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PubMed · 15543997

Sleep disorders: an overview.

Abstract

Although sleep disorders medicine is a relatively young discipline, understanding of the diagnosis, pathophysiology, and treatment of sleep disorders is evolving at a rapid pace. This overview discusses the history of the development of sleep disorders medicine, tracing changes in the diagnostic classification of sleep disorders as well as the role of polysomnography in diagnosis. This evolution is most evident for insomnia, one of the major sleep disturbances. The accumulation of epidemiologic data on the prevalence and temporal course of insomnia and emerging information regarding its pathophysiology derived from laboratory assessments have led to the development of new therapeutic approaches for primary insomnia and insomnia associated with medical and psychiatric disorders.

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BibTeXRIS

Timothy Roehrs, Thomas Roth. 2004. Sleep disorders: an overview.. https://doi.org/10.1016/s1098-3597(04)80043-7

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Assessing the comorbidity between asthma and depression through polygenic risk scoring and time-to-event models.

BACKGROUND: Patients with asthma have an increased risk of developing depression, affecting their quality of life. To date, the processes contributing to this comorbidity remain unclear. METHODS: We integrated two large genome-wide association studies (88,486 patients with asthma and 447,859 controls; 412,024 patients with depression and 1,587,577 controls) with cross-sectional and longitudinal information available from the All of Us Research Program (N = 87,167) through polygenic risk scoring (PRS), Cox proportional-hazards models, one-sample Mendelian randomization (MR), and gene-set and drug-repurposing analyses. RESULTS: We observed that depression PRS was associated with increased asthma risk (hazard ratio, HR = 1.13, 95% CI = 1.09-1.17), also when accounting for comorbidity status (HR = 1.08, 95% CI = 1.04-1.12). Conversely, the effect of asthma PRS was null after accounting for comorbidity status. One-sample MR analysis showed an effect of depression genetic liability on asthma, ranging from beta = 0.36 ± 0.03 when considering a linear relationship to beta = 3.21 ± 0.31 when considering possible nonlinear relationships. Conversely, the effect of asthma genetic risk on depression was null after accounting for potential confounders. The gene-set analyses showed that asthma and depression polygenic risks share biological processes, molecular functions, and cellular components related to the immune system and the lung-brain axis. CONCLUSIONS: Genetic predisposition contributes to asthma-depression comorbidity through direct effects and shared pathogenic processes. These findings highlight the potential to develop targeted interventions to prevent and treat the co-occurrence of respiratory and neuropsychiatric disorders.

Comorbidity↗