The escalating social and economic burden of an aging world population has placed aging research at center stage. The hallmarks of aging comprise diverse molecular mechanisms and cellular systems that are interrelated and act in concert to drive the aging process. Here, through the lens of telomere biology, we examine how telomere dysfunction may amplify or drive molecular biological processes underlying each hallmark of aging and contribute to development of age-related diseases such as neurodegeneration and cancer. The intimate link of telomeres to aging hallmarks informs preventive and therapeutic interventions designed to attenuate aging itself and reduce the incidence of age-associated diseases.
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http://dx.doi.org/10.1016/j.cell.2020.12.028 | DOI Listing |
Ecotoxicol Environ Saf
January 2025
Chinese Medicine Guangdong Laboratory, Hengqin 519031, China; State Key Laboratory of Traditional Chinese Medicine Syndrome, Guangzhou University of Chinese Medicine, Guangzhou 510006, China. Electronic address:
Aging populations are susceptible to climate change due to physiological factors and comorbidities. Most relevant studies reported the effect of temperature on cardiovascular disease (CVD)-related mortality in aging populations. However, the combined effects of temperature and humidity on CVD-related mortality remain unclear.
View Article and Find Full Text PDFNeurology
February 2025
Department of Laboratory Medicine and Pathology, Mayo Clinic, Rochester, MN.
Background And Objectives: Chronic kidney disease (CKD) is known to be associated with increased plasma phosphorylated tau217 (p-tau217) concentrations, potentially confounding the utility of plasma p-tau217 measurements as a marker of amyloid pathology in individuals with suspected Alzheimer disease (AD). In this study, we quantitatively investigate the relationship of plasma p-tau217 concentrations vs estimated glomerular filtration rate (eGFR) in individuals with CKD with and without amyloid pathology.
Methods: This was a retrospective examination of data from 2 observational cohorts from either the Mayo Clinic Study of Aging or the Alzheimer's Disease Research Center cohorts.
Neurology
February 2025
Departments of Child Neurology and General Practice, University of Turku and Turku University Hospital, Finland.
Background And Objectives: Previous research has demonstrated increased brain amyloid plaque load in individuals with childhood-onset epilepsy in late middle age. However, the trajectory of this process is not yet known. The aim of this study was to determine whether individuals with a history of childhood-onset epilepsy show progressive brain aging in amyloid accumulation in late adulthood (Turku Adult Childhood-Onset Epilepsy study, TACOE).
View Article and Find Full Text PDFPLoS One
January 2025
Research Department of Primary Care & Population Health, Centre for Ageing Population Studies, University College London, London, United Kingdom.
Introduction: Evidence suggests that social prescribing might have a positive impact on identity, control, creativity and quality of life in people with dementia. While evidence on the benefits of social prescribing is accumulating, there is a sparsity of research on the experiences of social prescribers. This study aims to identify the challenges that social prescribers face when supporting people with dementia and their families and strategies to address these.
View Article and Find Full Text PDFJ Neurochem
January 2025
Department of Pathology, University of Alabama at Birmingham, Birmingham, Alabama, USA.
Enhancing protein O-GlcNAcylation by pharmacological inhibition of the enzyme O-GlcNAcase (OGA) has been considered as a strategy to decrease tau and amyloid-beta phosphorylation, aggregation, and pathology in Alzheimer's disease (AD). There is still more to be learned about the impact of enhancing global protein O-GlcNAcylation, which is important for understanding the potential of using OGA inhibition to treat neurodegenerative diseases. In this study, we investigated the acute effect of pharmacologically increasing O-GlcNAc levels, using the OGA inhibitor Thiamet G (TG), in normal mouse brains.
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