preventing Alzheimer’s disease and related dementias (ADRD) has been recognized, epidemiologic evidence remains limited for non-White or low-income individuals who bear disproportionate burdens of ADRD. This population-based cohort study aims to investigate associations of lifestyle factors, individually and together, with the risk of ADRD among socioeconomically disadvantaged Americans. Methods: In the Southern Community Cohort Study, comprising two-thirds self-reported Black and primarily low-income Americans, we identified incident ADRD using claims data among participants enrolled in Medicare for at least 12 consecutive months after age 65. Five lifestyle factors—tobacco smoking, alcohol consumption, leisure-time physical activity (LTPA), sleep hours, and diet quality— were each scored 0 (unhealthy), 1 (intermediate), or 2 (healthy) based on health guidelines. A composite lifestyle score was created by summing all scores. Cox regression was used to estimate hazard ratios (HRs, 95% CIs) for incident ADRD, treating death as a competing risk. Results: We identified 1,694 patients with newly diagnosed ADRD among 17,209 participants during a median follow-up of 4.0 years in claims data; the mean age at ADRD diagnosis was 74.0 years. Healthy lifestyles were individually associated with 11%-25% reduced risk of ADRD: multivariable-adjusted HR (95% CI) was 0.87 (0.76-0.99) for never vs. current smoking, 0.81 (0.72-0.92) for low-to-moderate vs. no alcohol consumption, 0.89 (0.77-1.03) for ≥150 minutes of moderate or ≥75 minutes of vigorous LTPA each week vs. none, 0.75 (0.64-0.87) for 7-9 hours vs. >9 hours of sleep, and 0.85 (0.75-0.96) for the highest vs. lowest tertiles of Healthy Eating Index. The composite lifestyle score showed a dose-response association with up to 36% reduced risk of ADRD: multivariable-adjusted HRs (95% CIs) across quartiles were 1 (ref), 0.88 (0.77-0.99), 0.79 (0.70-0.90), and 0.64 (0.55-0.74); p-trend<0.001. The beneficial associations were observed regardless of participants’ sociodemographics (e.g., race, education, and income) and health conditions (e.g., history of cardiometabolic diseases and depression). Conclusion: Our findings support significant benefits of healthy lifestyles for ADRD prevention among socioeconomically disadvantaged Americans, suggesting that promoting healthy lifestyles and reducing barriers to lifestyle changes are crucial to tackling the growing burden and disparities posed by ADRD.
... Chronic sleep disturbance is a risk factor for dementia diseases and is commonly seen in dementias such as Alzheimer's and Parkinson's diseases, [1][2][3][4] as well as in other dementing brain diseases, e.g. after traumatic brain injury (TBI). 5 While it is disputed whether sleep disturbance is cause or consequence of dementia disease, impaired glymphatic function may represent a direct link between chronic sleep deprivation and the aggregation of toxic by-products of brain metabolism in dementia disease, i.e. ...
... 61 (3) Evidence of sleep-dependent tracer enrichment within brain tissue. 17 (4) Centripetal enrichment of brain tissue from outside cerebral cortex of a tracer strictly confined outside vessels due to the blood-brain-barrier. 18 Concerning the latter, it should be noticed that the tracer enriches the brain centripetally while soluble waste is expected to be cleared centrifugally under physiological conditions. ...
Article
Chronic sleep disturbance is a risk factor for dementia disease, possibly due to impaired sleep-dependent clearance of toxic metabolic by-products. We compared enrichment of a cerebrospinal fluid (CSF) tracer within brain of patients reporting good or poor sleep quality, assessed by the Pittsburgh Sleep Quality Index (PSQI) questionnaire. Tracer enrichment in a selection of brain regions was assessed using multiphase magnetic resonance imaging up to 48 hours after intrathecal administration of the contrast agent gadobutrol (0.5 ml of 1 mmol/ml) serving as tracer. Tracer enrichment differed between patients with good (PSQI ≤5) and poor (PSQI >5) sleep quality in a cohort of non-dementia individuals (n = 44; age 42.3 ± 14.5 years), and in patients with the dementia subtype idiopathic normal pressure hydrocephalus (n = 24; age 71.0 ± 4.9 years). Sleep impairment was associated with increased CSF tracer enrichment in several brain regions. Cortical brain volume as well as entorhinal cortex thickness was reduced in the oldest cohort and was correlated with the severity of sleep disturbance and the degree of cortical tracer enrichment. We suggest chronic sleep disturbance is accompanied by altered glymphatic function along enlarged perivascular spaces.
... Recent prospective cohort studies conducted around 2000s revealed that disturbances and disorders related with sleep might be related with the elevated risk of cognitive impairment and dementia. Those studies revealed various forms of sleep disturbances and generally found them to be associated with dementia progression, for instance, the connection between insomnia [34], elevated daytime sleepiness [35,36], elongated sleep periods [37,38], shorter sleep period [37,39,40], and arising of cognitive impairment and/or dementia. As a summary, both short and long sleep durations might cause cognitive impairment/dementia [38,39]. ...
... According to the findings, insomnia is associated with AD, and sleep-related respiratory difficulties are associated with all types of dementia, including AD and vascular dementia. [40]. However, further researches should be conducted for more significant claims. ...
Article
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Sleep disturbances, as well as sleep-wake rhythm disorders, are characteristic symptoms of Alzheimer’s disease (AD) that may head the other clinical signs of this neurodegenerative disease. Age-related structural and physiological changes in the brain lead to changes in sleep patterns. Conditions such as AD affect the cerebral cortex, basal forebrain, locus coeruleus, and the hypothalamus, thus changing the sleep-wake cycle. Sleep disorders likewise adversely affect the course of the disease. Since the sleep quality is important for the proper functioning of the memory, impaired sleep is associated with problems in the related areas of the brain that play a key role in learning and memory functions. In addition to synthetic drugs, utilization of medicinal plants has become popular in the treatment of neurological diseases. Curcuminoids, which are in a diarylheptanoid structure, are the main components of turmeric. Amongst them, curcumin has multiple applications in treatment regimens of various diseases such as cardiovascular diseases, obesity, cancer, inflammatory diseases, and aging. Besides, curcumin has been reported to be effective in different types of neurodegenerative diseases. Scientific studies exclusively showed that curcumin leads significant improvements in the pathological process of AD. Yet, its low solubility hence low bioavailability is the main therapeutic limitation of curcumin. Although previous studies have focused different types of advanced nanoformulations of curcumin, new approaches are needed to solve the solubility problem. This review summarizes the available scientific data, as reported by the most recent studies describing the utilization of curcumin in the treatment of AD and sleep deprivation-related consequences.
... In the recent decades, emerging studies have explored the associations between sleep disturbances and cognitive impairment, and some kinds of sleep disturbances were identified to be associated with cognitive impairment, such as insomnia and 11 sleep disordered breathing. 12,13 However, the results about the associations between some other kinds of sleep disturbances and cognitive impairment are varied. For example, the associations between REM (rapid eye movement) sleep behavior disorder and cognitive impairment were conflicted, [14][15][16][17] the associations between narcolepsy and cognitive impairment were lack of evidence in the population, 18 and the associations between restless leg syndrome and cognitive impairment were less reported. ...
Article
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Objective: Cognitive impairment is a rapidly growing global public health problem in China and worldwide. In the recent decades, emerging studies have explored the associations between sleep disturbances and cognitive impairment. However, the variety of the results imply us that further studies should be conducted for the associations. Methods: This is a cross-sectional study conducted between August and October 2018 in five cities in Hebei province, China. Subjects were 21,376 community residents. Cognitive impairment was screened by the Chinese version of the Mini-Mental State Examination (MMSE). Scales of Athens Insomnia Scale (AIS), Berlin Questionnaire (BQ), REM (rapid eye movement) Sleep Behavior Disorder Questionnaire (RBDQ-HK), Ullanlinna Narcolepsy Scale (CUNS), and Cambridge-Hopkins Restless Legs Syndrome Questionnaire (CH-RLSq) were used to access insomnia, sleep apnea, REM sleep behavior disorder, narcolepsy, and restless leg syndrome. Results: The mean ± SD (standard error) of MMSE, AIS, RBDQ-HK, and CUNS were 27.95 ± 4.79, 2.16 ± 3.39, 5.55 ± 7.75, and 3.76 ± 2.31, respectively. Among the participants, 10.6% and 1.5% of the participants were identified as having a high risk of sleep apnea and restless leg syndrome, respectively. The results of multiple linear regression showed that cognitive impairment was associated with insomnia (β = -0.037, p < 0.001) and narcolepsy (β = -0.023, p < 0.001). The association between sleep apnea (β = -0.002, p > 0.05), REM sleep behavior disorder (β = 0.006, p > 0.05), restless leg syndrome (β = -0.007, p > 0.05), and cognitive impairment were not supported. Other factors associated with cognitive impairment were gender, age, education level, married status, and region. Conclusion: This study provides some epidemiological evidence for the association between sleep disturbances and cognitive impairment among community residents in central China. In this study, the associations between insomnia, narcolepsy, and cognitive impairment were identified, but the associations between sleep apnea, REM sleep behavior disorder, narcolepsy, restless leg syndrome, and cognitive impairment were not supported among community residents.
... The progression from early to end stages of ADRD also include profound changes in personality, mood and social interactions, including anterograde amnesia (i.e., inability to acquire new memories), retrograde amnesia (i.e., trouble recalling past memories), and even psychiatric symptoms such as delusions and hallucinations [46,47]. Those with ADRD also show poorer social functioning and self-care routines, score higher on tests of anxiety, and have greater sleep disturbances [48,49]. ...
