Background: Obstructive Sleep Apnea (OSA) is a highly prevalent and underdiagnosed sleep disorder. Recent studies suggest that OSA might disrupt the biological clock, potentially causing or worsening OSA-associated comorbidities. However, the effect of OSA treatment on clock disruption is not fully understood. Methods: The impact of OSA and short-(four months) and long-term (two years) OSA treatment, with Continuous Positive Airway Pressure (CPAP), on the biological clock was investigated at four time points within 24 h, in OSA patients relative to controls subjects (no OSA) of the same sex and age group, in a case-control study. Plasma melatonin and cortisol, body temperature and the expression levels and rhythmicity of eleven clock genes in peripheral blood mononuclear cells (PBMCs) were assessed. Additional computational tools were used for a detailed data analysis. Findings: OSA impacts on clock outputs and on the expression of several clock genes in PBMCs. Neither shortnor long-term treatment fully reverted OSA-induced alterations in the expression of clock genes. However, long-term treatment was able to re-establish levels of plasma melatonin and cortisol and body temperature. Machine learning methods could discriminate controls from untreated OSA patients. Following long-term treatment, the distinction between controls and patients disappeared, suggesting a closer similarity of the phenotypes. Interpretation: OSA alters biological clock-related characteristics that differentially respond to short-and long-term CPAP treatment. Long-term CPAP was more efficient in counteracting OSA impact on the clock, but the obtained results suggest that it is not fully effective. A better understanding of the impact of OSA and OSA treatment on the clock may open new avenues to OSA diagnosis, monitoring and treatment.
Throughout the course of life, there are age-related changes in sleep. Despite these normal changes, there is a high percentage of older adults that report sleep dissatisfaction with a high pervasiveness of chronic insomnia, the most common sleep disorder worldwide, with its prevalence being expected to continuously increase due to the growing rates of aging and obesity. This can have different adverse health outcomes, especially by promoting both physical and cognitive decline, which ultimately may aggravate frailty in older adults. Moreover, age-related frailty and sleep dysfunction may have a common mechanism related to the hallmarks of cellular aging. Cellular aging was categorized into nine hallmarks, such as DNA damage, telomere attrition and epigenetic changes. In the context of geriatric and chronic insomnia research, this review aims at discussing the current evidence from both animal models and human cohorts addressing the link between chronic insomnia, the hallmarks of aging and their impact on frailty. Moreover, the most recent research about the putative effect of insomnia therapeutic approaches on hallmarks of aging will be also highlighted.
Background: Obstructive Sleep Apnea (OSA) is a highly prevalent and underdiagnosed sleep disorder. Recent studies suggest that OSA might disrupt the biological clock, potentially causing or worsening OSA-associated comorbidities. However, the effect of OSA treatment on clock disruption is not fully understood. Methods: The impact of OSA and short-(four months) and long-term (two years) OSA treatment, with Continuous Positive Airway Pressure (CPAP), on the biological clock was investigated at four time points within 24 h, in OSA patients relative to controls subjects (no OSA) of the same sex and age group, in a case-control study. Plasma melatonin and cortisol, body temperature and the expression levels and rhythmicity of eleven clock genes in peripheral blood mononuclear cells (PBMCs) were assessed. Additional computational tools were used for a detailed data analysis. Findings: OSA impacts on clock outputs and on the expression of several clock genes in PBMCs. Neither shortnor long-term treatment fully reverted OSA-induced alterations in the expression of clock genes. However, long-term treatment was able to re-establish levels of plasma melatonin and cortisol and body temperature. Machine learning methods could discriminate controls from untreated OSA patients. Following long-term treatment, the distinction between controls and patients disappeared, suggesting a closer similarity of the phenotypes. Interpretation: OSA alters biological clock-related characteristics that differentially respond to short-and long-term CPAP treatment. Long-term CPAP was more efficient in counteracting OSA impact on the clock, but the obtained results suggest that it is not fully effective. A better understanding of the impact of OSA and OSA treatment on the clock may open new avenues to OSA diagnosis, monitoring and treatment.
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