scholarly journals Does selection for short sleep duration explain human vulnerability to Alzheimer’s disease?

2017 ◽  
Vol 2017 (1) ◽  
pp. 39-46 ◽  
Author(s):  
Randolph M Nesse ◽  
Caleb E Finch ◽  
Charles L Nunn
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Sleep Duration ◽  
Short Sleep Duration ◽  
Human Vulnerability ◽  
Short Sleep ◽  
Selection For

scholarly journals 1152 Genetic Risk Of Alzheimer’S Disease Is Linked To Short Sleep Duration

SLEEP ◽  
2020 ◽  
Vol 43 (Supplement_1) ◽  
pp. A439-A439
Author(s):  
Y Leng ◽  
K Yaffe ◽  
S Ackley ◽  
M Glymour ◽  
W Brenowitz
Keyword(s):  
Alzheimer’S Disease ◽  
Older Adults ◽  
Alzheimer's Disease ◽  
Sleep Duration ◽  
Genetic Risk ◽  
Genetic Risk Score ◽  
Genetic Ancestry ◽  
European Ancestry ◽  
Short Sleep Duration ◽  
Short Sleep

Abstract Introduction Sleep disturbances including short sleep duration are common in older adults, especially in those with Alzheimer’s disease (AD). However, it is unclear to what extent sleep duration is a manifestation of AD disease process. We examined whether genetic variants related to AD influence sleep duration in middle-aged and older adults and estimated the causal effects of AD on sleep duration using a mendelian randomization (MR) analysis. Methods We examined 406,687 UK Biobank participants with Caucasian genetic ancestry who self-reported sleep duration at baseline (2006-2010). Sleep duration was assessed by asking: “About how many hours sleep do you get in every 24 hours? (please include naps).” A genetic risk score for AD (AD-GRS) was calculated as a weighted sum of 23 previously identified AD-related single nucleotide polymorphisms in individuals of European ancestry. We evaluated whether AD-GRS predicted sleep duration using linear regression, adjusting for age, sex and principle components for genetic ancestry. We also stratified the analysis by age at baseline (≤55y or >55y) and conducted a MR analysis to estimate the effect of AD (ICD-9/10 codes for AD/dementia diagnosis) on sleep duration. Results The participants (aged 56.91±8.00y) had an average sleep duration of 7.2 (Standard deviation [SD]=1.1) hours and AD-GRS of 0.11 (SD=0.40) (range: -1.15~1.85). Higher AD-GRS score predicted shorter sleep duration (b= -0.013, 95%CI:-0.022,-0.005), mainly among those aged over 55y (b= -0.023, 95%CI:-0.034,-0.012) and not in those 55y or younger (b= 0.006, 95%CI:-0.012,0.013); p for interaction by age=0.02. MR analysis using AD-GRS as an instrumental variable suggested that AD was associated with 1.76 hrs (b=-1.76, -2.62~ -0.90) shorter sleep duration in those aged >55y. Conclusion Using a novel analytical approach, we found that higher genetic risk for AD predicted shorter sleep duration among older adults. This suggests shared genetic pathways; the biologic processes that lead to AD may also affect sleep duration. Support Dr. Leng received support from the National Institute on Aging (NIA) 1K99AG056598, and from GBHI, Alzheimer’s Association, and Alzheimer’s Society (GBHI ALZ UK-19-591141).

scholarly journals Sleep experiences during different lifetime periods and in vivo Alzheimer pathologies

2019 ◽  
Vol 11 (1) ◽  
Author(s):  
Young Min Choe ◽  
◽  
Min Soo Byun ◽  
Dahyun Yi ◽  
Jun Ho Lee ◽  
...  
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Sleep Quality ◽  
Sleep Duration ◽  
Young Adulthood ◽  
Short Sleep Duration ◽  
Old Adults ◽  
Short Sleep ◽  
The Relationship

