GeroScience最新文献

{"title":"Chronic alcohol consumption accelerates cardiovascular aging and decreases cardiovascular reserve capacity","authors":"Partha Mukhopadhyay, Burhan Yokus, Bruno Paes-Leme, Sándor Bátkai, Zoltán Ungvári, György Haskó, Pal Pacher","doi":"10.1007/s11357-025-01613-w","DOIUrl":"https://doi.org/10.1007/s11357-025-01613-w","url":null,"abstract":"<p>The pathology of cardiovascular aging is complex, involving mitochondrial dysfunction, oxidative and nitrative stress, oxidative DNA injury, impaired lipid metabolism, cell death, senescence, and chronic inflammation. These processes lead to remodeling and structural changes in the cardiovascular system, resulting in a progressive decline in cardiovascular reserve capacity and health, and an increased risk of diseases and mortality. Excessive alcohol consumption exacerbates these risks by promoting hypertension, stroke, arrhythmias, coronary artery disease, cardiomyopathy, and sudden cardiac death, yet the effects of chronic alcohol consumption on cardiovascular aging remain unclear. Herein, we explored the impact of a 6-month 5% Lieber-DeCarli alcohol diet in young (3 months old) and aging (24–26 months old) Fisher F344BNF1 rats. We assessed detailed hemodynamics, mitochondrial function, oxidative/nitrative stress, lipid metabolism, inflammation, cell death, senescence, and myocardial fibrosis using the pressure–volume system, isolated vascular rings, and various histological, biochemical, and molecular biology methods. Alcohol consumption in both young and aging rats impaired mitochondrial function, disrupted cholesterol and triglyceride metabolism, and increased oxidative/nitrative stress, inflammation, cell death, and senescence, leading to a decline in systolic contractile function. In aging rats, alcohol further exacerbated diastolic dysfunction and myocardial fibrosis. Alcohol also increased oxidative/nitrative stress, apoptosis, and senescence in the vasculature, contributing to endothelial dysfunction and increased total peripheral resistance. Additionally, alcohol exacerbated the aging-related ventriculo-arterial uncoupling and diminished cardiac efficiency, further reducing cardiovascular reserve capacity. In conclusion, chronic alcohol consumption promotes cardiovascular aging and further diminishes the already impaired cardiac and vascular reserve capacity associated with aging.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"34 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143661370","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Age-related alterations of angiogenesis, inflammation and bone microarchitecture during fracture healing in mice","authors":"Maximilian M. Menger, Ruben Manuschewski, Sandra Hans, Benedikt J. Braun, Moses K. D. El Kayali, Sabrina Ehnert, Emmanuel Ampofo, Selina Wrublewsky, Michael D. Menger, Tina Histing, Matthias W. Laschke","doi":"10.1007/s11357-025-01584-y","DOIUrl":"https://doi.org/10.1007/s11357-025-01584-y","url":null,"abstract":"<p>The surgical treatment of geriatric patients represents a major challenge in traumatology. It is well known that aging affects fracture healing. However, the exact pathophysiology of age-related changes in angiogenesis, inflammation and bone remodeling remains still elusive. Therefore, we herein studied the differences of femoral fracture healing in young adult (3–4 months) and aged (16–18 months) CD-1 mice by using a stable closed femoral fracture model with intramedullary screw fixation. The callus tissue was analyzed by means of X-ray, micro-computed tomography (µCT), histology and immunohistochemistry. We found a deteriorated trabecular architecture and a reduced bone formation within the callus tissue of aged mice. Moreover, aged animals showed an increased number of tartrate-resistant acid phosphatase (TRAP)-positive osteoclasts at an early healing time point, whereas the fraction of mature α-smooth muscle actin (SMA)-positive microvessels was significantly reduced. Furthermore, the numbers of macrophages and granulocytes were higher in the callus tissue of aged animals at the end of the healing process. Taken together, these results demonstrate a delayed femoral fracture healing in aged CD-1 mice. This is most likely caused by an early overshooting osteoclast response, a decelerated maturation of the callus microvasculature and a late increased recruitment of pro-inflammatory cells. Targeting these alterations may contribute to the development of novel treatment approaches for the stimulation of bone regeneration in geriatric patients.