Article
Converging evidence from biopsychosocial research in humans and animals demonstrates that chronic sensory stimulation (via excessive screen exposure) affects brain development increasing the risk of cognitive, emotional, and behavioural disorders in adolescents and young adults. Emerging evidence suggests that some of these effects are similar to those seen in adults with symptoms of mild cognitive impairment (MCI) in the early stages of dementia, including impaired concentration, orientation, acquisition of recent memories (anterograde amnesia), recall of past memories (retrograde amnesia), social functioning, and self-care. Excessive screen time is known to alter gray matter and white volumes in the brain, increase the risk of mental disorders, and impair acquisition of memories and learning which are known risk factors for dementia. Chronic sensory overstimulation (i.e., excessive screen time) during brain development increases the risk of accelerated neurodegeneration in adulthood (i.e., amnesia, early onset dementia). This relationship is affected by several mediating/moderating factors (e.g., IQ decline, learning impairments and mental illness). We hypothesize that excessive screen exposure during critical periods of development in Generation Z will lead to mild cognitive impairments in early to middle adulthood resulting in substantially increased rates of early onset dementia in later adulthood. We predict that from 2060 to 2100, the rates of Alzheimer’s disease and related dementias (ADRD) will increase significantly, far above the Centres for Disease Control (CDC) projected estimates of a two-fold increase, to upwards of a four-to-six-fold increase. The CDC estimates are based entirely on factors related to the age, sex, race and ethnicity of individuals born before 1950 who did not have access to mobile digital technology during critical periods of brain development. Compared to previous generations, the average 17–19-year-old spends approximately 6 hours a day on mobile digital devices (MDD) (smartphones, tablets, and laptop computers) whereas individuals born before 1950 at the same age spent zero. Our estimates include the documented effects of excessive screen time on individuals born after 1980, Millennials and Generation Z, who will be the majority of individuals ≥65 years old. An estimated 4-to-6-fold increase in rates of ADRD post-2060 will result in widespread societal and economic distress and the complete collapse of already overburdened healthcare systems in developed countries. Preventative measures must be set in place immediately including investments and interventions in public education, social policy, laws, and healthcare.
... The literature seems to confirm an important association between sleep duration and global cognitive decline, especially in individuals with insufficient (four hours a night) or excessive sleep (10 hours a night). 1 A recent meta-analysis found that people with the most frequent sleep disorders in the general population (insomnia, sleep apnea, excessive daytime sleepiness, sleep-related movement disorder, and circadian rhythm disorder) may be vulnerable to all-cause dementia, Alzheimer's disease and vascular dementia. 2 In recent years, laboratory studies have revealed the pathophysiological mechanisms involved in this relationship. A recent gold-standard real-time iontophoretic method for exploring and quantifying the extracellular space of the living brain has shown that deep sleep (natural or induced) increases interstitial fluid by 60%, resulting in a remarkable increase in the convective exchange between cerebrospinal fluid and interstitial fluid, which substantially increases the rate of β-amyloid protein clearance during sleep. ...
... Recent evidence has suggested that sleep disturbance may lead to increased inflammatory processes, which in turn may lead to Alzheimer's disease (Irwin and Vitiello, 2019). Several metaanalyses and systematic reviews indicated that sleep disturbance may be an important risk factor, and thus an important target for Alzheimer's disease prevention (Bubu et al., 2017;Shi et al., 2018;Livingston et al., 2020). Furthermore, the Hisayama epidemiological study in Fukuoka, Japan provided clear evidence that sleep disorders and the concomitant use of hypnotic drugs resulted in an increased risk of dementia in elderly patients. ...
Article
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The objective of this review is to evaluate the anti-dementia activities of saffron and its combination with Kampo medicine. The Kampo formula Kamiuntanto composed of 13 crude drugs is well known for its anti-dementia activity. A significant increase in choline acetyltransferase activity and mRNA levels were observed. Polygala radix was identified as the most essential component drug in Kamiuntanto, probably due to the saponins, tenuifolin, and sinapinic acid. Ginseng was also identified as an essential Kamiuntanto component in terms of its synergistic functions with Polygala radix. Saffron, which was recommended in the Bencao Gangmu for memory and dementia, and is used as an anti-spasmodic, anti-catarrhal, and sedative herbal drug. Saffron and its major constituent, crocin were shown to enhance learning-memory, non-rapid eye movement (rem) sleep, and inhibit depression and neuronal cell death due to strong anti-oxidant and anti-inflammation activities. In addition based on the epidemiological studies such as the treatment of sleeping disorders and the clinical trials of saffron for Alzheimer patients, we demonstrated the indirect and direct anti-dementia activities of crocin and saffron.
... We showed that lower integrity of the middle-to-caudal LC, as measured with a 7 T LC-NE MRI sequence, is associated with more frequent selfreported nocturnal awakenings in 72 cognitively unimpaired older adults, particularly in individuals with higher plasma levels of total tau protein burden [113], a biomarker of increased risk for cognitive decline and incident dementia. Additional longitudinal designs with repeated cognitive, sleep-wake, and LC MRI assessments in cognitively impaired and unimpaired older individuals will be crucial to shed light on the temporal ordering of events, and will contribute to understanding the isolated protective effects of preserved sleep-wake regulation [114] and LC-NE integrity [115] for cognitive performance in aging and AD. ...
Article
Five decades ago, seminal studies positioned the brainstem locus coeruleus (LC) norepinephrine (NE) system as a key substrate for the regulation of wakefulness and sleep, and this picture has recently been elaborated thanks to methodological advances in the precise investigation and experimental modulation of LC structure and functions. This review presents and discusses findings that support the major role of the LC-NE system at different levels of sleep-wake organization, ranging from its involvement in the overall architecture of the sleep-wake cycle to its associations with sleep microstructure, while accounting for the intricate neuroanatomy surrounding the LC. Given the particular position held by the LC-NE system by being at the intersection of sleep-wake dysregulation and initial pathophysiological processes of Alzheimer’s disease (AD), we conclude by examining emerging opportunities to investigate LC-NE mediated relationships between sleep-wake alteration and AD in human aging. We further propose several research perspectives that could support the LC-NE system as a promising target for the identification of at-risk individuals in the preclinical stages of AD, and for the development of novel preventive interventions.
... Predictably, dementia imposes an extreme economic cost that is globally estimated to be around 818 billion dollars per year; therefore, it represents a significant barrier to both social and economic development [1,2]. Hence there is a need for special attention on prevention and management of dementia risk factors including age-related psychophysiological decline, unhealthy lifestyle habits [3,4], environmental factors [5], cardiocerebrovascular diseases [6,7], sleep disturbances [8,9], anxiety [10,11], and apathetic symptoms [12,13], particularly in patients suffering from Mild Cognitive Impairment (MCI) [14][15][16][17][18]. ...
Article
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Decreased upper-extremity/visuomotor abilities are frequently encountered in healthy aging. However, few studies have assessed hand movements in the prodromal stage of dementia. The evaluation of visuomotor skills in patients with Mild Cognitive Impairment (PwMCI) may have non-negligible clinical relevance both in diagnostic and prognostic terms, given the strong relationships with executive functioning and functional autonomies. In the present review paper, these issues will be disclosed by describing general pathophysiological and neuropsychological mechanisms responsible for visuomotor deficits, and by reporting the available experimental results on differences in visuomotor functioning between PwMCI, healthy controls and/or patients with dementia. Moreover, the relationships binding visuomotor and executive domains to functional autonomies will be then addressed. Finally, we will propose insights for future research.
... Finally, physical activity appears as a protective factor as in other elderly cohorts [37,38], although reverse causation cannot be excluded in our cohort with a short follow-up period. The RF "sleeping > 8 h" (symptom of excessive day sleepiness) could be a preclinical manifestation of dementia, and, in general, may predict incident dementia risk (39). The most relevant and relatively novel finding in this study is that "poor" SPH ("bad" and "very bad" answers to the SPH-G and SPH-C questions) appears as a relevant RF of dementia and AD. ...
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Background The causes of the dementia decrease in affluent countries are not well known but health amelioration could probably play a major role. Nevertheless, although many vascular and systemic disorders in adult life are well-known risk factors (RF) for dementia and Alzheimer disease (AD), health status is rarely considered as a single RF. Aim To analyse whether the health status and the self-perceived health (SPH) could be RF for dementia and AD and to discuss its biological basis. Methods We analysed different objective health measures and SPH as RF for dementia and AD incidence in 4569 participants of the NEDICES cohort by means of Cox-regression models. The mean follow-up period was 3.2 (range: 0.03–6.6) years. Results Ageing, low education, history of stroke, and “poor” SPH were the main RF for dementia and AD incidence, whereas physical activity was protective. “Poor” SPH had a hazard ratio = 1.66 (95% CI 1.17–2.46; p = 0.012) after controlling for different confounders. Discussion According to data from NEDICES cohort, SPH is a better predictor of dementia and AD than other more objective health status proxies. SPH should be considered a holistic and biologically rooted indicator of health status, which can predict future development of dementia and AD in older adults. Conclusions Our data indicate that it is worthwhile to include the SPH status as a RF in the studies of dementia and AD incidence and to explore the effect of its improvement in the evolution of this incidence.
... A handful of studies have now also prospectively assessed whether insomnia was associated with greater risk for developing dementia. Cumulatively, these studies suggest that individuals with insomnia have a 53% increase in risk for developing dementia later in life (de Almondes et al., 2016) and a 51% greater risk of developing Alzheimer's Disorder (AD) (Shi et al., 2018). One study found that patients 50 years and older were more than twice as likely to develop dementia during a three-year period if they had a history of chronic insomnia compared to those with no history of insomnia. ...
Chapter
Chronic insomnia is one of the most prevalent sleep disorders in the general population. It is also a significant risk factor for multiple medical and psychiatric disorders. Initial data suggests that sleep disturbances and insomnia may disproportionately affect members of certain racial/ethnic minority groups. The goal of the current article was to provide an overview of the symptoms and physical health consequences of insomnia, describe the prevalence at the population level, highlight sociodemographic (e.g., racial/ethnic) differences, and offer conjecture related to the possible causes of these differences, including the potential downstream adverse health consequence for racial/ethnic minorities.
... Previous studies based primarily on self-reported and fewer more recent based on objective measures, have indicated that short sleep duration is associated with adverse effects on cardiovascular function [30][31][32][33] and memory [34,35]. Additionally, it has been reported that insomniatype symptoms in community-dwelling elderly are associated with cognitive decline [36][37][38][39][40]. Furthermore, insomnia with objective short sleep duration (ISS) has been proposed as a novel more severe phenotype associated with activation of the stress system, particularly the HPA axis and significant impact on health such as increased hypertension, impaired heart rate variability, diabetes type II, neurocognitive impairment, and mortality [30,[41][42][43][44]. ...
