Research into aging has grown substantially with the creation of molecular biomarkers of biological age that can be used to determine age acceleration. Concurrently, nuclear magnetic resonance (NMR) assessment of biomarkers of inflammation and metabolism provides researchers with new ways to examine intermediate risk factors for chronic disease. We used data from a cardiac catheterization cohort to examine associations between biomarkers of cardiometabolic health and accelerated aging assessed using both gene expression (Transcriptomic Age) and DNA methylation (Hannum Age, GrimAge, Horvath Age, and Phenotypic Age). Linear regression models were used to associate accelerated aging with each outcome (cardiometabolic health biomarkers) while adjusting for chronological age, sex, race, and neighborhood socioeconomic status. Our study shows a robust association between GlycA and GrimAge (5.71, 95% CI = 4.36, 7.05, = 7.94 × 10), Hannum Age (1.81, 95% CI = 0.65, 2.98, = 2.30 × 10), and Phenotypic Age (2.88, 95% CI = 1.91, 3.87, = 1.21 × 10). We also saw inverse associations between apolipoprotein A-1 and aging biomarkers. These associations provide insight into the relationship between aging and cardiometabolic health that may be informative for vulnerable populations.
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http://dx.doi.org/10.18632/aging.205758 | DOI Listing |
Sci Rep
December 2024
Department of Medicinal Chemistry, University of Minnesota, Minneapolis, MN, 55455, USA.
Exposure to reactive oxygen species (ROS) can induce DNA-protein crosslinks (DPCs), unusually bulky DNA lesions that block replication and transcription and play a role in aging, cancer, cardiovascular disease, and neurodegenerative disorders. Repair of DPCs depends on the coordinated efforts of proteases and DNA repair enzymes to cleave the protein component of the lesion to smaller DNA-peptide crosslinks which can be processed by tyrosyl-DNA phosphodiesterases 1 and 2, nucleotide excision and homologous recombination repair pathways. DNA-dependent metalloprotease SPRTN plays a role in DPC repair, and SPRTN-deficient mice exhibit an accelerated aging phenotype and develop liver cancer early in life.
View Article and Find Full Text PDFJ Geriatr Oncol
December 2024
Institute for Physical Activity and Nutrition, Deakin University, Geelong, Australia; School of Exercise and Nutrition Sciences, Deakin University, Burwood, Victoria, Australia; Nutrition and Speech Pathology Department, Peter MacCallum Cancer Centre, Melbourne, Victoria 3000, Australia; Sir Peter MacCallum Department of Oncology, The University of Melbourne, Victoria 3010, Australia.
Introduction: Older patients with cancer (65 years and older) are a growing population with unique nutrition-and treatment-related issues that accelerate aging. Nutrition interventions attenuate nutritional decline, muscle loss, and risk of malnutrition and sarcopenia in patients with cancer, however the evidence for older patients with cancer is limited. The aim of this systematic review was to evaluate the efficacy of nutrition interventions on nutritional status, body weight/composition and clinical outcomes in older patients with cancer and to identify future research priority areas.
View Article and Find Full Text PDFFEMS Microbiol Lett
December 2024
Department of Biophysics, Yeditepe University School of Medicine, Yeditepe University, Istanbul, Turkey.
Chronological lifespan (CLS) in budding yeast Saccharomyces cerevisiae, which is defined as the time nondividing cells in saturation remain viable, has been utilized as a model to study post-mitotic aging in mammalian cells. CLS is closely related to entry into and maintenance of a quiescent state. Many rearrangements that direct the quiescent state enhance the ability of cells to endure several types of stress.
View Article and Find Full Text PDFBrain Behav Immun
December 2024
Department of Geriatrics, University Medical Center Goettingen, Robert-Koch-Str. 42, 37075 Goettingen, Germany; DZHK (German Center for Cardiovascular Research), Partner Site Göttingen, 37075 Göttingen, Germany. Electronic address:
Obesity, a pandemic, worldwide afflicts almost one billion people. Obesity and ageing share several pathological pathways leading to neurological disorders. However, due to a lack of suitable animal models, the long-term effects of obesity on age-related disorders- cognitive impairment and dementia have not yet been thoroughly investigated.
View Article and Find Full Text PDFBiogerontology
December 2024
Second Affiliated Hospital of Heilongjiang University of Chinese Medicine, Harbin, China.
Mitochondrial DNA encodes essential components of the respiratory chain complexes, serving as the foundation of mitochondrial respiratory function. Mutations in mtDNA primarily impair energy metabolism, exerting far-reaching effects on cellular physiology, particularly in the context of aging. The intrinsic vulnerability of mtDNA is increasingly recognized as a key driver in the initiation of aging and the progression of its related diseases.
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