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"92 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143661364","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effect of acipimox on skeletal muscle biochemistry, structure and function in older people with probable sarcopenia: an experimental medicine study","authors":"Claire McDonald, Craig Alderson, Matthew G. Birkbeck, Silvia Del Din, Gráinne S. Gorman, Kieren G. Hollingsworth, Cameron Kirk, Clare Massarella, Lynn Rochester, Helen A. L. Tuppen, Charlotte Warren, Avan A. Sayer, Miles D. Witham","doi":"10.1007/s11357-025-01606-9","DOIUrl":"https://doi.org/10.1007/s11357-025-01606-9","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Background</h3><p>Skeletal muscle nicotinamide adenine dinucleotide (NAD) concentrations are low in people with sarcopenia. Increasing NAD concentrations may offer a novel therapy. This study tested if acipimox (a NAD precursor) improves skeletal muscle NAD concentration and function in people with probable sarcopenia. Participants aged 65 and over with low walk speed (&lt; 0.8 m/s) and low muscle strength (by 2019 European Working Group criteria) were recruited to this before and after, proof-of-concept study. Participants received acipimox 250 mg orally (twice or thrice daily according to creatinine clearance) + aspirin 75 mg daily (to prevent facial flushing) for 4 weeks. Muscle biopsy of the vastus lateralis, ³¹P magnetic resonance spectroscopy and a 7-digital mobility assessment were performed before starting acipimox and after 3 weeks of treatment. The primary outcome was change in skeletal muscle NAD concentration. Secondary outcomes included change in phosphocreatine recovery rate and measures of physical performance. Eleven participants (8 women), mean age 78.9 years (SD 4.3), were recruited. Mean walk speed at baseline was 0.69 m/s (SD 0.07). All completed baseline and follow-up visits. Median medication adherence was 95% (range 91–104%). There was no statistically significant difference in the primary outcome of change in NAD concentrations in skeletal muscle between baseline and follow-up [median difference: − 0.003 umol/g (IQR − 0.058 to 0.210); <i>P</i> = 0.26] or secondary outcomes. Nineteen none-serious adverse events were reported. Although the study protocol was feasible and well tolerated, acipimox did not improve skeletal muscle NAD concentration, biochemical markers or physical function in people with probable sarcopenia. ClinicalTrials.gov Identifier: ISRCTN (ISRCTN87404878).</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"33 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143640842","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"An incidental finding during a brain plasticity study: substantial telomere length shortening after COVID-19 lockdown in the older population","authors":"Kirsten Jahn, Shambhabi Chatterjee, Christopher Sinke, Jonas Janik Ralf Koberschinski, Kristin Jünemann, Clara Eline James, Florian Worschech, Damien Marie, Eckart Altenmüller, Christian Bär, Tillmann Horst Christoph Krüger","doi":"10.1007/s11357-025-01602-z","DOIUrl":"https://doi.org/10.1007/s11357-025-01602-z","url":null,"abstract":"<p>The detrimental effects of lockdowns have already been proven by numerous studies, mainly using psychometric measurements. Since telomere shortening is a driver of aging and aging-associated disorders, including cognitive decline, the telomere length in the older population has been investigated in the current study. Measurements were taken over a 6-month period just before and during the 6 months that included the first lockdown. The cohort of 55 persons aged 64 to 70 years was investigated in the context of a study focusing on neuroplasticity. Participants were recruited in Germany and Switzerland and characterized by psychometric measurements concerning neurocognition and neuroplasticity. Telomere lengths were measured by real-time PCR-based LTL measurement. We found an impressive and significant decline in telomere lengths in the period that included the lockdown (2.33 (± 0.1) at T1 vs. 1.35 (± 0.1) at T2), whereas it was stable in the phase before the lockdown in the same individuals (T0 was 2.25 (± 0.1 S.E.M.) vs. T1, 2.33 (± 0.1)). Correlation of the sudden decrease revealed no linkage to health issues or general physical activity but was in trend related to a decline in the WHOQOL-BREF Social Score referring to the social interaction of the study participants. Our data support, at a biological level, the results of clinical and psychosocial studies showing the detrimental effects of lockdowns.