Article
Background: Mild cognitive impairment (MCI) is frequent in elderly and a risk factor for dementia. Both insomnia and increased cortisol levels are risk factors for MCI. Objective: We examined cross-sectionally whether increased cortisol levels are associated with short sleep duration (SSD) and/or the insomnia short sleep duration (ISS) phenotype, in elderly with MCI. Methods: One hundred twenty-four participants with MCI and 84 cognitively non-impaired controls (CNI)≥60 years underwent medical history, physical examination, neuropsychiatric evaluation, neuropsychological testing, 3-day actigraphy, assessment of subjective insomnia symptoms, and a single morning plasma cortisol level. The short sleep phenotypes were defined by sleep efficiency below the median of the entire sample (i.e.,≤81%) with at least one insomnia symptom (ISS) or without (SSD). ANOVA models were used to compare the various sleep phenotypes to those who did not present either short sleep or insomnia symptoms [non-insomnia (NI)]. Results: MCI participants had higher cortisol levels compared to the CNI group (p = 0.009). MCI participants with insomnia (n = 44) or SSD (n = 38) had higher cortisol levels compared to the NI group (n = 42; p = 0.014 and p = 0.045, respectively). Furthermore, MCI participants with ISS phenotype but not those with insomnia with normal sleep duration had higher cortisol levels compared to NI (p = 0.011 and p = 0.4, respectively). Both linear trend analyses showed that cortisol reached the highest levels in the ISS phenotype. Conclusion: The ISS and SSD phenotypes are associated with increased cortisol levels in elderly with MCI. Improving sleep quality and duration and decreasing cortisol levels may delay further cognitive decline.
... Sleep disturbance is a symptom characterized by impaired sleep quality with abnormal sleep duration [9]. It can lead to poor sleep quality [10], which is considered a risk factor for many conditions, including cardiovascular disease, dementia, obesity, diabetes, depression, pain, and mortality [11][12][13][14][15]. ...
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Methods: A prospective, randomized study was conducted with 88 patients undergoing laparoscopic colorectal surgery. The experimental group (S group, n = 44) was given 10 mg of zolpidem tartrate one night before the surgical procedure, while no medication was given to the control group (C group, n = 44). The primary outcome was the intraoperative remifentanil consumption. Sufentanil consumption, average patient-controlled analgesia (PCA) effective press times, the visual analog scale (VAS) scores, and incidences of postoperative nausea and vomiting (PONV) were recorded at 6 h (T1), 12 h (T2), and 24 h (T3) postoperatively. Results: The intraoperative remifentanil consumption was significantly lower in the S group than that in the C group (p < 0.01). Sufentanil consumption at 6 h and 12 h postoperatively was significantly lower in the S group than that in the C group (p < 0.05); average PCA effective press times and VAS scores, at 6 h and 12 h postoperatively, were significantly lower in the S group than those in the C group (p < 0.01); differences between groups 24 h postoperatively were not significant. No significant between-group difference was noted in the incidence of nausea and vomiting. Conclusion: Improving patients' sleep quality the night before surgical procedure by zolpidem can decrease the usage of intraoperative analgesics and reduce postoperative pain.
... Des patients souffrant d'insomnie au long cours, encourent quatre à huit fois plus de risque de développer un trouble mental que la population générale [478], alors que jusqu'à 80 % des patients présentant une dépression sévère, sont atteints d'insomnie chronique [472]. Une méta-analyse sur 18 articles rapporte un risque de démence augmenté significativement, pour les patients atteints d'insomnie ou de trouble respiratoire du sommeil [479]. ...
Thesis
Toxoplasma gondii est un parasite intra-cellulaire infectant près d’un tiers de la population mondiale. Généralement asymptomatique, la toxoplasmose est associée à une symptomatologie grave chez les patients immunodéprimés et dans le cas d’infection congénitale. Négligée par les pouvoirs publics, la phase chronique de l’infection a longtemps été sous-estimée. Cette méconnaissance entraîne donc des questions telles que quel est le meilleur protocole thérapeutique ? quelle est la meilleure stratégie diagnostique ? Récemment une stratégie de dissémination très avancée a été suspectée, sur la base de la théorie de la manipulation comportementale de l’hôte. Chez l’Homme, une telle manipulation peut avoir des effets majeurs cérébraux, neurologiques ou psychologiques. Quoi qu’il en soit, son impact sur le sommeil, qui constitue un index particulièrement sensible des fonctions cérébrales, est pour le moment inconnu. C’est pourquoi nous avons établi un modèle murin expérimental afin d’étudier les effets de Toxoplasma gondii sur le cycle éveil-sommeil. Nous avons montré que l’infection chronique par T. gondii était associée de manière persistante avec une augmentation de l’éveil et une diminution du sommeil, ce qui cadre avec la stratégie du parasite pour faciliter sa dissémination grâce à la prédation de son hôte. Nos résultats montrent pour la première fois les conséquences directes de l’infection toxoplasmique sur le comportement, pouvant avoir un impact majeur sur l’apparition de pathologies neuropsychiatriques et neurodégénératives.
... Modifying these 12 factors may prevent or delay dementia by 40% (4). Moreover, many other modifiable protective/risk factors for dementia have been identified, such as sleep disturbances, sleep duration, Mediterranean diet, marital status, vitamin D deficiency, and cardiovascular disease (5)(6)(7)(8)(9)(10). A growing body of research suggests that the immune system and infections play an important role in the development of dementia; bacterial, fungal, and viral infections may cause neurotoxic inflammation and oxidative stress in the brain, which can lead to neurodegeneration (11)(12)(13). ...
Article
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Background Common vaccinations may have impacts on dementia risk, but current evidence is inconsistent. We therefore investigated the association between vaccinations and dementia risk by systematic review and meta-analysis approach. Methods We conducted an extensive search of PubMed, Embase, Cochrane Library, and Web of Science to identify studies that compared the risk of dementia in vaccinated versus unvaccinated populations. The adjusted hazard ratio (HR) and corresponding 95% confidence intervals (CIs) were pooled as measures. Results Of the 9124 records initially retrieved, 17 studies with 1857134 participants were included in our analysis. The overall pooled results showed that vaccinations were associated with a 35% lower dementia risk (HR=0.65, 95% CI: 0.60-0.71, P overall effect < 0.001; I 2 = 91.8%, P heterogeneity <0.001). All types of vaccination were associated with a trend toward reduced dementia risk, with rabies (HR=0.43), tetanus & diphtheria & pertussis (Tdap) (HR=0.69), herpes zoster (HR=0.69), influenza (HR=0.74), hepatitis A (HR=0.78), typhoid (HR=0.80), and hepatitis B (HR=0.82) vaccinations being significant. Individuals with more full vaccination types and more annual influenza vaccinations were less likely to develop dementia. Gender and age had no effect on this association. Conclusion Routine adult vaccinations are associated with a significant reduction in dementia risk and may be an effective strategy for dementia prevention. Further research is needed to elucidate the causal effects of this association and the underlying mechanisms.
... Some longitudinal studies have shown that sleep problems (e.g., short or long sleep duration, prolonged sleep latency, and EDS), which are common among patients with dementia living in care homes [8], are also risk factors for dementia [9,10]. The associations between poor sleep and dementia were supported in a meta-analysis and systematic review [11]. These findings indicate a potential bidirectional association between poor sleep quality and dementia. ...
Article
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Background Sleep characteristics associated with dementia are poorly defined and whether their associations vary by demographics and APOE genotype among older adults are unclear. Methods This population-based cross-sectional study included 4742 participants (age ≥ 65 years, 57.1% women) living in rural China. Sleep parameters were measured using the self-rated questionnaires of the Pittsburgh Sleep Quality Index and Epworth Sleepiness Scale. Global cognitive function was assessed with the Mini-Mental State Examination (MMSE). Dementia was diagnosed following the Diagnostic and Statistical Manual of Mental Disorders, Fourth Edition, criteria, and the National Institute on Aging-Alzheimer’s Association criteria for Alzheimer’s disease (AD). Data were analysed using multiple logistic and general linear regression models. Results Dementia was diagnosed in 173 participants (115 with AD). Multivariable-adjusted odds ratio (OR) of dementia was 1.71 (95%CI, 1.07-2.72) for sleep duration ≤4 h/night (vs. > 6-8 h/night), 0.76 (0.49-1.18) for > 4-6 h/night, 1.63 (1.05-2.55) for > 8 h/night, 1.11 (1.03-1.20) for lower sleep efficiency (per 10% decrease), and 1.85 (1.19-2.89) for excessive daytime sleepiness. Very short sleep duration (≤4 h/night), lower sleep efficiency, and excessive daytime sleepiness were significantly associated with being diagnosed with AD (multivariable-adjusted OR range = 1.12-2.07; p < 0.05). The associations of sleep problems with dementia and AD were evident mainly among young-old adults (65-74 years) or APOE ε4 carriers. Among dementia-free participants, these sleep characteristics were significantly associated with a lower MMSE score. Conclusions Self-reported sleep problems in dementia are characterized by very short or long sleep duration, low sleep efficiency, and excessive daytime sleepiness, especially among young-old people and APOE ε4 carriers. Trial registration ChiCTR1800017758 (Aug 13, 2018).
... Growing evidence indicates that AD patients frequently have sleep disorders, implying common causes of these complex phenotypes. Emerging epidemiological studies suggest that AD is associated with a significantly increased risk of sleep disorders and vice versa (Andrade et al., 2018;Brzecka et al., 2018;Shi et al., 2018;Sadeghmousavi et al., 2020). Furthermore, neuropathological studies have shown that extracellular levels of both Aβ and tau fluctuate during the normal sleep-wake cycle (Wang and Holtzman, 2020). ...
Article
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Late-onset Alzheimer’s disease (AD) is associated with sleep-related phenotypes (SRPs). The fact that whether they share a common genetic etiology remains largely unknown. We explored the shared genetics and causality between AD and SRPs by using high-definition likelihood (HDL), cross-phenotype association study (CPASSOC), transcriptome-wide association study (TWAS), and bidirectional Mendelian randomization (MR) in summary-level data for AD (N = 455,258) and summary-level data for seven SRPs (sample size ranges from 359,916 to 1,331,010). AD shared a strong genetic basis with insomnia (r g = 0.20; p = 9.70 × 10–5), snoring (r g = 0.13; p = 2.45 × 10–3), and sleep duration (r g = −0.11; p = 1.18 × 10–3). The CPASSOC identifies 31 independent loci shared between AD and SRPs, including four novel shared loci. Functional analysis and the TWAS showed shared genes were enriched in liver, brain, breast, and heart tissues and highlighted the regulatory roles of immunological disorders, very-low-density lipoprotein particle clearance, triglyceride-rich lipoprotein particle clearance, chylomicron remnant clearance, and positive regulation of T-cell–mediated cytotoxicity pathways. Protein–protein interaction analysis identified three potential drug target genes (APOE, MARK4, and HLA-DRA) that interacted with known FDA-approved drug target genes. The CPASSOC and TWAS demonstrated three regions 11p11.2, 6p22.3, and 16p11.2 may account for the shared basis between AD and sleep duration or snoring. MR showed insomnia had a causal effect on AD (ORIVW = 1.02, P IVW = 6.7 × 10–6), and multivariate MR suggested a potential role of sleep duration and major depression in this association. Our findings provide strong evidence of shared genetics and causation between AD and sleep abnormalities and advance our understanding of the genetic overlap between them. Identifying shared drug targets and molecular pathways can be beneficial for treating AD and sleep disorders more efficiently.
