Pub Date : 2026-02-03DOI: 10.1007/s11357-026-02113-1
Imnameren Longkumer, Soohyeon Ko, Priyanka deSouza, Rohit Bhatia, Rockli Kim, S V Subramanian
Polluting cooking fuels are a major source of household air pollution and may reduce life satisfaction (LS). Yet, this relationship remains unexplored in India where polluting fuel use is still widespread. We utilized cross-sectional data from the Longitudinal Aging Study in India, a nationally representative study of individuals aged 45 years and above. Cooking fuel type was classified as households using clean fuels (CF) or non-CF. Based on kitchen type, non-CF was categorized into non-CF in separate kitchen, and non-CF without separate kitchen. We used multivariable regression to examine the association between polluting cooking fuels and LS and explored gender differences in this association. The analytical sample comprised 62,822 respondents (mean age 59.56 ± 10.52 years). The use of non-CF in separate and non-separate kitchen was 27.08% (n = 17,010) and 18.89% (n = 11,868), respectively. We observed that LS scores were highest among households using CF, followed by those using non-CF in separate kitchen, and lowest among households using non-CF without separate room for cooking. Additionally, in the fully adjusted model, a dose-response association with LS was observed corresponding to different levels of polluting cooking fuels (non-CF in separate kitchen: β = -0.51 [95% CI: -0.71, -0.31]; non-CF without separate kitchen: β = -1.42 [95% CI: -1.65, -1.19]). Multiple sensitivity analyses support the robustness of our findings. Gender was a significant effect modifier, with the interaction model revealing a stronger negative association between non-CF use and LS among women than among men. Our findings highlight the need for policies that promote an equitable clean fuel transition to enhance life satisfaction and well-being.
{"title":"Polluting cooking fuels and life satisfaction among middle-aged and older adults: a cross-sectional study from the Longitudinal Ageing Study in India.","authors":"Imnameren Longkumer, Soohyeon Ko, Priyanka deSouza, Rohit Bhatia, Rockli Kim, S V Subramanian","doi":"10.1007/s11357-026-02113-1","DOIUrl":"https://doi.org/10.1007/s11357-026-02113-1","url":null,"abstract":"<p><p>Polluting cooking fuels are a major source of household air pollution and may reduce life satisfaction (LS). Yet, this relationship remains unexplored in India where polluting fuel use is still widespread. We utilized cross-sectional data from the Longitudinal Aging Study in India, a nationally representative study of individuals aged 45 years and above. Cooking fuel type was classified as households using clean fuels (CF) or non-CF. Based on kitchen type, non-CF was categorized into non-CF in separate kitchen, and non-CF without separate kitchen. We used multivariable regression to examine the association between polluting cooking fuels and LS and explored gender differences in this association. The analytical sample comprised 62,822 respondents (mean age 59.56 ± 10.52 years). The use of non-CF in separate and non-separate kitchen was 27.08% (n = 17,010) and 18.89% (n = 11,868), respectively. We observed that LS scores were highest among households using CF, followed by those using non-CF in separate kitchen, and lowest among households using non-CF without separate room for cooking. Additionally, in the fully adjusted model, a dose-response association with LS was observed corresponding to different levels of polluting cooking fuels (non-CF in separate kitchen: β = -0.51 [95% CI: -0.71, -0.31]; non-CF without separate kitchen: β = -1.42 [95% CI: -1.65, -1.19]). Multiple sensitivity analyses support the robustness of our findings. Gender was a significant effect modifier, with the interaction model revealing a stronger negative association between non-CF use and LS among women than among men. Our findings highlight the need for policies that promote an equitable clean fuel transition to enhance life satisfaction and well-being.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":" ","pages":""},"PeriodicalIF":5.4,"publicationDate":"2026-02-03","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146112860","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}
Pub Date : 2026-01-31DOI: 10.1007/s11357-025-02087-6
Kyra Jennifer Waligora Mendez,Sang Kyu Lee,Casey Dagnall,Tsung-Po Lai,Hormuzd Katki,Stephen R Spellman,Valerie Stewart,Abraham Aviv,Shahinaz M Gadalla,Hyokyoung G Hong
Telomere length (TL) is associated with health outcomes. Southern Blotting (SB) is the gold standard of TL measurements, while qPCR-based TL measurements are the most used because of their high throughput. We compared leukocyte TL (LTL) measurements by SB and qPCR, and their ability to capture LTL associations with demographic factors. This study included 908 healthy donors for hematopoietic cell transplantation who had blood samples and data available at CIBMTR®. We used quantile regression (QR) to assess the associations between selected demographic factors and LTL across the LTL distribution. Pearson correlation coefficient and Bland-Altman plot were used to compare SB-LTL and qPCR-LTL measurements. SB-LTL and qPCR-LTL were modestly correlated (r = 0.58, P < 0.001). On average, SB-LTL shortened by 29 base pairs (bp) per year and was 190 bp longer in females than in males. QR analyses showed that the association between SB-LTL and age varied across the LTL distribution, with stronger age-related shortening at higher percentiles (25 bp at the 25th percentile vs. 31 bp at the 75th percentile; P = 0.003). Females had longer SB-LTL than males across all percentiles (P < 0.05 in SB-LTL analysis), and the magnitude of this sex difference did not vary significantly across the LTL distribution (157 bp at the 25th percentile vs. 221 bp at the 75th percentile; P = 0.33). Both SB and qPCR showed an inverse relationship between LTL and age, though the magnitudes differed between methods. Considering the full LTL distribution in studies of lifestyle factors and diseases may provide better molecular insights and guide LTL utilization in health applications.