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"42 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143640841","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Insomnia accelerates the epigenetic clocks in older adults","authors":"Nadia Alejandra Rivero-Segura, Julian Daniel Rodriguez Cuartas, Paola Garcia-delaTorre, Sergio Sanchez-Garcia, Ricardo Ramirez-Aldana, Juan Carlos Gomez-Verjan","doi":"10.1007/s11357-025-01608-7","DOIUrl":"https://doi.org/10.1007/s11357-025-01608-7","url":null,"abstract":"<p>Insomnia is a common sleep disorder characterized mainly by poor sleep quality and insufficient sleep duration. It affects a significant proportion of the global population and is correlated with physical and mental consequences such as cognitive decline, anxiety, chronic fatigue, poor concentration, and memory impairment. Interestingly, it is also linked to ageing and age-related diseases (cardiovascular, metabolic, and neurodegenerative). On the other hand, as we age, DNA methylation patterns undergo significant changes. These have been used to develop the so-called epigenetic clocks that estimate the biological age linked to the environment and the risk of diseases. Few studies have evaluated the association between insomnia and epigenetic clocks, providing insight into the role of insomnia in ageing acceleration. Therefore, in the present study, we carried out an epigenetic analysis by using Illumina EPICv.2 array on 63 older adults (&gt; 60 years old, <i>n</i> = 33 with insomnia vs. <i>n</i> = 30 control) to evaluate the relation between insomnia and epigenetic ages (HorvathAGE, HannumAGE, PhenoAGE, SkinBloodClock, GrimAGE, DunedinPACE, DNAmTL). As a result, we found an increased acceleration and correlation between GrimAGE and SkinBloodClock and a significant reduction in the DNAmTL in individuals with insomnia. An EWAS analysis showed a global pattern of hypomethylation and an enrichment of several proteostasis and oxidative pathways. In conclusion, our results suggest that insomnia increases GrimAGE and SkinBloodClock acceleration and may be participating in telomere shortening. Additionally, changes in DNA methylation patterns induced by insomnia impact proteostasis and oxidative stress.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"69 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143640849","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Sex differences in cognitive performance persist into your 80s","authors":"Ross Julian, Stephanie Fröhlich, Katrin Müller, Melanie Dammhahn, Claudia Voelcker-Rehage","doi":"10.1007/s11357-025-01585-x","DOIUrl":"https://doi.org/10.1007/s11357-025-01585-x","url":null,"abstract":"<h3 data-test=\"abstract-sub-heading\">Background</h3><p>Sex differences in cognitive performance have been extensively documented. Understanding the underlying factors contributing to sex differences in older adults is imperative to promote healthy cognitive aging. Sex hormones, estrogens, and testosterone have been suggested to be associated with cognition. Nevertheless, there is a scarcity of studies investigating the sex difference in cognitive performance and the contribution of gonadal hormones in older adults. Hence, the current study aimed to investigate sex differences in cognitive performance and elucidate the association between gonadal hormones and cognitive performance in 80+ -year-olds.</p><h3 data-test=\"abstract-sub-heading\">Methods</h3><p>Using confirmatory factor analysis in a sample of 131 older adults (aged 80 to 92 years), 17 cognitive performance measures were divided into two cognitive components: executive functioning and memory. Subsequently, mediation analyses were conducted to determine the direct effect of sex and the indirect effect mediated by gonadal hormones on executive functioning and memory.</p><h3 data-test=\"abstract-sub-heading\">Results</h3><p>Females outperformed males in executive functioning and memory. However, gonadal hormones did not mediate the sex effect on cognitive performance. Estrogen levels significantly predicted executive functioning but not memory. Testosterone levels did neither predict executive functioning nor memory.