... Both sleep stages are important for learning and memory consolidation. It has been shown that the risk of developing Alzheimer's disease and the prevalence of all-cause dementia increases with sleep disorders (Shi et al., 2018). In clinical observation, sleep disturbance is often present years before the symptomatic stages of neurodegenerative diseases and becomes more severe along with the disease progression (Guarnieri et al., 2012;Irwin and Vitiello, 2019). ...
Article
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Chronic sleep insufficiency is becoming a common issue in the young population nowadays, mostly due to life habits and work stress. Studies in animal models of neurological diseases reported that it would accelerate neurodegeneration progression and exacerbate interstitial metabolic waste accumulation in the brain. In this paper, we study whether chronic sleep insufficiency leads to neurodegenerative diseases in young wild-type animals without a genetic predisposition. To this aim, we modeled chronic sleep fragmentation (SF) in young wild-type mice. We detected pathological hyperphosphorylated-tau (Ser396/Tau5) and gliosis in the SF hippocampus. 18 F-labeled fluorodeoxyglucose positron emission tomography scan (18 F-FDG-PET) further revealed a significant increase in brain glucose metabolism, especially in the hypothalamus, hippocampus and amygdala. Hippocampal RNAseq indicated that immunological and inflammatory pathways were significantly altered in 1.5-month SF mice. More interestingly, differential expression gene lists from stress mouse models showed differential expression patterns between 1.5-month SF and control mice, while Alzheimer's disease, normal aging, and APOEε4 mutation mouse models did not exhibit any significant pattern. In summary, 1.5-month sleep fragmentation could generate AD-like pathological changes including tauopathy and gliosis, mainly linked to stress, as the incremented glucose metabolism observed with PET imaging suggested. Further investigation will show whether SF could eventually lead to chronic neurodegeneration if the stress condition is prolonged in time.
... and AD dementia (RR 1.6; 95% CI 1.3-1.9) compared with the absence of sleep disturbance [19,20]. Even if less evidence is available on the potential cognitive benefits of meditation, relaxation, and spirituality, there is growing interest in these factors, as they have been suggested to be related to AD risk [21]. ...
Article
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Dementia, the most severe expression of cognitive impairment, is among the main causes of disability in older adults and currently affects over 55 million individuals. Dementia prevention is a global public health priority, and recent studies have shown that dementia risk can be reduced through non-pharmacological interventions targeting different lifestyle areas. The FINnish GERiatric Intervention Study to Prevent Cognitive Impairment and Disability (FINGER) has shown a positive effect on cognition in older adults at risk of dementia through a 2-year multidomain intervention targeting lifestyle and vascular risk factors. The LETHE project builds on these findings and will provide a digital-enabled FINGER intervention model for delaying or preventing the onset of cognitive decline. An individualised ICT-based multidomain, preventive lifestyle intervention program will be implemented utilising behaviour and intervention data through passive and active data collection. Artificial intelligence and machine learning methods will be used for data-driven risk factor prediction models. An initial model based on large multinational datasets will be validated and integrated into an 18-month trial integrating digital biomarkers to further improve the model. Furthermore, the LETHE project will investigate the concept of federated learning to, on the one hand, protect the privacy of the health and behaviour data and, on the other hand, to provide the opportunity to enhance the data model easily by integrating additional clinical centres.
... In modern society, sleep pattern is highly influenced by a large number of social and individual factors, such as employment, gender, age, culture, race and ethnicity, and has great impact on health. 1 Late bedtime has developed into a new kind of sleep habit, and short sleep duration and low sleep quality have been found to be strongly linked with both physical and mental problems, [2][3][4] such as anxiety symptoms, dental caries, obesity, heart disease, high blood pressure and diabetes. [5][6][7] It has been reported that low sleep efficiency and chronically poor sleep quality are significantly associated with TEWL, a direct indicator of skin barrier function. ...
Article
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Background: Late bedtime is a common form of unhealthy sleep pattern in adulthood, which influences circadian rhythm, and negatively affects health. However, little is known about the effect of regular late bedtime on skin characteristics, particularly on skin microbiome. Objective: To investigate the changes and effects of the regular late bedtime on skin physiological parameters and facial bacterial microbiome of 219 cases of Chinese women aged 18-38 years living in Shanghai. Methods: Based on the Self-Evaluation Questionnaire, bedtime was categorized as 11:00 PM; thus, the volunteers were divided into early bedtime group (S0) and late bedtime group (S1). The physiological parameters of facial skin were measured by non-invasive instrumental methods, and the skin microbiome was analyzed by 16S rRNA high-throughput sequencing. Results: The skin physiological parameters of the late bedtime group exhibited significant decrease in skin hydration content, skin firmness (F4) and elasticity (R2), while TEWL, sebum and wrinkle significantly increased. The result indicated that late bedtime significantly impaired the integrity of skin barrier, damaged skin structure, and disrupted water-oil balance. Furthermore, the analysis of α-diversity, Sobs, Ace and Chao index were found to significantly decrease (P < 0.05) in the late bedtime group, suggesting that late bedtime reduced both the abundance and the diversity of facial bacterial microbiota. Moreover, the abundance of Pseudomonas increased significantly, while Streptococcus, Stenotrophomonas, Acinetobacter, Haemophilus, Actinomyces and Neisseria decreased significantly. In addition, Spearman correlation analysis revealed strong correlations between the microbiota and the physiological parameters. Notably, the abundance of Pseudomonas significantly positively correlated with skin firmness and elasticity, but significantly negatively correlated with skin hemoglobin content, melanin content and skin hydration. Conclusion: Bedtime is an important factor in maintaining skin health. Regular late bedtime not only damages the skin barrier and skin structure but also reduces the diversity and composition of facial bacterial microbiome.
... As people get older, sleep becomes more fragmented (e.g., Bliwise et al., 2009), less efficient (Gadie et al., 2017) and there is a decline in the quantity and quality of the "deep" stages of sleep, such as slowwave sleep (SWS) and REM sleep (Ohayon et al., 2004;Mander et al., 2017). Among older adults, sleep problems have been associated with increased risk of developing cardiovascular disease (Wu et al., 2018), dementia (Shi et al., 2018), and mental health problems (Roberts et al., 2000). An outstanding question is how these variations in sleep quality are related to brain function and cognitive performance, which also change with age. ...
Article
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Sleep quality changes dramatically from young to old age, but its effects on brain dynamics and cognitive functions are not yet fully understood. We tested the hypothesis that a shift in brain networks dynamics relates to sleep quality and cognitive performance across the lifespan. Network dynamics were assessed using Hidden Markov Models (HMMs) in resting-state MEG data from a large cohort of population-based adults ( N = 564, aged 18–88). Using multivariate analyses of brain-sleep profiles and brain-cognition profiles, we found an age-related “neural shift,” expressed as decreased occurrence of “lower-order” brain networks coupled with increased occurrence of “higher-order” networks. This “neural shift” was associated with both increased sleep dysfunction and decreased fluid intelligence, and this relationship was not explained by age, sex or other covariates. These results establish the link between poor sleep quality, as evident in aging, and a behavior-related shift in neural dynamics.
Thesis
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Die vorliegende Forschungsarbeit befasst sich mit der Entwicklung und Gestaltung von körpernahen, tragbaren Artefakten für den digitalisierten Gesundheitsbereich. Unter dem entwickelten Begriff des Wearable Enhancements werden die verschiedenen Termini aus smarten Textilien, Fashion Technologies, Wearable Technologies sowie elektronischen Textilien zusammengefasst und zwei zentrale Forschungsfragen untersucht. Wie kann Wearable Enhancement im Bereich Smart Health ethisch, sozial und ökologisch entwickelt und gestaltet werden? Inwiefern können textile Schnittstellen die Wahrnehmung und die Wahrnehmbarkeit des Körpers verändern? Mit der ersten Forschungsfrage sollen vorrangig Ansätze und Strategien der Sichtbarkeit für die Entwicklung und Gestaltung diskutiert werden, welche Aussagen für die Designpraxis, den Gestaltungs- und Designforschungsprozess sowie die Designlösungen selbst generieren sollen. Die zweite Forschungsfrage zielt darauf, Formen der Sichtbarmachung von sowie für Wearable Enhancement zu untersuchen. Anhand von drei konkreten Fallstudien werden wesentliche Aspekte der Rezeption, Perzeption, Konstruktion, Konfiguration und Konzeption von soziotechnischen Artefakten zur Funktionssteigerung des menschlichen Körpers untersucht und verschiedene Formen der Sichtbarkeit und Sichtbarmachung entwickelt. In der Arbeit wird ein dual-angelegter transdisziplinärer Designforschungsansatz entwickelt und praktiziert, welcher sowohl die menschlichen Bedürfnisse der Nutzer*innen als auch die Weiterentwicklung von Technologien berücksichtigt. Auf dieser Grundlage wird versucht Anregungen für ein zukunftsfähiges und zugleich verantwortungsorientiertes Design zu geben.
