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Sleep Initiation and Maintenance Disorders: HELP
Articles by Henning Tiemeier
Based on 2 articles published since 2010
(Why 2 articles?)
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Between 2010 and 2020, Henning Tiemeier wrote the following 2 articles about Sleep Initiation and Maintenance Disorders.
 
+ Citations + Abstracts
1 Article Genome-wide analysis of insomnia in 1,331,010 individuals identifies new risk loci and functional pathways. 2019

Jansen, Philip R / Watanabe, Kyoko / Stringer, Sven / Skene, Nathan / Bryois, Julien / Hammerschlag, Anke R / de Leeuw, Christiaan A / Benjamins, Jeroen S / Muñoz-Manchado, Ana B / Nagel, Mats / Savage, Jeanne E / Tiemeier, Henning / White, Tonya / Anonymous16401124 / Tung, Joyce Y / Hinds, David A / Vacic, Vladimir / Wang, Xin / Sullivan, Patrick F / van der Sluis, Sophie / Polderman, Tinca J C / Smit, August B / Hjerling-Leffler, Jens / Van Someren, Eus J W / Posthuma, Danielle. ·Department of Complex Trait Genetics, Center for Neurogenomics and Cognitive Research, Amsterdam Neuroscience, VU University Amsterdam, Amsterdam, the Netherlands. · Department of Child and Adolescent Psychiatry, Erasmus University Medical Center, Rotterdam, the Netherlands. · Laboratory of Molecular Neurobiology, Department of Medical Biochemistry and Biophysics, Karolinska Institutet, Stockholm, Sweden. · UCL Institute of Neurology, Queen Square, London, UK. · Department of Medical Epidemiology and Biostatistics, Karolinska Institutet, Stockholm, Sweden. · Department of Social, Health and Organisational Psychology, Utrecht University, Utrecht, the Netherlands. · Department of Experimental Psychology, Helmholtz Institute, Utrecht University, Utrecht, the Netherlands. · Department of Clinical Genetics, Section of Complex Trait Genetics, Amsterdam Neuroscience, VU University Medical Center, Amsterdam, The Netherlands. · Department of Psychiatry, Erasmus University Medical Center, Rotterdam, the Netherlands. · 23andMe, Inc., Mountain View, CA, USA. · Department of Genetics, University of North Carolina, Chapel Hill, NC, USA. · Department of Psychiatry, University of North Carolina, Chapel Hill, NC, USA. · Department of Molecular and Cellular Neurobiology, Center for Neurogenomics and Cognitive Research, Amsterdam Neuroscience, VU University Amsterdam, Amsterdam, The Netherlands. · Department of Sleep and Cognition, Netherlands Institute for Neuroscience (an institute of the Royal Netherlands Academy of Arts and Sciences), Amsterdam, The Netherlands. · Departments of Psychiatry and Integrative Neurophysiology, Center for Neurogenomics and Cognitive Research, Amsterdam Neuroscience, VU University, Amsterdam University Medical Center, Amsterdam, The Netherlands. · Department of Complex Trait Genetics, Center for Neurogenomics and Cognitive Research, Amsterdam Neuroscience, VU University Amsterdam, Amsterdam, the Netherlands. d.posthuma@vu.nl. · Department of Clinical Genetics, Section of Complex Trait Genetics, Amsterdam Neuroscience, VU University Medical Center, Amsterdam, The Netherlands. d.posthuma@vu.nl. ·Nat Genet · Pubmed #30804565.

ABSTRACT: Insomnia is the second most prevalent mental disorder, with no sufficient treatment available. Despite substantial heritability, insight into the associated genes and neurobiological pathways remains limited. Here, we use a large genetic association sample (n = 1,331,010) to detect novel loci and gain insight into the pathways, tissue and cell types involved in insomnia complaints. We identify 202 loci implicating 956 genes through positional, expression quantitative trait loci, and chromatin mapping. The meta-analysis explained 2.6% of the variance. We show gene set enrichments for the axonal part of neurons, cortical and subcortical tissues, and specific cell types, including striatal, hypothalamic, and claustrum neurons. We found considerable genetic correlations with psychiatric traits and sleep duration, and modest correlations with other sleep-related traits. Mendelian randomization identified the causal effects of insomnia on depression, diabetes, and cardiovascular disease, and the protective effects of educational attainment and intracranial volume. Our findings highlight key brain areas and cell types implicated in insomnia, and provide new treatment targets.

2 Article Associations of the 24-h activity rhythm and sleep with cognition: a population-based study of middle-aged and elderly persons. 2015

Luik, Annemarie I / Zuurbier, Lisette A / Hofman, Albert / Van Someren, Eus J W / Ikram, M Arfan / Tiemeier, Henning. ·Department of Epidemiology, Erasmus University Medical Center, Rotterdam, The Netherlands. · Department of Sleep and Cognition, Netherlands Institute for Neuroscience, an Institute of the Netherlands Royal Academy of Arts and Sciences, Amsterdam, The Netherlands; Departments of Integrative Neurophysiology and Medical Psychology, Center for Neurogenomics and Cognitive Research, Neuroscience Campus Amsterdam, VU University and Medical Center, Amsterdam, The Netherlands. · Department of Epidemiology, Erasmus University Medical Center, Rotterdam, The Netherlands; Department of Neurology, Erasmus University Medical Center, Rotterdam, The Netherlands; Department of Radiology, Erasmus University Medical Center, Rotterdam, The Netherlands. · Department of Epidemiology, Erasmus University Medical Center, Rotterdam, The Netherlands; Department of Child and Adolescent Psychiatry, Erasmus University Medical Center, Rotterdam, The Netherlands; Department of Psychiatry, Erasmus University Medical Center, Rotterdam, The Netherlands. Electronic address: h.tiemeier@erasmusmc.nl. ·Sleep Med · Pubmed #26028055.

ABSTRACT: BACKGROUND: Cognitive functioning changes with age, sleep, and the circadian rhythm. We investigated whether these factors are independently associated with different cognitive domains assessed in middle-aged and elderly persons. METHODS: In 1723 middle-aged and elderly persons (age 62 ± 9.4 years, mean ± standard deviation, SD) of the Rotterdam Study, we collected actigraphy recordings of on average 138 h. Actigraphy was used to quantify 24-h rhythms by calculating the stability of the rhythm over days and the fragmentation of the rhythm. Sleep parameters including total sleep time, sleep-onset latency, and wake after sleep onset were also estimated from actigraphy. Cognitive functioning was assessed with the word learning test (WLT), word fluency test (WFT), letter digit substitution task (LDST), and Stroop color word test (Stroop). RESULTS: Persons with less stable 24-h rhythms performed worse on the LDST (B = 0.42 per SD increase, p = 0.004) and the Stroop interference trial (B = -1.04 per SD increase, p = 0.003) after full adjustment. Similarly, persons with more fragmented rhythms performed worse on the LDST (B = -0.47 per SD increase, p = 0.002) and the Stroop (B = 1.47 per SD increase, p <0.001). By contrast, longer observed sleep-onset latencies were related to worse performance on the WLT delayed recall (B = -0.19 per SD increase, p = 0.027) and the WFT (B = -0.45 per SD increase, p = 0.007). CONCLUSIONS: Disturbances of sleep and the 24-h activity rhythm were independently related to cognition; while persons with longer sleep-onset latencies had worse performance on memory and verbal tasks, persons with 24-h rhythm disturbances performed less on executive functioning and perceptual speed tasks.