</p><h3 data-test=\"abstract-sub-heading\">Conclusion</h3><p>Our study confirms enduring sex differences in memory and executive function, even among individuals aged 80 and above. Current gonadal hormone levels do not mediate these differences. While estrogen may predict executive function, its influence does not explain the sex differences. These findings underscore the complex nature of cognitive disparities between sexes in older age, warranting further investigation into underlying mechanisms.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"39 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143635160","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Frailty incidence by diabetes treatment regimens in older adults with diabetes mellitus in the ASPirin in Reducing Events in the Elderly Study","authors":"Sara E. Espinoza, Jonathan C. Broder, Rory Wolfe, Michael E. Ernst, Raj C. Shah, Suzanne G. Orchard, Robyn L. Woods, Joanne Ryan, Anne Murray","doi":"10.1007/s11357-025-01598-6","DOIUrl":"https://doi.org/10.1007/s11357-025-01598-6","url":null,"abstract":"<p>Diabetes mellitus is a major risk factor for frailty in older adults, and studies suggest that frailty risk may differ by diabetes treatment regimen. To investigate the association between diabetes medication use and frailty, we conducted an observational cohort analysis of older adults with diabetes enrolled in the ASPirin in Reducing Events in the Elderly (ASPREE) study. Diabetes at baseline (<i>N</i> = 2045) was defined as self-reported diabetes, fasting blood glucose levels &gt; 125 mg/dL, or use of diabetes medication. Diabetes medication exposure at baseline was categorized as use of metformin only (monotherapy) (<i>N</i> = 545), metformin combined with other diabetes medications (<i>N</i> = 420), other diabetes medications only (<i>N</i> = 200), or no diabetes medications (<i>N</i> = 880). Frailty was defined using a modified Fried frailty phenotype (presence of ≥ 3 of 5 criteria) and a deficit accumulation frailty index (FI, score &gt; 0.21/1.00). Mixed effects ordinal logistic regression models revealed the odds of frailty at baseline were highest for the other diabetes medications only group, but this difference remained consistent over follow-up. After adjustment for covariates, including baseline pre-frailty, no differences in the rates of Fried or FI frailty were observed among the diabetes medication exposure groups. These findings suggest that diabetes medication exposure in older adults with diabetes does not directly impact frailty risk.</p><h3 data-test=\"abstract-sub-heading\">Graphical abstract</h3>\u0000","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"24 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143640840","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Machine vision-based frailty assessment for genetically diverse mice","authors":"Gautam S. Sabnis, Gary A. Churchill, Vivek Kumar","doi":"10.1007/s11357-025-01583-z","DOIUrl":"https://doi.org/10.1007/s11357-025-01583-z","url":null,"abstract":"<p>Frailty indexes (FIs) capture health status in humans and model organisms. To accelerate our understanding of biological aging and carry out scalable interventional studies, high-throughput approaches are necessary. We previously introduced a machine vision-based visual frailty index (vFI) that uses mouse behavior in the open field to assess frailty using C57BL/6J (B6J) data. Aging trajectories are highly genetic and are frequently modeled in genetically diverse animals. In order to extend the vFI to genetically diverse mouse populations, we collect frailty and behavior data on a large cohort of aged Diversity Outbred (DO) mice. Combined with previous data, this represents one of the largest video-based aging behavior datasets to date. Using these data, we build accurate predictive models of frailty, chronological age, and even the proportion of life lived. The extension of automated and objective frailty assessment tools to genetically diverse mice will enable better modeling of aging mechanisms and enable high-throughput interventional aging studies.