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Background: Sleep disturbances are frequent in Alzheimer's disease (AD). Objective: To summarize the impact of sleep disturbances on AD patients and their caregivers and the effects of currently available sleep therapies. Methods: Published studies (January 1985-March 2020) assessing the burden associated with insomnia/sleep disturbances in the AD population and insomnia treatment effects were identified by searching PubMed, Embase, and Cochrane Library and screened against inclusion criteria. Results: 58 studies assessing patient and caregiver burden, institutionalization, and insomnia treatments in AD patients with sleep disturbances were identified. Sleep disturbances were associated with worse cognition, functional ability, and behavioral and neuropsychological functioning. Health status and quality of life of both patients and caregivers were reduced in the presence of sleep disturbances. Sleep disturbances were also associated with institutionalization. Although significant associations between sleep problems and clinical outcomes were apparent, there was generally no control for other influencing factors (e.g., cognitive status). Bright light and behavioral therapies as well as drugs showed some promise in AD patients, but studies were primarily small and limited data were available, particularly in regard to the effect on associated clinical burden. Conclusion: Sleep disturbances are a significant problem for AD patients and caregivers, associated with behavioral and psychological problems and cognitive decline. However, they remain poorly characterized and under-researched. As the global population is aging and AD is on thes rise, data from larger, prospective trials are required to fully understand the clinical correlates of sleep disturbances and the impact insomnia treatments can have.
Article
Population aging is inextricably linked to an increase in the prevalence of dementia, which are one of the main causes of loss of autonomy in old age. However, early detection of cognitive decline is critical to proactively implementing interventions to slow the progression of cognitive decline and maintain the ability to live independently of outside help. Therefore, early detection of cognitive decline is one of the primary tasks of the general practitioner. The aim of the lecture is to present a low gait speed, frailty, neuropsychiatric symptoms, sleep disorders and hearing loss as biomarkers of high risk to development of dementia risk and suggest ways measuring these risk factors in primary health care.
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Background Individuals with Down syndrome (DS) are at significant risk for early onset Alzheimer’s disease (AD), likely due to the triplication of genes on chromosome 21that facilitate AD neuropathology. To aid the effective early diagnosis of dementia in DS, we demonstrate the strategy of using single point assessment of cognitive performance with scoring normed for degree of intellectual disability to generate age related prevalence data for acquired mild cognitive impairment (AMCI). Methods 412 adults with DS were assessed using the Neuropsychological Assessment of Dementia in Adults with Intellectual Disability. Normative data, banded by degree of intellectual disability, allowed identification of AMCI by atypical deviation from expected performance. Results AMCI was evident in approximately 20% of adults with DS aged 40 and under, 40% aged 41-50 and 45% aged 51 and over. Relative risk increased significantly in those aged 46 and over. Analysis of prevalence by five year age bands revealed two peaks for higher prevalence of AMCI. Conclusions Psychometric data indicate single point assessment of AMCI is possible for the majority of adults with DS. Two peaks for age related prevalence of AMCI suggest the risk for onset of AD conferred by trisomy of chromosome 21 is moderated by another factor, possibly APOE status. This article is protected by copyright. All rights reserved.
Article
Background: The American Heart Association, in conjunction with the National Institutes of Health, annually reports the most up-to-date statistics related to heart disease, stroke, and cardiovascular risk factors, including core health behaviors (smoking, physical activity, diet, and weight) and health factors (cholesterol, blood pressure, and glucose control) that contribute to cardiovascular health. The Statistical Update presents the latest data on a range of major clinical heart and circulatory disease conditions (including stroke, congenital heart disease, rhythm disorders, subclinical atherosclerosis, coronary heart disease, heart failure, valvular disease, venous disease, and peripheral artery disease) and the associated outcomes (including quality of care, procedures, and economic costs). Methods: The American Heart Association, through its Statistics Committee, continuously monitors and evaluates sources of data on heart disease and stroke in the United States to provide the most current information available in the annual Statistical Update. The 2022 Statistical Update is the product of a full year's worth of effort by dedicated volunteer clinicians and scientists, committed government professionals, and American Heart Association staff members. This year's edition includes data on the monitoring and benefits of cardiovascular health in the population and an enhanced focus on social determinants of health, adverse pregnancy outcomes, vascular contributions to brain health, and the global burden of cardiovascular disease and healthy life expectancy. Results: Each of the chapters in the Statistical Update focuses on a different topic related to heart disease and stroke statistics. Conclusions: The Statistical Update represents a critical resource for the lay public, policymakers, media professionals, clinicians, health care administrators, researchers, health advocates, and others seeking the best available data on these factors and conditions.
Article
Objectives: Perioperative neurocognitive disorders (PND) is one of the important factors affecting the recovery of the elderly after surgery, and sleep disorders are also one of the common diseases of the elderly. Previous studies have shown that the quality of postoperative sleep may be factor affecting postoperative cognitive function, but there are few studies on the relationship between preoperative sleep disorders and postoperative cognitive dysfunction. This study aims to explore the relationship between preoperative sleep disorders and postoperative delayed neurocognitive recovery in elderly patients, and provide references for improving the prognosis and quality of life of patients. Methods: This study was porformed as a prospective cohort study. Elderly patients (age≥65 years old) underwent elective non-cardiac surgery at Xiangya Hospital of Central South University from October 2019 to January 2020 were selected and interviewed 1 day before the operation. The Mini-Mental State Examination (MMSE) and Montreal Cognitive Assessment Scale (MoCA) were used to assess the patient's baseline cognitive status. Patients with preoperative MMSE scores of less than 24 points were excluded. For patients meeting the criteria of inclusion, Pittsburgh Sleep Quality Index (PSQI) scale was used to evaluate the patients, and the patients were divided into a sleep disorder group and a non-sleep disorder group according to the score. General data of patients were collected and intraoperative data were recorded, such as duration of surgery, anesthetic time, surgical site, intraoperative fluid input, intraoperative blood product input, intraoperative blood loss and drug use. On consecutive 5 days after surgery, Numerical Rating Scale (NRS) was used to evaluate the sleep of the previous night and the pain of the day, which were recorded as sleep NRS score and pain NRS score; Confusion Assessment Method for ICU (CAM-ICU) scale and Confusion Assessment Method (CAM) scale were used to assess the occurrence of delirium. On the 7th day after the operation, the MMSE and MoCA scales were used to evaluate cognitive function of patients. We compared the incidence of postoperative complications, the number of deaths, the number of unplanned ICU patients, the number of unplanned secondary operations, etc between the 2 groups. The baseline and prognosis of the 2 groups of patients were analyzed by univariate and multivariate logistics to analyze their correlation. Results: A total of 105 patients were collected in this study, including 32 patients in the sleep disorder group and 73 patients in the non-sleep disorder group. The general information of the 2 groups, such as age, gender, body mass index, and surgery site, were not statistically significant (all P>0.05). There was no statistically significant difference in the operation time, intraoperative bleeding, the number of delirium, and sleep NRS score at 5 days after operation between the 2 groups (all P>0.05). The incidence of unplanned second surgery after surgery and the NRS pain score on the first day in the sleep disorder group were significantly higher than those in the non-sleep disorder group (P=0.002, P=0.045, respectively). A total of 20 patients (19%) in the 2 groups had postoperative delayed neurocognitive recovery on the 7th day after surgery. Among them, 11 patients (34.4%) in the sleep disorder group, 9 patients (12.3%) in the non-sleep disorder group. The incidence of delayed neurocognitive recovery in the sleep disorder group was significantly higher than that in the non-sleep disorder group (P=0.008). The incidence of postoperative infection in the sleep disorder group was also higher than that in the non-sleep disorder group (P=0.020). After controlling for the confounding factors, preoperative sleep disorders were still independently associated with postoperative delayed neurocognitive recovery (OR=3.330, 95% CI 1.063-10.431, P=0.039). Conclusions: Preoperative sleep disorders can increase the risk of delayed neurocognitive function recovery in elderly patients. Active treatment of preoperative sleep disorders may improve perioperative neurocognitive function in elderly patients.
Article
Many epidemiologic and clinical studies have shown significant links between the degree of sleep disturbance and severity of impairment of selective cognitive functions, including the risk of neurodegenerative diseases. However, the sleep parameters that affect cognitive function in old age are unclear. Therefore, we investigated the association between sleep parameters and cognitive function in older patients. Patients aged above 65 years who complained of sleep-disordered breathing were enrolled consecutively. The Mini-Mental-State Examination tool was used to evaluate cognitive function. Eighty patients (normal cognitive function, n = 32 and cognitive impairment, n = 42) were included in this study. Multiple linear regression and binary logistic regression analyses were performed to explain the relationship between sleep parameters and cognitive function. We found that the body mass index (BMI) was significantly lower in the cognitive impairment group than in the normal cognitive function group. Additionally, the cognitive impairment group showed significantly decreased sleep efficiency and an increased apnea index compared with normal subjects. Moreover, lower BMI, reduced sleep efficiency, and high frequency of apnea events during sleep were associated with an increased risk of cognitive impairment.
Article
Sleep disturbances, including disrupted sleep and short sleep duration, are highly prevalent and are prospectively associated with an increased risk for various widespread diseases, including cardiometabolic, neurodegenerative, chronic pain, and autoimmune diseases. Systemic inflammation, which has been observed in populations experiencing sleep disturbances, may mechanistically link disturbed sleep with increased disease risks. To determine whether sleep disturbances are causally responsible for the inflammatory changes reported in population-based studies, we developed a 19-day in-hospital experimental model of prolonged sleep disturbance inducing disrupted and shortened sleep. The model included delayed sleep onset, frequent nighttime awakenings, and advanced sleep offset, interspersed with intermittent nights of undisturbed sleep. This pattern aimed at providing an ecologically highly valid experimental model of the typical sleep disturbances often reported in the general and patient populations. Unexpectedly, the experimental sleep disturbance model reduced several of the assessed proinflammatory markers, namely interleukin(IL)-6 production by monocytes and plasma levels of IL-6 and C-reactive protein (CRP), presumably due to intermittent increases in the counterinflammatory hormone cortisol. Striking sex differences were observed with females presenting a reduction in proinflammatory markers and males showing a predominantly proinflammatory response and reductions of cortisol levels. Our findings indicate that sleep disturbances causally dysregulate inflammatory pathways, with opposing effects in females and males. These results have the potential to advance our mechanistic understanding of the pronounced sexual dimorphism in the many diseases for which sleep disturbances are a risk factor.