Abstract Background Very little is known for the direction or causality of the relationship between lifetime sleep experiences and in vivo Alzheimer’s disease (AD) pathologies. This study aimed to examine the relationship between sleep experiences during the young adulthood, midlife, and late-life periods and in vivo cerebral beta-amyloid (Aβ) deposition and AD signature regional neurodegeneration in cognitively normal (CN) old adults. Methods This study included 202 CN old adults who participated in the Korean Brain Aging Study for the Early Diagnosis and Prediction of Alzheimer’s Disease (KBASE) study. All participants underwent a comprehensive clinical assessment, [11C] Pittsburgh Compound B positron emission tomography (PET), [18F] Fluorodeoxyglucose-PET, and magnetic resonance imaging. The quality and duration of sleep were assessed for the following age periods: 20–30s, 40–50s, and the most recent month. All analyses were adjusted for age, gender, education, apolipoprotein E ε4 status, vascular risk score, Hamilton Depression Rating Scale score, and use of sleep medication. Results Bad sleep quality and short sleep duration during midlife were significantly associated with increased Aβ deposition and AD signature regional hypometabolism, respectively. Although current bad sleep quality appeared to be associated with increased Aβ accumulation, this association disappeared after controlling for the effects of midlife sleep quality. Neither the quality nor duration of sleep during young adulthood was related to Aβ burden or neurodegeneration. Conclusions Bad sleep quality during midlife increases pathological Aβ deposition in the brain, while short sleep duration during the same period accelerates regional hypometabolism.

scholarly journals Genetic risk of Alzheimer’s disease is linked to short sleep duration

2020 ◽  
Vol 16 (S10) ◽  
Author(s):  
Yue Leng ◽  
Sarah F Ackley ◽  
M Maria Glymour ◽  
Kristine Yaffe ◽  
Willa D Brenowitz
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Sleep Duration ◽  
Genetic Risk ◽  
Short Sleep Duration ◽  
Short Sleep

scholarly journals Selection for long and short sleep duration in Drosophila melanogaster reveals the complex genetic network underlying natural variation in sleep

PLoS Genetics ◽  
2017 ◽  
Vol 13 (12) ◽  
pp. e1007098 ◽  
Author(s):  
Susan T. Harbison ◽  
Yazmin L. Serrano Negron ◽  
Nancy F. Hansen ◽  
Amanda S. Lobell
Keyword(s):  
Drosophila Melanogaster ◽  
Sleep Duration ◽  
Natural Variation ◽  
Genetic Network ◽  
Short Sleep Duration ◽  
Short Sleep ◽  
Selection For

scholarly journals 0011 ARTIFICIAL SELECTION FOR LONG AND SHORT SLEEP DURATION IN DROSOPHILA MAPS TO BROAD DEVELOPMENTAL AND SIGNALING PATHWAY GENES

SLEEP ◽  
2017 ◽  
Vol 40 (suppl_1) ◽  
pp. A4-A4
Author(s):  
ST Harbison ◽  
Y Serrano Negron ◽  
NF Hansen ◽  
AS Lobell
Keyword(s):  
Signaling Pathway ◽  
Sleep Duration ◽  
Artificial Selection ◽  
Short Sleep Duration ◽  
Short Sleep ◽  
Selection For

Relaksasi Benson Untuk Durasi Tidur Pasien Penyakit Jantung Koroner

2018 ◽  
Vol 3 (3) ◽  
pp. 556
Author(s):  
Mulyanti Roberto Muliantino ◽  
Tuti Herawati ◽  
Masfuri Masfuri
Keyword(s):  
Cardiac Rehabilitation ◽  
Sleep Duration ◽  
Intervention Group ◽  
Self Report ◽  
Pharmacological Intervention ◽  
Control Group ◽  
P Value ◽  
Short Sleep Duration ◽  
Short Sleep ◽  
Coronary Arterial Disease