端粒长度（TL）与健康状况相关。Southern Blotting （SB）是TL测定的金标准，而基于qpcr的TL测定因其高通量而被广泛使用。我们比较了SB和qPCR的白细胞TL （LTL）测量，以及它们捕捉LTL与人口统计学因素的相关性的能力。本研究包括908名健康的造血细胞移植供者，他们的血液样本和数据可在CIBMTR®获得。我们使用分位数回归（QR）来评估整个LTL分布中选定的人口统计学因素与LTL之间的关系。采用Pearson相关系数和Bland-Altman图比较SB-LTL和qPCR-LTL测量值。SB-LTL与qPCR-LTL呈正相关（r = 0.58, P < 0.001）。SB-LTL平均每年缩短29个碱基对（bp），雌性比雄性长190 bp。QR分析显示，在整个LTL分布中，SB-LTL与年龄之间的关联各不相同，在较高的百分位数上，年龄相关性缩短更强（第25百分位数为25 bp，第75百分位数为31 bp； P = 0.003）。在所有百分位数中，女性的SB-LTL都比男性长（在SB-LTL分析中P < 0.05），而且这种性别差异的幅度在整个LTL分布中没有显著差异（第25百分位数为157 bp，第75百分位数为221 bp， P = 0.33）。SB和qPCR均显示LTL与年龄呈负相关，但不同方法之间的差异程度不同。考虑LTL在生活方式因素和疾病研究中的完整分布，可以提供更好的分子认识，并指导LTL在健康应用中的应用。
{"title":"Quantile regression of the relationship between demographic factors and leukocyte telomere length, measured by Southern blot and qPCR.","authors":"Kyra Jennifer Waligora Mendez,Sang Kyu Lee,Casey Dagnall,Tsung-Po Lai,Hormuzd Katki,Stephen R Spellman,Valerie Stewart,Abraham Aviv,Shahinaz M Gadalla,Hyokyoung G Hong","doi":"10.1007/s11357-025-02087-6","DOIUrl":"https://doi.org/10.1007/s11357-025-02087-6","url":null,"abstract":"Telomere length (TL) is associated with health outcomes. Southern Blotting (SB) is the gold standard of TL measurements, while qPCR-based TL measurements are the most used because of their high throughput. We compared leukocyte TL (LTL) measurements by SB and qPCR, and their ability to capture LTL associations with demographic factors. This study included 908 healthy donors for hematopoietic cell transplantation who had blood samples and data available at CIBMTR®. We used quantile regression (QR) to assess the associations between selected demographic factors and LTL across the LTL distribution. Pearson correlation coefficient and Bland-Altman plot were used to compare SB-LTL and qPCR-LTL measurements. SB-LTL and qPCR-LTL were modestly correlated (r = 0.58, P < 0.001). On average, SB-LTL shortened by 29 base pairs (bp) per year and was 190 bp longer in females than in males. QR analyses showed that the association between SB-LTL and age varied across the LTL distribution, with stronger age-related shortening at higher percentiles (25 bp at the 25th percentile vs. 31 bp at the 75th percentile; P = 0.003). Females had longer SB-LTL than males across all percentiles (P < 0.05 in SB-LTL analysis), and the magnitude of this sex difference did not vary significantly across the LTL distribution (157 bp at the 25th percentile vs. 221 bp at the 75th percentile; P = 0.33). Both SB and qPCR showed an inverse relationship between LTL and age, though the magnitudes differed between methods. Considering the full LTL distribution in studies of lifestyle factors and diseases may provide better molecular insights and guide LTL utilization in health applications.","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"58 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146089131","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}
Frailty is a geriatric syndrome characterized by reduced physiological reserves and increased vulnerability to stressors. Given its complex phenotypes and underlying biology, robust multidimensional biomarkers are needed to advance personalized care. We aimed to identify serum metabolomics signatures associated with frailty phenotypes and related features. We analyzed serum metabolomics data in 901 participants (47.5% males, mean age 68.3 ± 3.5 years) from the Berlin Aging Study II, classified as non-frail, pre-frail, or frail using Fried's criteria at baseline (T0) and after 7 years (T1). Linear models assessed associations between metabolite levels, frailty, and related parameters. At T0, 1% were frail, increasing to 4.8% at T1. Over follow-up, 323 participants transitioned to a worse frailty category. Across 82 metabolites, no significant differences emerged for frailty status. However, in males, 27 and 30 circulating metabolites were negatively associated with handgrip strength at T0 and T1, respectively. Also in males, L-tyrosine was positively associated with fat mass, while 22 metabolites (carbohydrate-related, maltose, fructose, glucose, galactitol, mannose, lactate, acetylcarnitine; amino acid-related, valine, tyrosine, isoleucine, α-hydroxybutyrate) correlated with nutritional status at T0. In females, dimethylsulfone was positively associated with changes in handgrip strength over time, and glycerol with appendicular lean mass at T0. While serum metabolomics showed weak associations with frailty itself, clear links were observed with frailty-related features, notably muscle strength and nutritional status. These findings highlight insulin sensitivity as a central determinant, suggesting that early metabolic alterations may contribute to impaired muscle health in aging.