Article
The neurotrophin receptor p75 (p75NTR) is a circadian rhythm regulator and mediates cognitive deficits induced by sleep deprivation (SD). The soluble extracellular domain of p75NTR (p75ECD) has been shown to exert a neuroprotective function in Alzheimer’s disease (AD) and depression animal models. Nevertheless, the role of p75ECD in SD-induced cognitive dysfunction is unclear. In the present study we administrated p75ECD-Fc (10, 3 mg/kg), a recombinant fusion protein of human p75ECD and fragment C of immunoglobulin IgG1, to treat mice via intraperitoneal injection. The results revealed that peripheral supplementation of high-dose p75ECD-Fc (10 mg/kg) recovered the balance between Aβ and p75ECD in the hippocampus and rescued the cognitive deficits in SD mice. We also found that p75ECD-Fc ameliorated other pathologies induced by SD, including neuronal apoptosis, synaptic plasticity impairment and neuroinflammation. The current study suggests that p75ECD-Fc is a potential candidate for SD and peripheral supplementation of p75ECD-Fc may be a prospective preventive measure for cognitive decline in SD.
Article
Aims: The purpose of this study was to objectively quantify the sleep of elderly patients with dementia at home using a device and to investigate the factors associated with its identification. Methods: Sixteen patients (6 males [37.5%], 84.1±4.7 years old; and 10 patients with mild dementia [62.5%]) and their family caregivers who were using outpatient memory clinics and home-visiting nursing station in Japan were included. Demographic and clinical data of the patients and their family caregivers, subjective perceptions of patients' sleep, family caregivers' Zarit care burden, and whether or not they were aware of patients' sleep problems were determined. Nighttime sleep parameters were collected for one week using a non-wearable actigraph. Sleep parameters were compared with patients' subjective views and family caregivers' observations to investigate factors indicative of sleep disturbance. Results: Nighttime sleep parameters for 1 week (mean) were follows: sleep efficiency, 77.2%±9.3%; asleep time, 442.3±99.9 minutes; sleep latency, 18.2±15.8 minutes; awake time, 105.1±69.7 minutes; and number of times leaving the bed, 4.6±3.8 (maximum of 29/night). A significant positive correlation was found between sleep efficiency and duration of dementia (r=0.53, p=0.046), while no correlation was found with dementia severity or Zarit care burden score. The agreement between the patients' complaints about sleep and sleep efficiency (75%) was 30.7%, and family caregivers' awareness of patients' nighttime awakening and bed-leaving was significantly associated with patients' incontinence (p=0.024) and a greater dementia severity (p=0.027). Conclusions: Elderly dementia patients experienced sleep disturbance at home, such as nighttime awakening and associated bed-leaving; however, it might be difficult to identify these patients at an early stage based on their own complaints and observations by family caregivers. Identifying sleep problems at an early stage may thus require the use of objective measurement devices.
Article
Background and objective: The clinical significance of sleep-disordered breathing (SDB) in older age is uncertain. This study determined the prevalence and associations of SDB with mood, daytime sleepiness, quality of life (QOL) and cognition in a relatively healthy older Australian cohort. Methods: A cross-sectional analysis was conducted from the Study of Neurocognitive Outcomes, Radiological and retinal Effects of Aspirin in Sleep Apnoea. Participants completed an unattended limited channel sleep study to measure the oxygen desaturation index (ODI) to define mild (ODI 5-15) and moderate/severe (ODI ≥ 15) SDB, the Centre for Epidemiological Studies Scale, the Epworth Sleepiness Scale, the 12-item Short-Form for QOL and neuropsychological tests. Results: Of the 1399 participants (mean age 74.0 years), 36% (273 of 753) of men and 25% (164 of 646) of women had moderate/severe SDB. SDB was associated with lower physical health-related QOL (mild SDB: beta coefficient [β] -2.5, 95% CI -3.6 to -1.3, p < 0.001; moderate/severe SDB: β -1.8, 95% CI -3.0 to -0.6, p = 0.005) and with lower global composite cognition (mild SDB: β -0.1, 95% CI -0.2 to 0.0, p = 0.022; moderate/severe SDB: β -0.1, 95% CI -0.2 to 0.0, p = 0.032) compared to no SDB. SDB was not associated with daytime sleepiness nor depression. Conclusion: SDB was associated with lower physical health-related quality of life and cognitive function. Given the high prevalence of SDB in older age, assessing QOL and cognition may better delineate subgroups requiring further management, and provide useful treatment target measures for this age group.
Chapter
Globally, society is aging and changes to the timing and quality of sleep are often observed in older adults (aged ≥ 65 years). Good sleep quality, and sufficient sleep duration, is necessary to maintain good physical and psychological health, and strategies which optimize good sleep will be important in an aging society. Light has a very powerful effect upon sleep and circadian rhythms, and has specific advantages including the relative low cost, ease of administration and lack of interaction with other medications. For this reason, bright light treatment is a promising method for optimizing sleep and circadian rhythmicity in older adults. In this chapter, we examine whether bright light treatment could be used to optimize sleep, circadian rhythms, and health in older adults. We also outline a range of methodological considerations which need to be addressed to increase the feasibility, acceptability and effectiveness of light treatment in older adults.
Article
Background: Sleep disorders may cause dysregulation of cerebral glucose metabolism and synaptic functions, as well as alterations in cerebrospinal fluid (CSF) biomarker levels. Objective: This study aimed at measuring sleep, CSF Alzheimer's disease (AD) biomarkers, and cerebral glucose consumption in patients with obstructive sleep apnea syndrome (OSAS) and patients with periodic limb movement disorder (PLMD), compared to controls. Methods: OSAS and PLMD patients underwent 18F-fluoro-2-deoxy-D-glucose positron emission tomography (18F-FDG PET), polysomnographic monitoring, and lumbar puncture to quantify CSF levels of amyloid-β42 (Aβ42), total tau, and phosphorylated tau. All patients were compared to controls, who were not affected by sleep or neurodegenerative disorders. Results: Twenty OSAS patients, 12 PLMD patients, and 15 controls were included. Sleep quality and sleep structure were altered in both OSAS and PLMD patients when compared to controls. OSAS and PLMD patients showed lower CSF Aβ42 levels than controls. OSAS patients showed a significant increase in glucose uptake in a wide cluster of temporal-frontal areas and cerebellum, as well as a reduced glucose consumption in temporal-parietal regions compared to controls. PLMD patients showed increased brain glucose consumption in the left parahippocampal gyrus and left caudate than controls. Conclusion: Sleep dysregulation and nocturnal hypoxia present in OSAS patients, more than sleep fragmentation in PLMD patients, were associated with the alteration in CSF and 18F-FDG PET AD biomarkers, namely reduction of CSF Aβ42 levels and cerebral glucose metabolism dysregulation mainly in temporal areas, thus highlighting the possible role of sleep disorders in driving neurodegenerative processes typical of AD pathology.
Article
Background: Sleep problems may contribute to the disproportionate burden of Alzheimer's disease and related dementias (ADRD) among African Americans (AAs). Objective: To examine the role of sleep problems in contributing to cognitive function and clinically adjudicated cognitive impairment in a predominantly AA sample. Methods: This study (n = 216, 78.8% female; mean age = 67.7 years) examined associations between 1) the level (i.e., measured in 2018) and 2) change over time (from 2013 to 2018; n = 168) in actigraphy-assessed sleep with domain-specific cognitive function and clinically adjudicated cognitive impairment (2018) in a community-dwelling, predominantly AA (96.9%) sample. A comprehensive cognitive battery assessed global cognitive function (3MS) and domain-specific cognitive function (attention, visuo-spatial ability, language, delayed recall, immediate recall, and executive function) in 2018. Sleep was measured in 2013 and 2018 via actigraphy. Results: Higher sleep efficiency and less wakefulness after sleep onset (WASO; measured in 2018) were associated with greater attention, executive function, and visuospatial ability. Increases in sleep efficiency between 2013 and 2018 were associated with better executive function, language, immediate recall, and visuospatial ability, whereas increases in WASO (2013-2018) were associated with poorer attention, executive function, and visuospatial ability. Level or change in sleep duration were not associated with domain-specific cognitive function, nor were any sleep measures associated with clinically adjudicated cognitive impairment. Conclusion: In a predominantly AA sample of older adults, both the level and change (i.e., worsening) of sleep efficiency and WASO were associated with poorer cognitive function. Improving sleep health may support ADRD prevention and reduce health disparities.
Chapter
Sleep disorders are prevalent and pervasive across a wide range of dementias, including Alzheimer's disease, vascular dementia, and dementia with Lewy bodies. Herein, we review the links between sleep, circadian rhythms, across the spectrum of dementias, including the types of disorders, known alterations in sleep and circadian rhythms, and the effects of sleep on the underlying pathophysiologic mechanisms of dementia. Evaluation and management can be challenging in this population, particularly due to the atypical presentation of sleep complaints in this cohort and the need to be mindful about balancing pharmacotherapy and potential adverse events.
Article
The Indoor Air Quality (Indoor Air Quality (IAQ)) of the bedroom environment has recently garnered attention since air pollution can affect sleep. Previous studies investigated IAQ and sleep quality in controlled environments which impacts both self-reported and measured sleep quality. Studies within a participant’s home environment are ecologically valid and reduce participant bias. Here, we study 20 participants over 2.5 months in Austin, TX. We monitored five components of IAQ using the BEVO Beacon, a calibrated purpose-built environmental monitor, and measured participant sleep quality through wearable activity trackers and 4-question surveys sent four times a week. We found significant decreases in sleep quality during nights with elevated CO, CO2, and temperature. Elevated CO was associated with a mean increase in 0.9 self-reported awakenings and decreases in device-measured sleep time of 21.6 min and sleep efficiency of 0.6%. Increased CO2 and temperature were associated with decreases in device-measured sleep time of 17.5 and 15.2 min, respectively. Elevated PM2.5 and TVOCs concentrations were associated with overall improvements in sleep quality. Participants reported a mean of 4.4 fewer awakenings and had a 1.1% increased in measured sleep efficiency for nights with elevated PM2.5. Elevated TVOCs were associated with an increase in sleep time of 14.5 min. These findings indicate a need to study the relationship between these aggregate IAQ measures and sleep quality more closely. Our results also indicate that pollutants can independently affect sleep quality regardless of the CO2 measurements. Compared to literature, our study is the longest and includes the most IAQ parameters.
