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At least 19 recordsLinked to original sources
PubMedDate not supplied

Premature aging in male alcoholics: "accelerated aging" or "increased vulnerability"?

This study involved an evaluation of two versions of the "premature aging" theory of chronic alcoholism: the accelerated aging and increased vulnerability versions. The major dependent measures used were the tests included in Reitan's brain age quotient (BAQ), a series of neuropsychological tests known to be sensitive to the effects of alcoholism and aging. Subjects were 40 chronic alcoholic inpatients and 40 matched controls, divided into age groups by decade, ranging from the 30s to the 60s. It was proposed that an interaction between age and presence or absence of alcoholism, with BAQ test differences between alcoholics and controls widening as age increases, would support the increased vulnerability version, while the absence of such an interaction would support the accelerated aging version. The results clearly favored the accelerated aging version, with marked BAQ test differences between alcoholics and controls appearing even in the 30-year-old groups. It was concluded that chronic alcoholics tend to perform at levels found for nonalcoholics 10 years their senior, but the discrepancy between alcoholics and nonalcoholics does not increase with age.

Adult↗
PubMed1992

Acute wound repair in an aged animal: a model for accelerated aging of the microvasculature?

This study of wound repair in the aged rat is based on increased carbohydrate content of various proteins which occurs with aging and is readily seen in the microvasculature (MV). We have used the periodic acid-Schiff (PAS) reaction to identify histochemically the carbohydrate moiety of the glycoproteins found in these blood vessels. In the young rat, as in other young vertebrates, elements of the MV are PAS negative and become increasingly PAS+ beyond the half life span. During acute wound repair in an old animal, the new capillaries and venules are PAS- 2 weeks after injury, moderately PAS+ at 4 weeks, and intensely PAS+ at 8 weeks. Arterioles are present and PAS+ at 6 weeks, and intensively positive at 8 weeks, comparable to vessels remote from the wound site. The MV in wound repair in a young animal remains PAS- throughout healing. Rapid aging of the microvasculature in wound repair in an old animal reproduces histochemically the aging which occurs progressively during the prior 24 months. These histochemical changes may result from successive enzymatic and nonenzymatic glycosylation of the various basement membrane proteins in the microvasculature in both normal aging and wound repair in the aged animal. The latter may serve as a model for study of accelerated aging.

Aging↗
PubMed1978

Accelerated aging due to enzymatic racemization.

Thermodynamic racemization may be a cause of aging. Racemases might accelerate the aging process. If enzymatic racemization does accelerate aging, then the use of chemical or immunological inhibitors of racemases might retard aging.

Aging↗
PubMed2026

Identifying biomarkers of accelerated ageing in cancer patients from routine clinical data.

INTRODUCTION: Cancer and ageing have a bidirectional relationship: age is the strongest risk factor for cancer, and cancer and treatments can accelerate ageing. Therefore, biological age can differ from chronological age; biomarkers are needed to stratify interventions to minimise accelerated ageing. METHODS: PhenoAge was calculated from routine blood test results of patients attending a Geriatric Oncology clinic. PhenoAgeAccel was the residual from a regression of PhenoAge against age. RESULTS: Data were available for 173 patients (62% male). Mean PhenoAge was higher than age (84.3 (12.6) vs 76.2 (7.24), p&#x202f;<&#x202f;0.001), though the two were correlated (r&#x202f;=&#x202f;0.579, p&#x202f;<&#x202f;0.001). Unlike age, PhenoAge and PhenoAgeAccel were associated with one-year mortality (PhenoAge OR=1.083, 95% CI: 1.038-1.136; PhenoAgeAccel OR=1.096, 95% CI: 1.047-1.155). PhenoAge correlated with Clinical Frailty Score and Timed Up and Go (CFS: Rs=0.31, p&#x202f;<&#x202f;0.001; TUG: Rs=0.25, p&#x202f;<&#x202f;0.005); there were no correlations with age. PhenoAgeAccel correlated with the number of CGA interventions made (Rs=0.17, p&#x202f;<&#x202f;0.05), unlike age and PhenoAge. Patients with diabetes mellitus had a higher PhenoAgeAccel compared to those without (3.40 vs -1.71, p&#x202f;=&#x202f;0.002). In patients receiving systemic anti-cancer treatment, patients with PhenoAgeAccel calculated pre-treatment had less age acceleration than those with PhenoAgeAccel calculated post-treatment, both overall (2.18 vs -2.87; p&#x202f;=&#x202f;0.048) and in matched samples (n&#x202f;=&#x202f;21, 7.76 vs -2.87, p&#x202f;<&#x202f;0.001). CONCLUSIONS: PhenoAgeAccel is a greater predictor of risk than chronological age in older people with cancer. This makes it a promising biomarker to stratify patients for holistic geriatric assessment, dose reductions, or future geroprotective measures which could be integrated within electronic healthcare record systems.