{"title":"Serum metabolomic signatures associated with frailty-related phenotypes in a cohort of older people.","authors":"Céline Bougel,Rémi Servien,Nathalie Vialaneix,Elise Maigne,Yves Boirie,Clément Lahaye,Cécile Canlet,Laurent Debrauwer,Valentin Max Vetter,Kristina Norman,Dominique Dardevet,Ilja Demuth,Sergio Polakof","doi":"10.1007/s11357-026-02116-y","DOIUrl":"https://doi.org/10.1007/s11357-026-02116-y","url":null,"abstract":"Frailty is a geriatric syndrome characterized by reduced physiological reserves and increased vulnerability to stressors. Given its complex phenotypes and underlying biology, robust multidimensional biomarkers are needed to advance personalized care. We aimed to identify serum metabolomics signatures associated with frailty phenotypes and related features. We analyzed serum metabolomics data in 901 participants (47.5% males, mean age 68.3 ± 3.5 years) from the Berlin Aging Study II, classified as non-frail, pre-frail, or frail using Fried's criteria at baseline (T0) and after 7 years (T1). Linear models assessed associations between metabolite levels, frailty, and related parameters. At T0, 1% were frail, increasing to 4.8% at T1. Over follow-up, 323 participants transitioned to a worse frailty category. Across 82 metabolites, no significant differences emerged for frailty status. However, in males, 27 and 30 circulating metabolites were negatively associated with handgrip strength at T0 and T1, respectively. Also in males, L-tyrosine was positively associated with fat mass, while 22 metabolites (carbohydrate-related, maltose, fructose, glucose, galactitol, mannose, lactate, acetylcarnitine; amino acid-related, valine, tyrosine, isoleucine, α-hydroxybutyrate) correlated with nutritional status at T0. In females, dimethylsulfone was positively associated with changes in handgrip strength over time, and glycerol with appendicular lean mass at T0. While serum metabolomics showed weak associations with frailty itself, clear links were observed with frailty-related features, notably muscle strength and nutritional status. These findings highlight insulin sensitivity as a central determinant, suggesting that early metabolic alterations may contribute to impaired muscle health in aging.","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"26 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146089130","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}
Immune cells play a crucial role in maintaining tissue homeostasis during aging. However, the dynamics and functions of immune cells in testicular aging have not been well elucidated. In this study, we utilized single-cell RNA sequencing (scRNA-seq) to analyze CD45-enriched immune cells isolated from young and old mice testis. This approach yielded a comprehensive dataset comprising 6622 immune cells, encompassing macrophages, monocytes, and T cells. Our analysis revealed a significant decline in FOLR2 + resident macrophages, accompanied by a corresponding increase in pro-inflammatory CD74 + macrophages, CCR2 + monocytes, and CD8 + T cells in old mice testis. These findings were further validated by multiplex immunofluorescence staining. Notably, during testicular aging, FOLR2 + macrophages underwent a phenotypic transition towards a pro-inflammatory state. This transition subsequently facilitated the recruitment of monocytes and CD8 + T cells via the CCL8-CCR2/CCR5 axis. Furthermore, we discovered that mitochondrial metabolic dysfunction was a key driver of FOLR2 + macrophage activation. Specifically, inhibition of IDH2, a key catalytic enzyme in the TCA cycle, significantly induced this activation. Collectively, our findings provide a detailed immune atlas of testicular aging and suggest a potential role for FOLR2 + macrophages in maintaining testicular immune homeostasis.
{"title":"Single-cell immune atlas of mouse testes unveils metabolic reprogramming of FOLR2 + macrophages in orchestrating testicular immunity during aging.","authors":"Xinyu Li,Min Zhang,Ani Chi,Jiahui Mo,Xiaofeng Tan,Hongde Chen,Chunhua Deng,Xiangzhou Sun,Xin Feng,Zhihong Chen","doi":"10.1007/s11357-026-02109-x","DOIUrl":"https://doi.org/10.1007/s11357-026-02109-x","url":null,"abstract":"Immune cells play a crucial role in maintaining tissue homeostasis during aging. However, the dynamics and functions of immune cells in testicular aging have not been well elucidated. In this study, we utilized single-cell RNA sequencing (scRNA-seq) to analyze CD45-enriched immune cells isolated from young and old mice testis. This approach yielded a comprehensive dataset comprising 6622 immune cells, encompassing macrophages, monocytes, and T cells. Our analysis revealed a significant decline in FOLR2 + resident macrophages, accompanied by a corresponding increase in pro-inflammatory CD74 + macrophages, CCR2 + monocytes, and CD8 + T cells in old mice testis. These findings were further validated by multiplex immunofluorescence staining. Notably, during testicular aging, FOLR2 + macrophages underwent a phenotypic transition towards a pro-inflammatory state. This transition subsequently facilitated the recruitment of monocytes and CD8 + T cells via the CCL8-CCR2/CCR5 axis. Furthermore, we discovered that mitochondrial metabolic dysfunction was a key driver of FOLR2 + macrophage activation. Specifically, inhibition of IDH2, a key catalytic enzyme in the TCA cycle, significantly induced this activation. Collectively, our findings provide a detailed immune atlas of testicular aging and suggest a potential role for FOLR2 + macrophages in maintaining testicular immune homeostasis.","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"101 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146089132","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}
Pub Date : 2026-01-30DOI: 10.1007/s11357-026-02125-x
Catalina Trujillo-Llano,Nina M Ehrhardt,Anna Elisabeth Fromm,Friederike Thams,Dayana Hayek,Shu-Chen Li,Agnes Flöel,Daria Antonenko