Article
Sleep apnea (SA) is potentially a modifiable risk factor for dementia. However, its associations to specific aetiologies of dementia remain uncertain. A systematic review and meta‐analysis of cohort studies investigating the association between sleep apnea and specific aetiologies of dementia, including Alzheimer's disease (AD), Parkinson's disease (PD), Lewy body dementia (LBD), vascular dementia (VaD), and frontotemporal dementia (FTD) was performed. The use of biomarkers to support clinical diagnoses in eligible studies was collected. Eleven studies were included, comprising 1,333,424 patients. Patients with sleep apnea had an increased risk of developing any type of neurocognitive disorder (HR: 1.43 [95% CI 1.26–1.62]), Alzheimer's disease (HR: 1.28 [95% CI 1.16–1.41]), and Parkinson's disease (HR: 1.54 [95% CI 1.30–1.84]). No statistically significant association was found for vascular dementia. One study reported a two‐fold increased risk for Lewy body dementia (HR: 2.06 [95% CI 1.45–2.91]). No studies investigated the risk for frontotemporal dementia and none of the studies reported results pertaining to biomarkers. Sleep apnea is associated with a significantly increased risk of dementia, particularly for Alzheimer's disease and Parkinson's disease, but not for vascular dementia. Future studies should look at the impact of sleep apnea on specific dementia biomarkers.
Article
Background: Hospitalised older persons with dementia are commonly discharged with intensified sleep disturbances. These disturbances can impede the recovery process. Nurses are well-positioned to assist persons with dementia and their family caregivers in managing sleep disturbances during the transition from hospital to home. Objectives: To describe the development of a multi-component intervention to promote sleep. Methods: We applied three stages of the intervention mapping method to develop a non-pharmacological, multi-component sleep intervention. The first stage involved a review of the literature to generate an understanding of the determinants of sleep disturbances experienced by persons with dementia in hospital and home settings. The second stage consisted of a literature review to identify therapies for managing commonly reported determinants of sleep disturbances. The third stage entailed delineation of the intervention components. Results: The most common determinants of sleep disturbances experienced by persons with dementia in hospital and home settings were: physiological changes associated with ageing, sleep environments non-conducive to sleep, limited exposure to light and engagement in physical activity, stress and sleep-related beliefs and behaviours. Therapies found effective included: light therapy, physical activity therapy, sleep hygiene, and stimulus control therapy. These therapies were integrated into a multi-component sleep intervention to be provided using the teach-back technique, during and following hospitalisation. Discussion: Consistent with the principles of patient engagement, the multi-component sleep intervention will be evaluated for its acceptability and feasibility. Implications for practice: The intervention has potentials to improve sleep during the transition from hospital to home.
Article
Background Increasing evidence support the correlation between mental disorders and the likelihood of developing dementia. We aim to conduct an umbrella review to assess the risk of dementia in patients with eight mental disorders. Methods We searched PubMed, Embase, Web of science, CNKI, VIP, and Wanfang databases from inception to October 29, 2021. For each included meta-analysis, the effect size with a 95% confidence interval was estimated using either a random effect model or a fixed effect model, and between-study heterogeneity was expressed by I² and Cochran's Q test. The ROBIS tool was used to assess the risk of bias. Results A total of ten systematic reviews were included. Among these studies, we identified seven risk factors, including anxiety disorder, bipolar disorder, depression, late-life depression, post-traumatic stress disorder, schizophrenia, and sleep disorder. Light to moderate alcohol drinking was identified as a protective factor. The evaluation results of the ROBIS tool showed that nine systematic reviews had high risk of bias and one had low risk of bias. The strength of evidence supporting the associations between late-life depression and all-cause dementia, Alzheimer's disease, and vascular dementia was high; the strength of evidence supporting the association between depression and all-cause dementia was moderate. Limitations Most associations had low strength of evidence and high risk of bias. Conclusions This umbrella review shows that high and moderate evidence supports the associations between some mental disorders and dementia. More cohort studies are needed to support the associations between mental disorders and dementia.
Article
Poor sleep, which is reportedly prevalent among healthcare professionals, could lead to various detrimental consequences. This study aimed to investigate the sleep quality of individuals working in emergency departments of public hospitals in China and explore the potential factors influencing sleep disturbance. A self-administered questionnaire was completed by 7688 emergency workers from 147 public hospitals in Shandong, China. Log-binomial regression analysis was performed to explore the relationship of sleep disturbance with possible influencing factors, including individual and work characteristics, occupational stress, shift work, and musculoskeletal pain. The participants' mean Pittsburgh Sleep Quality Index score was 9.6 ± 4.8, with 5341 (69.5%, 68.2-70.7%) of them experiencing sleep disturbance. The sleep quality was poorer in doctors (10.2 ± 5.1, 71.0%, 69.0-73.0%) than in nurses (9.2 ± 4.5, 68.6%, 67.0-70.1%), and poorer in those working in secondary (9.9 ± 4.5, 70.2%, 68.0-72.3%) and tertiary (12.2 ± 4.9, 77.5%, 75.3-79.7%) hospitals than in primary hospitals (8.0 ± 4.1, 64.6%, 62.6-66.6%). High prevalence of sleep disturbance was significantly associated with shift work, occupational stress, musculoskeletal pain, fewer breaks in a work shift, and less exercise during leisure time, after adjusting for confounding variables. Sleep disturbance occurred in emergency workers in the following order: two-shift rotation > three-shift rotation > permanent night shift > permanent day shift. Emergency workers in public hospitals in China had poor sleep quality and commonly experienced musculoskeletal pain. Urgent and comprehensive measures are needed to combat these issues.
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Introduction: Few studies have evaluated the combined association between SDB with comorbid insomnia and mild cognitive impairment (MCI). To test the hypothesis that SDB with comorbid insomnia is associated with greater odds of MCI than either sleep disorder independently, we used ADNI data to evaluate cross-sectional associations between SDB risk with comorbid insomnia status and MCI. Methods: Participants with normal cognition or MCI were included. Insomnia was defined by self-report. SDB risk was assessed by modified STOP-BANG. Logistic regression models evaluated associations between four sleep disorder subgroups (low risk for SDB alone, low risk for SDB with insomnia, high risk for SDB alone, and high risk for SDB with insomnia) and MCI. Models adjusted for age, sex, BMI, APOE4 genotype, race, ethnicity, education, marital status, hypertension, cardiovascular disease, stroke, alcohol abuse, and smoking. Results: The sample (n = 1391) had a mean age of 73.5 ± 7.0 years, 44.9% were female, 72.0% were at low risk for SDB alone, 13.8% at low risk for SDB with insomnia, 10.1% at high risk for SDB alone, and 4.1% at high risk for SDB with insomnia. Only high risk for SDB with comorbid insomnia was associated with higher odds of MCI (OR 3.22, 95% CI 1.57–6.60). Conclusion: Studies are needed to evaluate SDB with comorbid insomnia as a modifiable risk factor for MCI.
Article
Background: The temporal relationship between sleep, Alzheimer's disease (AD), and cognitive impairment remains to be further elucidated. Objective: First, we aim to determine whether the Neuropsychiatric Inventory-Questionnaire (NPI-Q) assessed nighttime behaviors prior to cognitive decline influence the rate of cognitive deterioration in pathologically confirmed AD, and second, to assess the possible interactions with APOE allele and cerebral amyloid angiopathy (CAA). Methods: The rate of cognitive decline between cognitively asymptomatic participants from the National Alzheimer Coordinating Center who eventually received a neuropathologic diagnosis of AD with (+NTB) or without (-NTB) nighttime behaviors were compared using independent samples t-test. Participants were stratified by APOE carrier and CAA status. Demographic and patient characteristics were assessed using descriptive statistics, and the independent samples t-test was used for continuous variables and chi-square test for categorical variables. The significance level was set at p≤0.05. Results: The rate of cognitive decline was greater in +NTB (n = 74; 3.30 points/year) than -NTB (n = 330; 2.45 points/year) (p = 0.016), even if there was no difference in cognitive status at onset. This difference was restricted to APOE ɛ4 carriers (p = 0.049) and positive CAA participants (p = 0.020). Significance was not reached in non-carriers (p = 0.186) and negative CAA (p = 0.364). APOE and CAA were not differentially distributed between the NTB groups. Conclusion: NPI-Q assessed nighttime behaviors, a surrogate for sleep disturbances, are associated with more rapidly deteriorating cognition in patients with AD neuropathology who are also carriers of APOE ɛ4 or show CAA.
Article
Neurological disorders encompass an extremely broad range of conditions, including those that present early in development and those that progress slowly or manifest with advanced age. Although these disorders have distinct underlying etiologies, the activation of shared pathways, e.g., integrated stress response (ISR) and the development of shared phenotypes (sleep deficits) may offer clues toward understanding some of the mechanistic underpinnings of neurologic dysfunction. While it is incontrovertibly complex, the relationship between sleep and persistent stress in the brain has broad implications in understanding neurological disorders from development to degeneration. The convergent nature of the ISR could be a common thread linking genetically distinct neurological disorders through the dysregulation of a core cellular homeostasis pathway.
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STUDY OBJECTIVES: Mounting evidence implicates disturbed sleep or lack of sleep as one of the risk factors for Alzheimer's disease (AD) but the extent of the risk is uncertain. We conducted a broad systematic review and meta-analysis to quantify the effect of sleep problems/disorders on cognitive impairment and AD. METHODS: Original published literature assessing any association of sleep problems or disorders with cognitive impairment or AD was identified by searching PubMed, Embase, Web of Science, and the Cochrane library. Effect estimates of individual studies were pooled and relative risks (RR) and 95% confidence intervals (CI) were calculated using random effects models. We also estimated the population attributable risk (PAR). RESULTS: Twenty-seven observational studies (n = 69,216 participants) that provided 52 RR estimates were included in the meta-analysis. Individuals with sleep problems had a 1.55 (95% CI: 1.25-1.93), 1.65 (95% CI: 1.45-1.86) and 3.78 (95% CI: 2.27-6.30) times higher risk for AD, cognitive impairment and preclinical AD than individuals without sleep problems respectively. The overall meta-analysis revealed that individuals with sleep problems had a 1.68 (95% CI: 1.51-1.87) times higher risk for the combined outcome of cognitive impairment and/or AD. Approximately 15% of AD in the population may be attributed to sleep problems. CONCLUSION: This meta-analysis confirmed the association between sleep and cognitive impairment or AD and, for the first time, consolidated the evidence to provide an "average" magnitude of effect. As sleep problems are of a growing concern in the population, these findings are of interest for potential prevention of AD.