Humans↗
PubMed1990

Accelerated aging and male homosexuality: Australian evidence in a continuing debate.

The evidence of research looking at accelerated aging among gay men is contradictory. In this study the issue of accelerated aging is addressed by accounting for the duality of the gay man's lifestyle as he interacts in both the homosexual community and the larger society where heterosexuality is the presumed norm. The onset of middle and old age as self-perceived by gay men and as perceived by other gay men in the homosexual subculture is contrasted. The results indicate that existing contradictions and debates about gay men and accelerated aging are largely a function of their referent perceptual worlds.

Adaptation, Psychological↗
PubMed1985

Accelerated aging of the insect Drosophila melanogaster by gamma irradiations of pupae.

The purpose of this study was to induce accelerated aging in the fly Drosophila melanogaster (Diptera) using free radicals, and to distinguish aging from radiation syndrome. After irradiation of 12 to 24-hour-old pupae with does of 500-2500 rad, very similar fly emergence rates were observed in control and treated populations. The life span was shortened and dose-related in mixed populations and in both virgin and mated male and female populations. Males were more radiosensitive than females. In the 500-2500 rad dose range, all the populations tested were fertile after irradiation. Young treated as pupae and control adults both displayed similar mating ability and negative geotactic responses. Their response levels decreased with time, but the decline was faster and dose-related in the treated animals. This study demonstrates that irradiation of 12 to 24-hour-old pupae with doses of 500-2500 rad induces accelerated aging, without causing serious biological damage. For example, after an irradiation with 1750 rad, the "lethal time" (LT) 50 dropped by about 30%.

Aging↗
PubMed2026

Genetically Proxied Leukocyte Telomere Length and Epigenetic Age Acceleration in Relation to Healthspan: A Mendelian Randomization Study.

BACKGROUND: Leukocyte telomere length (LTL) and epigenetic age acceleration (EAA) are widely studied biomarkers of biological aging, but their potential roles in healthspan remain unclear. We evaluated whether genetically proxied LTL and EAA show evidence of potential effects on healthspan. METHODS: We conducted a two-sample Mendelian randomization study. Genetic instruments for LTL and four EAA biomarkers were obtained from published genome-wide association studies, including up to 472,174 individuals for LTL and approximately 35,000 individuals for each EAA biomarker. Summary statistics for healthspan, defined as age at first diagnosis of any of eight major chronic conditions or death, were derived from 300,447 unrelated European-ancestry participants in the UK Biobank. We used inverse-variance-weighted (IVW) models for the main analysis, with complementary MR estimators and sensitivity analyses to evaluate consistency, pleiotropy, instrument heterogeneity, and robustness. RESULTS: Genetically proxied longer LTL was associated with extended healthspan (IVW &#x3b2; = 0.106; 95% CI: 0.054-0.158; p = 6.9&#xa0;&#xd7;&#xa0;10-5). The association was robust across multiple sensitivity analyses. In contrast, the four genetically proxied EAA biomarkers did not show consistent MR evidence of an association with healthspan. CONCLUSIONS: These findings provide genetic evidence consistent with a potential role of LTL in healthspan, while providing little support for comparable associations involving the genetically proxied components of the evaluated EAA biomarkers. The findings do not exclude potential associations with environmentally or physiologically acquired EAA.