Episodic sequence memory is crucial for daily functioning and typically declines during aging. However, the neural mechanisms underlying this decline remain poorly understood. We examined the resting-state functional connectivity (FC) correlates of sequence memory in healthy older adults (OA), with a young adult (YA) group included for comparison. Thirty-eight OA (mean ± SD age: 69.9 ± 3.9 years; 24 women) and 20 YA (mean ± SD age: 24.2 ± 3.4 years; 14 women) completed a sequence memory task and resting-state functional magnetic resonance imaging (rsfMRI). Participants encoded sequences of greyscale pictures presented in colored frames and retrieved their sequential order. We compared the sequence memory performance (% correct) between age groups and examined associations between performance and seed-based FC patterns within each group, focusing on hippocampal and default mode network (DMN) regions. OA exhibited poorer sequence memory performance than YA. In OA, lower performance was associated with reduced FC between the left posterior hippocampus and DMN hubs, and the DMN and right posterior parietal cortex, suggesting that reduced intrinsic coupling within memory networks and between memory and attention networks contributes to sequence memory decline in aging. In YA, superior sequence memory performance correlated with higher FC between the left posterior hippocampus and right medial occipital cortex, indicating that hippocampal-perceptual integration benefits memory function. The FC in these networks did not differ between age groups, indicating a potential shift in memory-relevant connectivity in older adults rather than reduced network function per se. Our findings provide novel evidence of large-scale network correlates underlying sequence memory decline in old age and suggest qualitatively distinct connectivity patterns supporting sequence memory in young and older adults.
{"title":"Functional connectivity correlates of sequence memory decline in healthy older adults.","authors":"Catalina Trujillo-Llano,Nina M Ehrhardt,Anna Elisabeth Fromm,Friederike Thams,Dayana Hayek,Shu-Chen Li,Agnes Flöel,Daria Antonenko","doi":"10.1007/s11357-026-02125-x","DOIUrl":"https://doi.org/10.1007/s11357-026-02125-x","url":null,"abstract":"Episodic sequence memory is crucial for daily functioning and typically declines during aging. However, the neural mechanisms underlying this decline remain poorly understood. We examined the resting-state functional connectivity (FC) correlates of sequence memory in healthy older adults (OA), with a young adult (YA) group included for comparison. Thirty-eight OA (mean ± SD age: 69.9 ± 3.9 years; 24 women) and 20 YA (mean ± SD age: 24.2 ± 3.4 years; 14 women) completed a sequence memory task and resting-state functional magnetic resonance imaging (rsfMRI). Participants encoded sequences of greyscale pictures presented in colored frames and retrieved their sequential order. We compared the sequence memory performance (% correct) between age groups and examined associations between performance and seed-based FC patterns within each group, focusing on hippocampal and default mode network (DMN) regions. OA exhibited poorer sequence memory performance than YA. In OA, lower performance was associated with reduced FC between the left posterior hippocampus and DMN hubs, and the DMN and right posterior parietal cortex, suggesting that reduced intrinsic coupling within memory networks and between memory and attention networks contributes to sequence memory decline in aging. In YA, superior sequence memory performance correlated with higher FC between the left posterior hippocampus and right medial occipital cortex, indicating that hippocampal-perceptual integration benefits memory function. The FC in these networks did not differ between age groups, indicating a potential shift in memory-relevant connectivity in older adults rather than reduced network function per se. Our findings provide novel evidence of large-scale network correlates underlying sequence memory decline in old age and suggest qualitatively distinct connectivity patterns supporting sequence memory in young and older adults.","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"182 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146073331","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}
Pub Date : 2026-01-30DOI: 10.1007/s11357-026-02124-y
María Del Mar Carcelén-Fraile,María Del Carmen Carcelén-Fraile,Fidel Hita-Contreras,Yolanda Castellote-Caballero,Agustín Aibar-Almazán
This study aimed to analyze the associations between cognitive function and factors linked to risk of falls in older adults with mild cognitive impairment (MCI). A cross-sectional design was applied in 129 older adults (mean age: 69.93 ± 3.84 years) diagnosed with MCI. Cognitive performance was evaluated with the MMSE, MoCA, Isaacs Test, Trail Making Test (TMT-A, TMT-B), D2 Test, and DSST. Risk of falls was assessed through the Tinetti Test, ABC-16 scale, and FES-I. Additional measures included gait speed, grip strength, and global physical function. Average MMSE and MoCA scores were 20.97 and 21.45, respectively. Regression models showed significant associations between cognitive and physical outcomes. Lower MMSE scores were related to weaker grip, slower gait, and greater risk of falls (R2 = 0.053; p < 0.05). Lower MoCA scores was associated with reduced physical function, lower balance confidence, increased fear of falling, weaker grip, and higher risk of falls (R2 = 0.107; p < 0.05). Isaacs performance was linked to grip strength, gait, balance, and fear of falling (R2 = 0.126; p < 0.05). Both TMT-A and TMT-B correlated with grip, balance confidence, and risk of falls; TMT-A also with gait speed (R2 = 0.059) and TMT-B with physical function (R2 = 0.087). D2 scores were associated with function, gait, balance, and risk of falls (R2 = 0.173 and 0.153). DSST performance correlated with all physical and psychological outcomes (R2 = 0.133; p < 0.05). Cognitive performance is closely tied to physical and psychological factors associated with risk of falls in older adults with MCI. These findings emphasize the need for comprehensive, multidimensional assessments to identify risk profiles and develop targeted preventive interventions.