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Sleep-related movement disorders (SRMD) are sleep disorders. As poor sleep quality is associated with cognitive impairment, we hypothesized that SRMD patients were exposed to a great risk for developing dementia. The present study was aimed to retrospectively examine the association of SRMD and dementia risk. A retrospective longitudinal study was conducted using the data obtained from the Longitudinal Health Insurance Database (LHID) in Taiwan. The study cohort enrolled 604 patients with SRMD who were initially diagnosed and 2416 patients who were randomly selected and age/gender matched with the study group. SRMD, dementia, and other confounding factors were defined according to International Classification of Diseases Clinical Modification Codes. Cox proportional-hazards regressions were employed to examine adjusted hazard ratios (HR) after adjusting with confounding factors. Our data revealed that patients with SRMD had a 3.952 times (95% CI = 1.124–4.767) higher risk to develop all-cause dementia compared with individuals without SRMD. The results showed that SRMD patients aged 45 to 64 exhibited highest risk of developing all-cause dementia (HR: 5.320, 95% CI = 1.770–5.991), followed by patients age ≥65 (HR: 4.123, 95% CI = 2.066–6.972) and <45 (HR: 3.170, 95% CI = 1.050–4.128), respectively. Females with SRMD were at greater risk to develop all-cause dementia (HR: 4.372, 95% CI = 1.175–5.624). The impact of SRMD on dementia risk was progressively increased by various follow-up time intervals (<1 year, 1–2 years, and ≥2 years). The results suggest that SRMD is linked to an increased risk for dementia with gender-dependent and time-dependent characteristics.
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Unlabelled: Although the functions of sleep remain to be fully elucidated, it is clear that there are far-reaching effects of its disruption, whether by curtailment for a single night, by a few hours each night over a long period, or by disruption in sleep continuity. Epidemiological and experimental studies of these different forms of sleep disruption show deranged physiology from subcellular levels to complex affective behavior. In keeping with the multifaceted influence of sleep on health and well-being, we illustrate how the duration of sleep, its timing, and continuity can affect cellular ultrastructure, gene expression, metabolic and hormone regulation, mood, and vigilance. Recent brain imaging studies provide some clues on mechanisms underlying the most common cause of disrupted sleep (insomnia). These insights should ultimately result in adequate interventions to prevent and treat sleep disruption because of their high relevance to our most prevalent health problems. Significance statement: Disruption of the duration, timing, and continuity of sleep affects cellular ultrastructure, gene expression, appetite regulation, hormone production, vigilance, and reward functions.
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To examine the association between self-reported sleep problems and incidence of dementia in community-dwelling elderly people. 1,041 nondemented participants over 65 years old were examined longitudinally. Sleep problems were estimated using the RAND Medical Outcomes Study Sleep Scale examining sleep disturbance, snoring, sleep short of breath or with a headache, sleep adequacy, and sleep somnolence. Cox regression analysis was used to examine the association between sleep problems and risk for incident dementia. Age, gender, education, ethnicity, APOE-ε4, stroke, heart disease, hypertension, diabetes, and depression were included as covariates. Over 3 years of follow-up, 966 (92.8%) participants remained nondemented, while 78 (7.2%) developed dementia. In unadjusted models, sleep inadequacy ('Get the amount of sleep you need') at the initial visit was associated with increased risk of incident dementia (HR = 1.20; 95% CI 1.02-1.42; p = 0.027). Adjusting for all the covariates, increased risk of incident dementia was still associated with sleep inadequacy (HR = 1.20; 95% CI 1.01-1.42; p = 0.040), as well as with increased daytime sleepiness ('Have trouble staying awake during the day') (HR = 1.24; 95% CI 1.00-1.54; p = 0.047). Our results suggest that sleep inadequacy and increased daytime sleepiness are risk factors for dementia in older adults, independent of demographic and clinical factors.
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Objective: To study the association between self-reported sleep disturbances and dementia risk. Methods: Self-reported sleep disturbances and established risk factors for dementia were measured in men at ages 50 (n = 1574) and 70 (n = 1029) years. Dementia incidence was determined by reviewing their patient history between ages 50 and 90 years. In addition, plasma levels of β-amyloid (Aβ) peptides 1-40 and 1-42 were measured at ages 70, 77, and 82 years. Results: Cox regression demonstrated that men with self-reported sleep disturbances had a higher risk of developing dementia (+33%) and Alzheimer's disease (AD, +51%) than men without self-reported sleep disturbances (both P < .05). Binary logistic regression showed the increased risk for both dementia (+114%) and AD (+192%) were highest when sleep disturbance was reported at age 70 years (both P < .001). No group differences were found in Aβ levels. Conclusion: Improving sleep quality may help reduce the neurodegenerative risk in older men.
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Sleep apnea (SA) has been associated with cognitive impairment. However, no data regarding the risk of dementia in patients with SA has been reported in the general population. This retrospective matched-control cohort study was designed to estimate and compare the risk of dementia in SA and non-SA patients among persons aged 40 and above over a 5-year period follow-up. We conducted a nationwide 5-year population-based study using data retrieved from the Longitudinal Health Insurance Database 2005 (LHID2005) in Taiwan. The study cohort comprised 1414 patients with SA aged 40 years who had at least 1 inpatient service claim or 1 ambulatory care claim. The comparison cohort comprised 7070 randomly selected patients who were matched with the study group according to sex, age, and index year. We performed Cox proportional-hazards regressions to compute the 5-year dementia-free survival rates after adjusting for potentially confounding factors. The SA patients in this study had a 1.70-times greater risk of developing dementia within 5 years of diagnosis compared to non-SA age- and sex-matched patients, after adjusting for other risk factors (95% confidence interval (CI) = 1.26-2.31; P < .01). For the gender-dependent effect, only females with SA were more likely to develop dementia (adjust HR: 2.38, 95% CI =1.51-3.74; P < .001). For the age-dependent effect of different genders, males with SA aged 50-59 years had a 6.08 times greater risk for developing dementia (95% CI = 1.96-18.90), and females with SA aged ≥ 70 years had a 3.20 times greater risk of developing dementia (95% CI =1.71-6.00). For the time-dependent effect, dementia may be most likely to occur in the first 2.5 years of follow-up (adjusted HR:2.04, 95% CI =1.35-3.07). SA may be a gender-dependent, age-dependent, and time-dependent risk factor for dementia.
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Importance: Older adults commonly report disturbed sleep, and recent studies in humans and animals suggest links between sleep and Alzheimer disease biomarkers. Studies are needed that evaluate whether sleep variables are associated with neuroimaging evidence of β-amyloid (Aβ) deposition. OBJECTIVE To determine the association between self-reported sleep variables and Aβ deposition in community-dwelling older adults. Design, setting, and participants: Cross-sectional study of 70 adults (mean age, 76 [range, 53-91] years) from the neuroimaging substudy of the Baltimore Longitudinal Study of Aging, a normative aging study. EXPOSURE Self-reported sleep variables. MAIN OUTCOMES AND MEASURES β-Amyloid burden, measured by carbon 11-labeled Pittsburgh compound B positron emission tomography distribution volume ratios (DVRs). Results: After adjustment for potential confounders, reports of shorter sleep duration were associated with greater Aβ burden, measured by mean cortical DVR (B = 0.08 [95% CI, 0.03-0.14]; P = .005) and precuneus DVR (B = 0.11 [0.03-0.18]; P = .007). Reports of lower sleep quality were associated with greater Aβ burden measured by precuneus DVR (B = 0.08 [0.01-0.15]; P = .03). Conclusions and relevance: Among community-dwelling older adults, reports of shorter sleep duration and poorer sleep quality are associated with greater Aβ burden. Additional studies with objective sleep measures are needed to determine whether sleep disturbance causes or accelerates Alzheimer disease.
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The conservation of sleep across all animal species suggests that sleep serves a vital function. We here report that sleep has a critical function in ensuring metabolic homeostasis. Using real-time assessments of tetramethylammonium diffusion and two-photon imaging in live mice, we show that natural sleep or anesthesia are associated with a 60% increase in the interstitial space, resulting in a striking increase in convective exchange of cerebrospinal fluid with interstitial fluid. In turn, convective fluxes of interstitial fluid increased the rate of β-amyloid clearance during sleep. Thus, the restorative function of sleep may be a consequence of the enhanced removal of potentially neurotoxic waste products that accumulate in the awake central nervous system.
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Sleep problems may adversely affect neuronal health. We examined a subjective report of change (reduced duration and/or depth) in sleep pattern in relation to subsequent risk of incident all-cause dementia and Alzheimer disease (AD) over 9 years. This longitudinal study used data from a population-based sample of 214 Swedish adults aged 75 and over who were dementia-free both at baseline and at first follow-up (3 years later). The sample was 80% female and, on average, 83.4 years of age at baseline. All participants underwent a thorough clinical examination to ascertain all-cause dementia and AD. Forty percent of participants reported a change in sleep duration at baseline. Between the 6th and 9th year after baseline, 28.5% were diagnosed with all-cause dementia, 22.0% of whom had AD. Reduced sleep was associated with a 75% increased all-cause dementia risk (hazard ratio: 1.75; 95% confidence interval: 1.04-2.93; Wald = 4.55, df = 1, p = 0.035) and double the risk of AD (hazard ratio: 2.01; 95% confidence interval: 1.12-3.61; Wald = 5.47, df = 1, p = 0.019) after adjusting for age, gender, and education. The results remained after adjusting for lifestyle and vascular factors but not after adjusting for depressive symptoms. No evidence supported a moderating effect of the use of sleeping pills, and the sleep-dementia relationship remained after controlling for the presence of the apolipoprotein E ε4 allele. Self-reported sleep problems may increase the risk for dementia, and depressive symptoms may explain this relationship. Future research should determine whether treatment, in particular, behavioral or nonpharmacologic treatment, may represent one avenue toward reduction of dementia risk in late life.
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Volgens rapport van de Wereld Gezondheidsorganisatie uit 2003 is de ziektelast van dementie hoger dan van welke andere aandoening dan ook. Zij brengt zeer hoge kosten met zich mee voor zowel de gezondheidszorg als de maatschappelijke dienstverlening en tevens door de grote behoefte aan institutionele zorg. Alzheimer Disease International, het overkoepelende orgaan van vele nationale Alzheimer organisaties, heeft een internationale groep van deskundigen bijeengeroepen om evidencebased ramingen te maken van de prevalentie van dementie in alle regio’s van de wereld voor nu en in de toekomst (2020- 2040).