Stress-induced biological aging: A review and guide for research priorities DOI Creative Commons

Lilian R. Polsky,

Kelly E. Rentscher, Judith Carroll

et al.

Brain Behavior and Immunity, Journal Year: 2022, Volume and Issue: 104, P. 97 - 109

Published: June 1, 2022

Exposure to chronic adverse conditions, and the resultant activation of neurobiological response cascade, has been associated with an increased risk early onset age-related disease and, recently, older biological age. This body research led hypothesis that exposure stressful life experiences, when occurring repeatedly or over a prolonged period, may accelerate rate at which ages. The mechanisms through psychosocial stress influences distinct aging pathways alter rates likely involve multiple layers in physiological-molecular network. In this review, we integrate using animal, human, vitro models begin delineate impact aging, as well neuroendocrine mediators (i.e., norepinephrine, epinephrine, glucocorticoids) drive these effects. Findings highlight key connections between namely cellular metabolic activity, DNA damage, telomere length, senescence, inflammatory patterns. We conclude guiding framework conceptual model outlines most promising by conditions could point missing gaps knowledge where future best answer pressing questions.

Language: Английский

Epigenetic-based age acceleration in a representative sample of older Americans: Associations with aging-related morbidity and mortality DOI Creative Commons
Jessica D. Faul, Jung Ki Kim, Morgan E. Levine

et al.

Proceedings of the National Academy of Sciences, Journal Year: 2023, Volume and Issue: 120(9)

Published: Feb. 21, 2023

Biomarkers developed from DNA methylation (DNAm) data are of growing interest as predictors health outcomes and mortality in older populations. However, it is unknown how epigenetic aging fits within the context known socioeconomic behavioral associations with aging-related a large, population-based, diverse sample. This study uses representative, panel US adults to examine relationship between DNAm-based age acceleration measures prediction cross-sectional longitudinal mortality. We whether recent improvements these scores, using principal component (PC)-based designed remove some technical noise unreliability measurement, improve predictive capability measures. also well perform against well-known such demographics, SES, behaviors. In our sample, calculated “second third generation clocks,” PhenoAge, GrimAge, DunedinPACE, consistently significant predictor including cognitive dysfunction, functional limitations chronic conditions assessed 2 y after DNAm 4-y PC-based do not significantly change or compared earlier versions While usefulness later life quite clear, other factors mental health, behaviors remain equally, if more robust, outcomes.

Language: Английский

Citations

103
Cell-type-specific aging clocks to quantify aging and rejuvenation in neurogenic regions of the brain DOI Creative Commons

Matthew T. Buckley,

Eric Sun, Benson M. George

et al.

Nature Aging, Journal Year: 2022, Volume and Issue: 3(1), P. 121 - 137

Published: Dec. 19, 2022

Abstract The diversity of cell types is a challenge for quantifying aging and its reversal. Here we develop ‘aging clocks’ based on single-cell transcriptomics to characterize cell-type-specific rejuvenation. We generated transcriptomes from the subventricular zone neurogenic region 28 mice, tiling ages young old. trained single-cell-based regression models predict chronological age biological (neural stem proliferation capacity). These clocks are generalizable independent cohorts other regions brains, species. To determine if these could quantify transcriptomic rejuvenation, datasets two interventions—heterochronic parabiosis exercise. Aging revealed that heterochronic exercise reverse in regions, but different ways. This study represents first development high-resolution data demonstrates their application

Language: Английский

Citations

98
Association of Pace of Aging Measured by Blood-Based DNA Methylation With Age-Related Cognitive Impairment and Dementia DOI Creative Commons
Karen Sugden, Avshalom Caspi, Maxwell L. Elliott

et al.

Neurology, Journal Year: 2022, Volume and Issue: 99(13)

Published: July 6, 2022

Background and Objectives

DNA methylation algorithms are increasingly used to estimate biological aging; however, how these proposed measures of whole-organism aging relate in the brain is not known. We data from Alzheimer9s Disease Neuroimaging Initiative (ADNI) Framingham Heart Study (FHS) Offspring Cohort test association between blood-based cognitive impairment dementia older adults.