Mendelian randomization↗
PubMed1992

Progeria: a human-disease model of accelerated aging.

Progeria is a rare genetic disease with striking features that resemble accelerated aging. The inheritance pattern, paternal age effect, and lack of consanguinity argue that it is due to a sporadic dominant mutation. We have observed elevated levels of hyaluronic acid (HA) excretion in progeria patients. In several progeria patients we observed normal levels of growth hormone (GH) but very low levels of insulin-like growth factor I along with very high basal metabolic rates (BMRs). A trial of GH treatment was begun, which resulted in a marked increase in linear growth and a paradoxical drop in BMRs in these two patients. We hypothesize that the failure of patients with progeria to thrive may be due to a bioinactive form of GH and a lack of vasculogenesis caused by excess HA. An understanding of the progeria genetic mutation may define a key gene with a major effect on normal aging.

Basal Metabolism↗
PubMed2026

Epigenetic age acceleration is not strongly associated with cardiorespiratory fitness in heart failure: a pilot study.

BACKGROUND: In heart failure (HF), standard measures such as left ventricular ejection fraction and cardiopulmonary exercise testing incompletely capture interindividual differences in disease status or prognosis. DNA methylation (DNAm) epigenetic clocks, which estimate biological age and epigenetic age acceleration (EAA), may provide complementary insight into cardiorespiratory fitness and systemic aging in HF. RESEARCH DESIGN AND METHODS: We analyzed peripheral blood DNAm from fourteen patients enrolled in REDHART2, a clinical trial of interleukin-1 blockade following hospitalization for acute systolic HF. Genome-wide DNAm was assayed using Illumina EPIC arrays and several clocks were applied to these data. Associations between biological age or EAA and cardiorespiratory fitness measures, inflammatory markers, and clinical parameters were evaluated. RESULTS: All epigenetic clocks demonstrated moderate to strong correlations with chronological age. Biological age was consistently associated with measures of cardiorespiratory fitness, particularly oxygen consumption normalized to fat free mass (VO2_FFM). However, chronological age showed similar associations, and biological age did not significantly improve prediction of VO2 parameters beyond chronological age alone. EAA was not significantly associated with cardiorespiratory fitness for any clock. CONCLUSIONS: In this pilot study, neither biological age nor EAA provided significant predictive value beyond chronological age for cardiorespiratory fitness in patients with HF. CLINICAL TRIAL REGISTRATION NUMBER: NCT03797001.

DNA methylation↗
PubMed2026

Clonal haematopoiesis of indeterminate potential and epigenetic age acceleration: Systematic review and meta-analysis.

Clonal haematopoiesis of indeterminate potential (CHIP) represents somatic mutations in haematopoietic stem cells that drive clonal expansion. Epigenetic age acceleration (EAA), estimated from DNA methylation (DNAm) clocks, may capture age-related changes in haematopoiesis. This systematic review and meta-analysis was conducted to synthesise evidence on associations between CHIP and EAA and explore shared biological mechanisms that may underlie this relationship. Six databases were searched from January 1, 2011, to June 6, 2025, adhering to PRISMA 2020. Random-effects meta-analyses were performed. Five studies comprising 7483 individuals (ages 55-79, 67.1% female) assessing associations between CHIP and DNAm clocks were included. Across studies, CHIP individuals had higher EAA than no-CHIP individuals, and larger clones were associated with higher EAA. Meta-analysis of three cross-sectional studies (n&#x202f;=&#x202f;6946) showed that CHIP had higher EAA versus no-CHIP for Horvath1Age IEAA (mean difference, MD=2.84 years, 95% confidence interval, CI: 1.49-4.19), HannumAge EEAA (MD=2.31 years, 95% CI: 1.14-3.49), PhenoAge (MD=1.84 years, 95% CI: 0.96-2.71), and GrimAge (MD=1.20 years, 95% CI: 0.80-1.61). Both DNMT3A- and TET2-mutated CHIP were associated with higher EAA with TET2-mutated CHIP showing larger effect sizes and more consistent associations than DNMT3A-mutated CHIP across DNAm clocks tested. Higher EAA may also act as an effect modifier for morbidity and mortality in CHIP. Larger longitudinal studies are needed to verify a temporal relationship and determine whether EAA provides incremental prognostic value for morbidity and mortality in CHIP.