本研究旨在分析轻度认知障碍（MCI）老年人认知功能与跌倒风险相关因素之间的关系。采用横断面设计对129名诊断为轻度认知障碍的老年人（平均年龄：69.93±3.84岁）进行研究。采用MMSE、MoCA、Isaacs测试、TMT-A、TMT-B、D2测试和DSST评估认知能力。通过Tinetti测试、ABC-16量表和FES-I评估跌倒风险。额外的测量包括步态速度、握力和整体身体功能。MMSE和MoCA的平均得分分别为20.97和21.45。回归模型显示认知和身体结果之间存在显著关联。MMSE评分越低，握力越弱、步态越慢、跌倒风险越大（R2 = 0.053; p < 0.05）。MoCA评分较低与身体功能降低、平衡信心降低、摔倒恐惧增加、握力较弱和摔倒风险增加相关（R2 = 0.107; p < 0.05）。艾萨克的表现与握力、步态、平衡和摔倒恐惧有关（R2 = 0.126; p < 0.05）。TMT-A和TMT-B与握力、平衡信心和跌倒风险相关；TMT-A与步态速度相关（R2 = 0.059）， TMT-B与身体功能相关（R2 = 0.087）。D2评分与功能、步态、平衡和跌倒风险相关（R2 = 0.173和0.153）。DSST表现与所有生理和心理结局相关（R2 = 0.133; p < 0.05）。认知表现与患有轻度认知障碍的老年人跌倒风险相关的生理和心理因素密切相关。这些发现强调需要进行全面、多维度的评估，以确定风险概况并制定有针对性的预防干预措施。
{"title":"Factors associated with the risk of falls and their relationship with cognitive function in older adults with cognitive impairment: a cross-sectional study.","authors":"María Del Mar Carcelén-Fraile,María Del Carmen Carcelén-Fraile,Fidel Hita-Contreras,Yolanda Castellote-Caballero,Agustín Aibar-Almazán","doi":"10.1007/s11357-026-02124-y","DOIUrl":"https://doi.org/10.1007/s11357-026-02124-y","url":null,"abstract":"This study aimed to analyze the associations between cognitive function and factors linked to risk of falls in older adults with mild cognitive impairment (MCI). A cross-sectional design was applied in 129 older adults (mean age: 69.93 ± 3.84 years) diagnosed with MCI. Cognitive performance was evaluated with the MMSE, MoCA, Isaacs Test, Trail Making Test (TMT-A, TMT-B), D2 Test, and DSST. Risk of falls was assessed through the Tinetti Test, ABC-16 scale, and FES-I. Additional measures included gait speed, grip strength, and global physical function. Average MMSE and MoCA scores were 20.97 and 21.45, respectively. Regression models showed significant associations between cognitive and physical outcomes. Lower MMSE scores were related to weaker grip, slower gait, and greater risk of falls (R2 = 0.053; p < 0.05). Lower MoCA scores was associated with reduced physical function, lower balance confidence, increased fear of falling, weaker grip, and higher risk of falls (R2 = 0.107; p < 0.05). Isaacs performance was linked to grip strength, gait, balance, and fear of falling (R2 = 0.126; p < 0.05). Both TMT-A and TMT-B correlated with grip, balance confidence, and risk of falls; TMT-A also with gait speed (R2 = 0.059) and TMT-B with physical function (R2 = 0.087). D2 scores were associated with function, gait, balance, and risk of falls (R2 = 0.173 and 0.153). DSST performance correlated with all physical and psychological outcomes (R2 = 0.133; p < 0.05). Cognitive performance is closely tied to physical and psychological factors associated with risk of falls in older adults with MCI. These findings emphasize the need for comprehensive, multidimensional assessments to identify risk profiles and develop targeted preventive interventions.","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"104 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-01-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146073332","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}
Pub Date : 2026-01-29DOI: 10.1007/s11357-026-02100-6
Maximilian Rentschler,Mohamed Ali-Jarboui,Christoph M Griessinger,Michael Rosen,Grégory Doré,Oliver Bischof,Manfred Kneilling,Martin Röcken,Heidi Braumüller,Thomas Wieder
Senescence is a tripartite cellular phenotype characterized by permanent growth arrest, resistance to apoptosis, and high secretory activity. Besides its physiological role in embryonic development and pathophysiological contribution to age-related tissue degeneration, in the context of tumor development senescence is an important suppressor mechanism, that counteracts accelerated proliferation. Among the many stressors that induce senescence is the external stimulation by cytokines. Although cytokine-induced senescence (CIS) has repeatedly been reported in the literature, the signaling networks leading to the senescent phenotype remained enigmatic. Here, we used two models of tumor-associated (TA)-CIS: (i) in vitro treatment of human A204 cancer cells with interferon (IFN)-γ and tumor necrosis factor (TNF) and (ii) in vivo senescence induction by adoptive transfer of T helper 1 (TH1) cells into tumor-bearing RIP-Tag2 mice. In both models, gene expression profiling and signal transduction analysis highlighted the persistent activation of IFN-receptor/STAT1 and TNF-receptor/NF-κB/p38 signaling leading to downregulation of cell cycle genes, upregulation of secretory factors and, remarkably, upregulation of pro-apoptotic as well as anti-apoptotic genes. Protein analysis further demonstrated that the growth-arrested tumor cells were not subject to apoptotic death. Altogether, we define a cross-species TA-CIS core gene and signal transduction signature that may be exploited for therapeutic ends for cancer.