Methods

tested 3 "generations" age (first generation: Horvath Hannum clocks; second PhenoAge GrimAge; third DunedinPACE, Dunedin Pace Aging Calculated Epigenome) against following ADNI: clinical diagnosis mild impairment, scores on Alzheimer disease (AD) / related dementias (ADRD) screening tests (Alzheimer9s Assessment Scale, Mini-Mental State Examination, Montreal Cognitive Assessment), (Rey Auditory Verbal Learning Test, Logical Memory test, Trail Making Test). In an independent replication FHS Cohort, we further longitudinal risk developing dementia.

Results

ADNI (N = 649 individuals), first-generation (Horvath clocks) second-generation (PhenoAge GrimAge) were consistently associated with By contrast, a third-generation measure aging, was (beta [95% CI] 0.28 [0.08–0.47]), poorer disease/ADRD [Robust SE] −0.10 [0.04] 0.08[0.04]), −0.12 0.10 [0.03]). The faster pace as measured by confirmed analysis 2,264 individuals, hazard ratio 1.27 [1.07–1.49]).

Discussion

Third-generation could prove valuable for measuring differences individuals rate at which they their decline, evaluating interventions slow aging.

Language: Английский

Citations

84
Role of sleep quality in the acceleration of biological aging and its potential for preventive interaction on air pollution insults: Findings from the UK Biobank cohort DOI Creative Commons
Xu Gao, Ninghao Huang, Xinbiao Guo

et al.

Aging Cell, Journal Year: 2022, Volume and Issue: 21(5)

Published: April 14, 2022

Sleep has been associated with aging and relevant health outcomes, but the causal relationship remains inconclusive. In this study, we investigated associations of sleep behaviors biological ages (BAs) among 363,886 middle elderly adults from UK Biobank. index (0 [worst]-6 [best]) each participant was retrieved following six behaviors: snoring, chronotype, daytime sleepiness, duration, insomnia, difficulties in getting up. Two BAs, KDM-biological age PhenoAge, were estimated by corresponding algorithms based on clinical traits, their residual discrepancies chronological defined as accelerations (AAs). We first observed negative between two AAs, demonstrated that change AAs could be consequence quality using Mendelian randomization genetic risk scores BAs. Particularly, a one-unit increase 0.104- 0.119-year decreases AA PhenoAge acceleration, respectively. Air pollution is another key driver aging. further significant independent joint effects air (PM2.5 NO2 ) AAs. also showed modifying effect elevated PM2.5 levels accelerated For instance, an interquartile range level 0.009-, 0.044-, 0.074-year acceleration people high (5-6), medium (3-4), low (0-2) index, Our findings elucidate better lessen resulting pollution.

Language: Английский

Citations

76
Stress-induced biological aging: A review and guide for research priorities DOI Creative Commons

Lilian R. Polsky,

Kelly E. Rentscher, Judith Carroll

et al.

Brain Behavior and Immunity, Journal Year: 2022, Volume and Issue: 104, P. 97 - 109

Published: June 1, 2022

Exposure to chronic adverse conditions, and the resultant activation of neurobiological response cascade, has been associated with an increased risk early onset age-related disease and, recently, older biological age. This body research led hypothesis that exposure stressful life experiences, when occurring repeatedly or over a prolonged period, may accelerate rate at which ages. The mechanisms through psychosocial stress influences distinct aging pathways alter rates likely involve multiple layers in physiological-molecular network. In this review, we integrate using animal, human, vitro models begin delineate impact aging, as well neuroendocrine mediators (i.e., norepinephrine, epinephrine, glucocorticoids) drive these effects. Findings highlight key connections between namely cellular metabolic activity, DNA damage, telomere length, senescence, inflammatory patterns. We conclude guiding framework conceptual model outlines most promising by conditions could point missing gaps knowledge where future best answer pressing questions.

Language: Английский

Citations

73