Humans↗
PubMedDate not supplied

Color stability of restorative resins under accelerated aging.

The color stability of seven commercial composite resins, an unfilled resin, and three glazes was studied under conditions of accelerated aging by reflection spectrophotometry and visually with Munsell color tabs. After aging for 900 hours, most of the resins had lower values of luminous reflectance and excitation purity and higher values of dominant wavelength and contrast ratio compared to values at baseline.

Acrylic Resins↗
PubMed1975

Apparent accelerated aging of human collagen in diabetes mellitus.

The chronologic ages of human subjects were determined experimentally by enzymatic digestion of tendon collagen samples. Determined age closely matched actual age for individuals dying with a variety of major diseases. Juvenile diabetics did not fit this pattern; their experimentally determined ages were significantly greater than their actual ages. This raises the possibility of relationships between diabetes mellitus, changes in connective tissue, and accelerated aging.

Adult↗
PubMed2020

Tissue specificity of senescent cell accumulation during physiologic and accelerated aging of mice.

Senescent cells accumulate with age in vertebrates and promote aging largely through their senescence-associated secretory phenotype (SASP). Many types of stress induce senescence, including genotoxic stress. ERCC1-XPF is a DNA repair endonuclease required for multiple DNA repair mechanisms that protect the nuclear genome. Humans or mice with reduced expression of this enzyme age rapidly due to increased levels of spontaneous, genotoxic stress. Here, we asked whether this corresponds to an increased level of senescent cells. p16Ink4a and p21Cip1 mRNA were increased ~15-fold in peripheral lymphocytes from 4- to 5-month-old Ercc1-/&#x2206; and 2.5-year-old wild-type (WT) mice, suggesting that these animals exhibit a similar biological age. p16Ink4a and p21Cip1 mRNA were elevated in 10 of 13 tissues analyzed from 4- to 5-month-old Ercc1-/&#x2206; mice, indicating where endogenous DNA damage drives senescence in vivo. Aged WT mice had similar increases of p16Ink4a and p21Cip1 mRNA in the same 10 tissues as the mutant mice. Senescence-associated &#x3b2;-galactosidase activity and p21Cip1 protein also were increased in tissues of the progeroid and aged mice, while Lamin B1 mRNA and protein levels were diminished. In Ercc1-/&#x394; mice with a p16Ink4a luciferase reporter, bioluminescence rose steadily with age, particularly in lung, thymus, and pancreas. These data illustrate where senescence occurs with natural and accelerated aging in mice and the relative extent of senescence among tissues. Interestingly, senescence was greater in male mice until the end of life. The similarities between Ercc1-/&#x2206; and aged WT&#xa0;mice support the conclusion that the DNA repair-deficient mice accurately model the&#xa0;age-related accumulation of senescent cells, albeit six-times faster.

Aging↗
PubMed1990

Does progeria provide the best model of accelerated ageing in humans?

Studies of the causes of ageing are often obscured by the complexity of this phenomenon, hindering investigations in this area. In particular, the variable characteristics of ageing complicate analysis at a molecular level. It is proposed that to gain insight into ageing, the problem must first be simplified by restricting studies to an aspect of the ageing processes. It is suggested that progeria, which presents a less complicated etiology and phenotype than other accelerated ageing diseases, allows research to focus on a regulation site involved in development and ageing.

Aging↗
PubMed1990

Accelerated ageing of metallic biomaterials: principle and results.

Electrochemical methods such as voltammetry and chronoamperometry are very useful in the study of biodegradation processes. Voltammetry gives qualitative information on the behaviour of a biomaterial in an electrolytic medium. Accelerated ageing of a metallic biomaterial can be obtained using chronoamperometry. Quantitative information on elements released in a solution is also obtained.

Biocompatible Materials↗