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.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC9895045 | PMC |
| http://dx.doi.org/10.1007/s40520-022-02310-w | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Amyloid-associated hyperconnectivity drives tau spread across connected brain regions in Alzheimer's disease.
Sci Transl Med
January 2025
Institute for Stroke and Dementia Research (ISD), University Hospital, LMU Munich, 81377 Munich, Germany.
In Alzheimer's disease (AD), amyloid-β (Aβ) triggers the aggregation and spreading of tau pathology, which drives neurodegeneration and cognitive decline. However, the pathophysiological link between Aβ and tau remains unclear, which hinders therapeutic efforts to attenuate Aβ-related tau accumulation. Aβ has been found to trigger neuronal hyperactivity and hyperconnectivity, and preclinical research has shown that tau spreads across connected neurons in an activity-dependent manner.
View Article and Find Full Text PDFMineral Stress Drives Loss of Heterochromatin: An Early Harbinger of Vascular Inflammaging and Calcification.
Circ Res
January 2025
British Heart Foundation Centre for Research Excellence, School of Cardiovascular and Metabolic Medicine and Sciences, James Black Centre, King's College London, United Kingdom (C.Y.H., M.-Y.W., J.T., S.A., L.D., G.A., R.H., C.M.S.).
Background: Vascular calcification is a detrimental aging pathology markedly accelerated in patients with chronic kidney disease. Prelamin A is a biomarker of vascular smooth muscle cell aging that accelerates calcification however the mechanisms remain undefined.
Methods: Vascular smooth muscle cells were transduced with prelamin A using an adenoviral vector and epigenetic modifications were monitored using immunofluorescence and targeted polymerase chain reaction array.
Hallmarks of aging: middle-aging hypovascularity, tissue perfusion and nitric oxide perspective on healthspan.
Front Aging
January 2025
Molecular Medicine, NSW Health Pathology, John Hunter Hospital, Newcastle, NSW, Australia.
Aging is a complex process marked by various changes at both cellular and systemic levels, impacting the functioning and lifespan of organisms. Over time, researchers have pinpointed several significant hallmarks of aging that lead to the gradual deterioration of tissue function, regulation, and homeostasis associated with aging in humans. Despite this, the intricate interactions and cumulative effects of these hallmarks are still mostly uncharted territory.
View Article and Find Full Text PDFMitochondrial DNA variants and their impact on epigenetic and biological aging in young adulthood.
Transl Psychiatry
January 2025
Campbell Family Mental Health Research Institute, Centre for Addiction and Mental Health, Toronto, ON, Canada.
The pace of biological aging varies between people independently of chronological age and mitochondria dysfunction is a key hallmark of biological aging. We hypothesized that higher functional impact (FI) score of mitochondrial DNA (mtDNA) variants might contribute to premature aging and tested the relationships between a novel FI score of mtDNA variants and epigenetic and biological aging in young adulthood. A total of 81 participants from the European Longitudinal Study of Pregnancy and Childhood (ELSPAC) prenatal birth cohort had good quality genetic data as well as blood-based markers to estimate biological aging in the late 20.
View Article and Find Full Text PDFInsights and Interventions in Age-Associated Inflammation.
Curr Opin Genet Dev
January 2025
National Clinical Research Center for Geriatric Disorders, Aging Translational Medicine Center, International Center for Aging and Cancer, Xuanwu Hospital Capital Medical University, Beijing 100053, China; University of Chinese Academy of Sciences, Beijing, 100049, China; Aging Biomarker Consortium (ABC), Beijing 100101, China; Beijing Institute for Stem Cell and Regenerative Medicine, Beijing, 100101, China; Key Laboratory of Organ Regeneration and Reconstruction, State Key Laboratory of Membrane Biology, Institute of Zoology, Chinese Academy of Sciences, Beijing, 100101, China. Electronic address:
Aging is a systemic, complex, and heterogeneous process characterized by a progressive decline in physiological functions, rendering it a major risk factor for various chronic diseases. Chronic inflammation has emerged as both a hallmark and a driver in this complicated process. This persistent inflammatory state arises from a spectrum of stimuli, ranging from external pathogens to internal cellular remnants, to metabolic dysregulation, and to chronic stress.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!