<p><em>Coronary Arterial Disease (CAD) is one of cardiovaskular disease that remain leading cause death and disability. Short sleep duration is the major symptoms in patients with CAD, during recovery period after cardiac events and during cardiac rehabilitation. Benson’s relaxation is one of relaxation as modalities therapy to increase sleep duration, </em><em>however few studies related to this</em><em> technique in planned</em><em> intervention</em><em>.</em><em> This study was to measured the effectiveness of Benson’s relaxation in short sleep duration of CAD patients during cardiac rehabilitation. It was a </em><em>quasi experimental pretest posttest control group design.</em><em> This study included 29 respondens in Dr.M.Djamil Hospital were assigned to intervention group which receiving Benson’s relaxation technique (n=15) and control group with routine care (n=14). </em><em>Benson’s relaxation </em><em>technique</em><em> was administered for 5 days 2 times a day, each 20 minutes to intervention group.</em><em> Short sleep duration was measured using </em><em>sleep diary (self report).</em><em> The result indicated significant increasing in mean of  sleep duration  before and after Benson’s relaxation in intervention group </em><em>(p value &lt; 0,001). </em><em>The study concluded that </em><em>Benson’s relaxation </em><em>technique is an effective non-pharmacological intervention to increase sleep duration in CAD patients.</em></p><p><em><br /></em></p><p>Penyakit jantung koroner menjadi masalah kardiovaskular yang mengakibatkan angka mortalitas yang tinggi. Durasi tidur pendek termasuk salah satu keluhan utama pasien penyakit jantung koroner pada masa recovery setelah serangan dan menjalani rehabilitasi fase 2. Relaksasi Benson merupakan teknik relaksasi sebagai terapi modalitas untuk mengurangi keluhan durasi tidur pendek, namum belum banyak penelitian terkait intervensi ini. Penelitian ini bertujuan untuk mengidentifikasi pengaruh relaksasi Benson terhadap durasi tidur pasien penyakit jantung koroner yang menjalani rehabilitasi fase 2. Penelitian ini menggunakan desain Quasi Eksperimen dengan pendekatan <em>control group pretest posttest design</em> pada 29 responden di RSUP. Dr.M.Djamil Padang yang dibagi dalam dua kelompok (kelompok intervensi dan kelompok kontrol). Hasil penelitian menunjukan ada perbedaan rerata durasi tidur yang signifikan antara sebelum dan setelah dilakukan intervensi relaksasi Benson pada kelompok intervensi (p value &lt; 0,001). Simpulan hasil penelitian ini dapat menjadi salah satu terapi modalitas bagi perawat untuk mengatasi masalah durasi tidur pendek pada pasien penyakit jantung koroner.</p><p><em><br /></em></p>

374 Cognitive Behavioral Therapy with Exercise in Adults with Insomnia and Short Sleep: Daytime Function Outcomes from a Pilot Study

SLEEP ◽  
2021 ◽  
Vol 44 (Supplement_2) ◽  
pp. A149-A149
Author(s):  
Andrew Kubala ◽  
Mara Egeler ◽  
Daniel Buysse ◽  
Martica Hall ◽  
Emma Barinas-Mitchell ◽  
...  
Keyword(s):  
Sleep Duration ◽  
Behavioral Therapy ◽  
Exercise Program ◽  
Short Sleep Duration ◽  
Post Intervention ◽  
Short Sleep ◽  
Supervised Exercise ◽  
Daytime Function ◽  
Supervised Exercise Program ◽  
Insomnia Severity

Abstract Introduction Cognitive behavioral therapy for insomnia (CBT-I) is efficacious, but there is mixed evidence as to whether improvement is blunted in adults with insomnia and short sleep duration. Exercise training can reduce physiologic hyperarousal and may increase homeostatic sleep drive, which could potentiate CBT-I treatment effects. This pilot study explored changes in self-reported outcomes from a CBT-I intervention augmented by exercise training in a sample of adults with insomnia and objective short sleep duration. Methods Eight adults (50% female, 62.5% white) with insomnia disorder and short sleep duration (mean actigraphic TST &lt;6.5 hr) completed a 12-week single-arm trial. Participants self-administered the online “Sleep Healthy Using the Internet” (SHUT-I) CBT-I program with additional staff guidance while completing a supervised exercise program (EX; 150 min/wk of moderate-intensity aerobic exercise and 2 days/wk of strength training). Participants completed assessments of self-reported sleep and daytime function pre- and post-intervention, including the Insomnia Severity Index (ISI), Flinders Fatigue Scale (FFS), Ford Insomnia Response to Stress Test (FIRST), Perceived Stress Scale (PSS), and Epworth Sleepiness Scale (ESS). Differences between timepoints were analyzed using paired t-tests and Cohen’s d effect size calculations. Results Insomnia severity significantly decreased after the intervention (ISI: p&lt;0.001, d=2.99), with 75% reporting post-intervention ISI ≤ 7. Likewise, fatigue significantly decreased after the intervention (FFS: p=0.032, d=0.95). Symptoms of stress-related sleep reactivity and stress were also reduced (FIRST: p=0.012, d=1.19; PSS: p=0.014, d=1.14). Though nonsignificant, large reductions in sleepiness were additionally observed (ESS: p=0.058, d=0.80). Conclusion In this pilot trial among patients with insomnia and short sleep duration, online CBT-I plus a supervised exercise program resulted in a significant reduction in insomnia severity. The intervention also produced large and meaningful reductions in fatigue and stress, which are common daytime impairments in patients with insomnia. Future research should attempt to disentangle the independent contributions of CBT-I and exercise on outcomes in this population. Support (if any) NIH: K23HL118318

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