{"title":"Cytokine-induced senescence in tumors is based on sustained activation of STAT1- and NFκB-dependent gene regulatory signatures.","authors":"Maximilian Rentschler,Mohamed Ali-Jarboui,Christoph M Griessinger,Michael Rosen,Grégory Doré,Oliver Bischof,Manfred Kneilling,Martin Röcken,Heidi Braumüller,Thomas Wieder","doi":"10.1007/s11357-026-02100-6","DOIUrl":"https://doi.org/10.1007/s11357-026-02100-6","url":null,"abstract":"Senescence is a tripartite cellular phenotype characterized by permanent growth arrest, resistance to apoptosis, and high secretory activity. Besides its physiological role in embryonic development and pathophysiological contribution to age-related tissue degeneration, in the context of tumor development senescence is an important suppressor mechanism, that counteracts accelerated proliferation. Among the many stressors that induce senescence is the external stimulation by cytokines. Although cytokine-induced senescence (CIS) has repeatedly been reported in the literature, the signaling networks leading to the senescent phenotype remained enigmatic. Here, we used two models of tumor-associated (TA)-CIS: (i) in vitro treatment of human A204 cancer cells with interferon (IFN)-γ and tumor necrosis factor (TNF) and (ii) in vivo senescence induction by adoptive transfer of T helper 1 (TH1) cells into tumor-bearing RIP-Tag2 mice. In both models, gene expression profiling and signal transduction analysis highlighted the persistent activation of IFN-receptor/STAT1 and TNF-receptor/NF-κB/p38 signaling leading to downregulation of cell cycle genes, upregulation of secretory factors and, remarkably, upregulation of pro-apoptotic as well as anti-apoptotic genes. Protein analysis further demonstrated that the growth-arrested tumor cells were not subject to apoptotic death. Altogether, we define a cross-species TA-CIS core gene and signal transduction signature that may be exploited for therapeutic ends for cancer.","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"3 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-01-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146072877","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}
Mitochondrial function is important to healthy aging, as it influences energy metabolism, oxidative stress, and physical performance. With age, mitochondrial function and biosynthesis of coenzyme Q10 (CoQ10) may change. CoQ10 serves as a key antioxidant and component of the electron transport system. Supplementation with CoQ10 may help preserve mitochondrial function and support healthy aging. Forty older community-dwelling adults (74 ± 4 years) received either daily oral CoQ10 supplementation (400 mg daily) or a placebo in a 12-week double-blinded, randomized, placebo-controlled design. Before and after the supplementation period, muscle biopsies were obtained. Subsequently, oral glucose tolerance tests (OGTT) and VO2max tests were conducted. Mitochondrial respiratory capacity (MRC), mitochondrial H2O2 emission, and mitochondrial content were assessed in both isolated mitochondria and permeabilized muscle fibers. Levels and redox status of CoQ10 were measured in plasma, muscle tissue, and isolated skeletal muscle mitochondria. Additionally, resting metabolic rate, cognitive function, and body composition were investigated. Plasma levels of CoQ10 increased significantly without changes in redox status after the intervention. No changes between groups or time were observed in muscle and isolated mitochondria regarding MRC, H2O2 emission, mitochondrial content, and levels of CoQ10. Glucose homeostasis, VO2max, and body composition were also unchanged. Twelve weeks of supplementation led to increased plasma levels of CoQ10, with unchanged levels in muscle tissue and isolated mitochondria. No differences in mitochondrial function, glucose homeostasis, and physical performance were found in a cohort of robust older adults.