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"5 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143635152","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Assessing the gut microbiota composition in older adults: connections to physical activity and healthy ageing","authors":"Catarina Ramos, Daniele Magistro, Gemma E. Walton, Anya Whitham, Nicola Camp, Carlos Poveda, Glenn R. Gibson, John Hough, Will Kinnear, Kirsty Hunter","doi":"10.1007/s11357-025-01605-w","DOIUrl":"https://doi.org/10.1007/s11357-025-01605-w","url":null,"abstract":"<p>The composition and functionality of the gut microbiota (GM) changes throughout the life course. As we move into older age, it starts to shift towards a less healthy one, which may lead to an imbalance in the GM community. Strategies that can reverse age-related dysbiosis are an important part of healthy aging. Little is known about the GM composition of older adults with different physical activity (PA) levels and whether it might contribute to healthy ageing. The aim of this study was to compare the GM composition of older adults with different PA levels and assess if it is associated with healthy ageing. 101 participants aged between 65–85 years undertook anthropometric measures, a 6-min walking test, wore an accelerometer for 7 days and provided a faecal sample. Faecal GM composition was analysed using 16S rRNA sequencing. We found that those who fulfilled the WHO/UK PA recommendations had higher relative abundance of several health-related bacteria such as <i>Lactobacillus, F. prausnitzii</i> and <i>Roseburia intestinalis</i> and lower abundance of disease-associated bacteria such as <i>D.piger</i> or Enterobacterales when compared to those who did not reach PA recommendations. These findings suggest that PA might improve the GM composition and has the potential to, at least partially, revert age-associated dysbiosis and promote healthy ageing.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"33 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143635096","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Epigenetic age acceleration and mortality risk prediction in US adults","authors":"Angelico Mendy, Tesfaye B. Mersha","doi":"10.1007/s11357-025-01604-x","DOIUrl":"https://doi.org/10.1007/s11357-025-01604-x","url":null,"abstract":"<p>Epigenetic clocks have emerged as novel measures of biological aging and potential predictors of mortality. We examined all-cause, cardiovascular, and cancer mortality prediction by epigenetic age acceleration (EAA) estimated using different epigenetic clocks. Among 2105 participants to the 1999–2002 National Health and Nutrition Examination Survey aged ≥ 50 years old and followed for mortality through 2019, we calculated EAAs from the residuals of nine epigenetic clocks regressed on chronological age. We assessed the association of EAAs and pace of aging with mortality adjusting for covariates. During 17.5 years of median follow-up, 998 deaths occurred, including 272 from cardiovascular disease and 209 from cancer. Overall mortality was most significantly predicted by Grim EAA (<i>P</i> &lt; 0.0001) followed by Hannum (<i>P</i> = 0.005), Pheno (<i>P</i> = 0.004), Horvath (<i>P</i> = 0.03), and Vidal-Bralo (<i>P</i> = 0.04) EAAs. Grim EAA predicted cardiovascular mortality (<i>P</i> &lt; 0.0001), whereas Hannum (<i>P</i> = 0.006), Horvath (<i>P</i> = 0.009), and Grim (<i>P</i> = 0.01) EAAs predicted cancer mortality. Overall mortality prediction differed by race/ethnicity between non-Hispanic White and White participants for Horvath (<i>P</i>_interaction = 0.048), Hannum (<i>P</i>_interaction = 0.01), and Grim (<i>P</i>_interaction = 0.04) EAAs. Hannum prediction of cancer mortality also differed between the two races/ethnicities (<i>P</i>_interaction = 0.007). Despite being predictive in non-Hispanic White participants, Horvath (<i>P</i> = 0.75), Hannum (<i>P</i> = 0.84), and Grim (<i>P</i> = 0.10) EAAs failed to predict overall mortality in Hispanic participants, and Hannum EAA was not associated with cancer mortality in Hispanic participants (<i>P</i> = 0.18). In a US representative sample, Horvath, Hannum, SkinBlood, Pheno, Vidal-Bralo, and Grim EAAs as well as pace of aging predict mortality. Howbeit, Horvath, Hannum, and Grim EAAs were less predictive in Hispanic participants.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"19 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2025-03-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143635159","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}