{"title":"Coenzyme Q10 supplementation raises plasma levels without improving mitochondrial function in older adults.","authors":"Malte Schmücker,Cathrine Tranberg,Jacob Borch,Mette Killerup Kaae,Michelle Damgaard,Mathias Flensted-Jensen,Ida Blom,Marco Morosetti,Sara Barbarossa,Patrick Orlando,Luca Tiano,Flemming Dela,Jørn Wulff Helge,Steen Larsen","doi":"10.1007/s11357-025-02068-9","DOIUrl":"https://doi.org/10.1007/s11357-025-02068-9","url":null,"abstract":"Mitochondrial function is important to healthy aging, as it influences energy metabolism, oxidative stress, and physical performance. With age, mitochondrial function and biosynthesis of coenzyme Q10 (CoQ10) may change. CoQ10 serves as a key antioxidant and component of the electron transport system. Supplementation with CoQ10 may help preserve mitochondrial function and support healthy aging. Forty older community-dwelling adults (74 ± 4 years) received either daily oral CoQ10 supplementation (400 mg daily) or a placebo in a 12-week double-blinded, randomized, placebo-controlled design. Before and after the supplementation period, muscle biopsies were obtained. Subsequently, oral glucose tolerance tests (OGTT) and VO2max tests were conducted. Mitochondrial respiratory capacity (MRC), mitochondrial H2O2 emission, and mitochondrial content were assessed in both isolated mitochondria and permeabilized muscle fibers. Levels and redox status of CoQ10 were measured in plasma, muscle tissue, and isolated skeletal muscle mitochondria. Additionally, resting metabolic rate, cognitive function, and body composition were investigated. Plasma levels of CoQ10 increased significantly without changes in redox status after the intervention. No changes between groups or time were observed in muscle and isolated mitochondria regarding MRC, H2O2 emission, mitochondrial content, and levels of CoQ10. Glucose homeostasis, VO2max, and body composition were also unchanged. Twelve weeks of supplementation led to increased plasma levels of CoQ10, with unchanged levels in muscle tissue and isolated mitochondria. No differences in mitochondrial function, glucose homeostasis, and physical performance were found in a cohort of robust older adults.","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"7 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146056874","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}
Pub Date : 2026-01-28DOI: 10.1007/s11357-026-02110-4
Thole H Hoppen,Nexhmedin Morina,Monica Aas,Julian Mutz
Exposure to non-relational trauma, such as serious accidents, war or life-threatening illness, is linked to poor mental and physical health. Its relationship with biological ageing markers, however, remains underexplored. This study's aim was to examine associations between non-relational trauma and multiple biological ageing markers, and to assess whether associations vary by trauma burden, trauma type and sex. We analysed UK Biobank data from 152,863 participants (mean age = 56.4 years; 56.5% female). Lifetime exposure to six non-relational traumatic experiences was assessed. Biological ageing markers included metabolomic age (MileAge) delta, a metabolomic mortality profile score, frailty, leukocyte telomere length and grip strength. Regression models, adjusted for demographic and socioeconomic confounders, estimated associations between trauma and biological ageing markers. We also examined trauma burden, trauma type-specific and sex-specific associations. Non-relational trauma was associated with a metabolite-predicted age exceeding chronological age (MileAge delta; β = 0.047, 95% CI 0.032-0.062), elevated metabolomic mortality scores (β = 0.102, 95% CI 0.051-0.153) and greater frailty (β = 0.298, 95% CI 0.290-0.307), with a graded, approximately linear pattern for frailty (i.e., higher non-relational trauma sum scores were associated with higher frailty scores). All trauma types were associated with greater frailty, with the strongest association for life-threatening illness. There was no evidence of associations with telomere length, and mixed findings for grip strength. Several associations differed by sex, for example overall trauma burden was more strongly associated with greater frailty in females compared to males. Lifetime non-relational trauma was associated with older biological ageing profiles, with the strongest associations with frailty. These findings support the notion that non-relational trauma exposure is associated with long-term health status, underscoring the need for mitigating ageing-related health decline in trauma-exposed populations.
遭受非关系性创伤，如严重事故、战争或危及生命的疾病，与精神和身体健康状况不佳有关。然而，它与生物衰老标志物的关系仍未得到充分探索。本研究的目的是研究非关系性创伤与多种生物衰老标志物之间的联系，并评估这种联系是否因创伤负担、创伤类型和性别而异。我们分析了英国生物银行152,863名参与者（平均年龄56.4岁，56.5%为女性）的数据。评估了六种非关系性创伤经历的终生暴露。生物老化标志物包括代谢组年龄（里程）delta、代谢组死亡率谱评分、虚弱、白细胞端粒长度和握力。根据人口统计学和社会经济混杂因素调整的回归模型估计了创伤和生物衰老标志物之间的关联。我们还研究了创伤负担、创伤类型特异性和性别特异性的关联。非关系性创伤与代谢预测年龄超过实际年龄（里程δ； β = 0.047, 95% CI 0.032-0.062）、代谢组学死亡率评分升高（β = 0.102, 95% CI 0.051-0.153）和更大的虚弱（β = 0.298, 95% CI 0.290-0.307）相关，虚弱呈分级近似线性模式（即，较高的非关系性创伤总评分与较高的虚弱评分相关）。所有的创伤类型都与更大的虚弱有关，与危及生命的疾病的联系最为密切。没有证据表明与端粒长度有关，握力也有不同的结果。一些关联因性别而异，例如，与男性相比，女性的总体创伤负担与更大的脆弱性联系更紧密。终生非关系性创伤与较老的生物老化特征有关，与脆弱的联系最为密切。这些发现支持了非关系性创伤暴露与长期健康状况相关的观点，强调了减轻创伤暴露人群中与年龄相关的健康下降的必要性。
{"title":"Lifetime non-relational traumatic experiences are associated with biological ageing.","authors":"Thole H Hoppen,Nexhmedin Morina,Monica Aas,Julian Mutz","doi":"10.1007/s11357-026-02110-4","DOIUrl":"https://doi.org/10.1007/s11357-026-02110-4","url":null,"abstract":"Exposure to non-relational trauma, such as serious accidents, war or life-threatening illness, is linked to poor mental and physical health. Its relationship with biological ageing markers, however, remains underexplored. This study's aim was to examine associations between non-relational trauma and multiple biological ageing markers, and to assess whether associations vary by trauma burden, trauma type and sex. We analysed UK Biobank data from 152,863 participants (mean age = 56.4 years; 56.5% female). Lifetime exposure to six non-relational traumatic experiences was assessed. Biological ageing markers included metabolomic age (MileAge) delta, a metabolomic mortality profile score, frailty, leukocyte telomere length and grip strength. Regression models, adjusted for demographic and socioeconomic confounders, estimated associations between trauma and biological ageing markers. We also examined trauma burden, trauma type-specific and sex-specific associations. Non-relational trauma was associated with a metabolite-predicted age exceeding chronological age (MileAge delta; β = 0.047, 95% CI 0.032-0.062), elevated metabolomic mortality scores (β = 0.102, 95% CI 0.051-0.153) and greater frailty (β = 0.298, 95% CI 0.290-0.307), with a graded, approximately linear pattern for frailty (i.e., higher non-relational trauma sum scores were associated with higher frailty scores). All trauma types were associated with greater frailty, with the strongest association for life-threatening illness. There was no evidence of associations with telomere length, and mixed findings for grip strength. Several associations differed by sex, for example overall trauma burden was more strongly associated with greater frailty in females compared to males. Lifetime non-relational trauma was associated with older biological ageing profiles, with the strongest associations with frailty. These findings support the notion that non-relational trauma exposure is associated with long-term health status, underscoring the need for mitigating ageing-related health decline in trauma-exposed populations.","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"42 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146056511","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}
Pub Date : 2026-01-28DOI: 10.1007/s11357-026-02103-3
Tianhao Wu,Chengnan Guo,Huangbo Yuan,Mingyi Du,Tiejun Zhang,Xingdong Chen,Zhenqiu Liu
Phenotypic age, an aging indicator derived from clinical biomarkers, is associated with morbidities and mortality. However, a liver-specific phenotypic aging indicator is still lacking, and its longitudinal associations with liver-related outcomes, as well as the underlying biological mechanisms, remain elusive. We developed a liver-specific phenotypic age using 11 selected clinical blood markers within the England-White cohort of the UK Biobank and validated this metric in both the Scotland-Wales cohort and Non-White-British cohort. We calculated phenotypic age acceleration (PhenoAgeAccel) and examined its association with long-term liver-related outcomes. We also explored the extent to which liver-specific PhenoAgeAccel mediated the impact of modifiable risk behaviors on liver-related outcomes. The metabolic and proteomic signatures of liver-specific PhenoAgeAccel were subsequently characterized. Liver-specific PhenoAgeAccel was significantly associated with a 1.23- to 2.97-fold increased risks of all-cause mortality and liver-related events. The impact of liver-specific PhenoAgeAccel on liver outcomes were more pronounced in males and in individuals with high genetic risk compared to their respective counterparts, and was stronger than that observed with systemic PhenoAgeAccel. Approximately 10-27% of the associations between risk behaviors and liver-related outcomes were mediated by liver-specific PhenoAgeAccel. Proteomic analysis identified 211 proteins associated with both liver-specific PhenoAgeAccel and liver-related outcomes, of which 22 (e.g., AGXT and SULT2A1) were liver-enriched and significantly mediated this relationship. Liver-specific PhenoAgeAccel is a strong predictor of liver-related outcomes, partially mediates the impact of modifiable behaviors, and is linked to liver-enriched proteins. This accessible tool may enhance risk stratification and support preventive strategies targeting liver health and aging.
{"title":"Liver-specific phenotypic aging, behavior and genetic risks, and long-term liver-related outcomes.","authors":"Tianhao Wu,Chengnan Guo,Huangbo Yuan,Mingyi Du,Tiejun Zhang,Xingdong Chen,Zhenqiu Liu","doi":"10.1007/s11357-026-02103-3","DOIUrl":"https://doi.org/10.1007/s11357-026-02103-3","url":null,"abstract":"Phenotypic age, an aging indicator derived from clinical biomarkers, is associated with morbidities and mortality. However, a liver-specific phenotypic aging indicator is still lacking, and its longitudinal associations with liver-related outcomes, as well as the underlying biological mechanisms, remain elusive. We developed a liver-specific phenotypic age using 11 selected clinical blood markers within the England-White cohort of the UK Biobank and validated this metric in both the Scotland-Wales cohort and Non-White-British cohort. We calculated phenotypic age acceleration (PhenoAgeAccel) and examined its association with long-term liver-related outcomes. We also explored the extent to which liver-specific PhenoAgeAccel mediated the impact of modifiable risk behaviors on liver-related outcomes. The metabolic and proteomic signatures of liver-specific PhenoAgeAccel were subsequently characterized. Liver-specific PhenoAgeAccel was significantly associated with a 1.23- to 2.97-fold increased risks of all-cause mortality and liver-related events. The impact of liver-specific PhenoAgeAccel on liver outcomes were more pronounced in males and in individuals with high genetic risk compared to their respective counterparts, and was stronger than that observed with systemic PhenoAgeAccel. Approximately 10-27% of the associations between risk behaviors and liver-related outcomes were mediated by liver-specific PhenoAgeAccel. Proteomic analysis identified 211 proteins associated with both liver-specific PhenoAgeAccel and liver-related outcomes, of which 22 (e.g., AGXT and SULT2A1) were liver-enriched and significantly mediated this relationship. Liver-specific PhenoAgeAccel is a strong predictor of liver-related outcomes, partially mediates the impact of modifiable behaviors, and is linked to liver-enriched proteins. This accessible tool may enhance risk stratification and support preventive strategies targeting liver health and aging.","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"293 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2026-01-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"146056875","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}
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