Jia Liu, Wei Xiang Gao, Wei Sen Zhang, Ya Li Jin, Lin Xu, Jiao Wang
Background China’s dramatic decline in fertility rates due to family planning policies and socioeconomic changes have significant impacts on women’s long-term health. We examined the associations of individual reproductive factors and reproductive risk scores (RRS) with all-cause, cardiovascular disease (CVD), and cancer mortality in Chinese women. Methods 19,833 women aged 50+ years from the Guangzhou Biobank Cohort Study were included. Reproductive factors include gravidity, parity, number of abortions, age at first pregnancy, duration of breastfeeding, age at menarche, age at menopause, and contraceptive use. Weighted and unweighted RRS was constructed by six reproductive characteristics associated with long-term mortality. Cox models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). Results During an average follow-up of 16.7 years, 4,310 deaths occurred. Per one-point increase in weighted RRS was associated with higher risks of all-cause (adjusted HR: 1.05, 95% CI: 1.03–1.07) and CVD mortality (1.07, 1.04–1.10), but not with cancer mortality (1.03, 0.99–1.07). Mortality was higher for 0 or ≥ 4 pregnancies than 3 pregnancies (1.32, 1.06–1.64 and 1.12, 1.02–1.22), 0 or ≥ 4 childbirths than 2 childbirths (1.46, 1.20–1.79 and 1.15, 1.05–1.25), ≥4 abortions than no abortions (1.10, 1.02–1.19), age at first pregnancy <22 years than 22–29 years (1.21, 1.13–1.30), and breastfeeding duration <3 months than the longer (1.23, 1.09–1.38). Age at menopause was negatively associated with all-cause mortality (0.99, 0.98–1.00 per one-year increase). Conclusion Reproductive factors, including gravidity, parity, abortion, age at first pregnancy, breastfeeding duration, and menopausal age, were significant determinants of mortality risk in older Chinese women.
{"title":"Reproductive Factors and Risk of Mortality in Older Women: A 16-year Follow-up of Guangzhou Biobank Cohort Study","authors":"Jia Liu, Wei Xiang Gao, Wei Sen Zhang, Ya Li Jin, Lin Xu, Jiao Wang","doi":"10.1093/gerona/glaf246","DOIUrl":"https://doi.org/10.1093/gerona/glaf246","url":null,"abstract":"Background China’s dramatic decline in fertility rates due to family planning policies and socioeconomic changes have significant impacts on women’s long-term health. We examined the associations of individual reproductive factors and reproductive risk scores (RRS) with all-cause, cardiovascular disease (CVD), and cancer mortality in Chinese women. Methods 19,833 women aged 50+ years from the Guangzhou Biobank Cohort Study were included. Reproductive factors include gravidity, parity, number of abortions, age at first pregnancy, duration of breastfeeding, age at menarche, age at menopause, and contraceptive use. Weighted and unweighted RRS was constructed by six reproductive characteristics associated with long-term mortality. Cox models were used to estimate hazard ratios (HRs) and 95% confidence intervals (CIs). Results During an average follow-up of 16.7 years, 4,310 deaths occurred. Per one-point increase in weighted RRS was associated with higher risks of all-cause (adjusted HR: 1.05, 95% CI: 1.03–1.07) and CVD mortality (1.07, 1.04–1.10), but not with cancer mortality (1.03, 0.99–1.07). Mortality was higher for 0 or ≥ 4 pregnancies than 3 pregnancies (1.32, 1.06–1.64 and 1.12, 1.02–1.22), 0 or ≥ 4 childbirths than 2 childbirths (1.46, 1.20–1.79 and 1.15, 1.05–1.25), ≥4 abortions than no abortions (1.10, 1.02–1.19), age at first pregnancy &lt;22 years than 22–29 years (1.21, 1.13–1.30), and breastfeeding duration &lt;3 months than the longer (1.23, 1.09–1.38). Age at menopause was negatively associated with all-cause mortality (0.99, 0.98–1.00 per one-year increase). Conclusion Reproductive factors, including gravidity, parity, abortion, age at first pregnancy, breastfeeding duration, and menopausal age, were significant determinants of mortality risk in older Chinese women.","PeriodicalId":22892,"journal":{"name":"The Journals of Gerontology Series A: Biological Sciences and Medical Sciences","volume":"42 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145472709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Fan Chen, Yi Guan, Bang-Bon Koo, Tammy M Scott, Wenjun Li, Kelsey M Mangano, Mahdi Garelnabi, Rafeeque Bhadelia, Katherine L Tucker
Background Magnesium’s (Mg) role in brain aging is under-studied. We examined associations of dietary and serum Mg with MRI and cognitive measures in a cohort with >10 y follow-up. Methods Adults from the Boston Puerto Rican Health Study who underwent MRI (n = 218 with serum Mg, n = 198 with Mg intake) and cognitive testing (n = 1049 with serum Mg, n = 1363 with Mg intake) were included. Hypomagnesemia was defined as serum Mg < 0.75 mmol/L, and adequate Mg intake as ≥ the Estimated Average Requirement (males : 350 mg/d, females : 265 mg/d). Multivariable linear regression and linear mixed-effects models were used to estimate associations of Mg with brain age gap (z-score), volumes (% of total intracranial volume), and cognitive scores (z-score). Effect modification by diabetes, hypertension, dyslipidemia, calcium: Mg intake ratio, or ApoE4 was evaluated. Results In the full sample, hypomagnesemia was not associated with brain MRI measures, but with global cognitive function [β (95% CI) = -0.058 (-0.11, -0.0020)], in fully adjusted models. Adequate Mg intake was associated with volumes of total gray matter [β (95% CI) = 2.83 (0.56, 5.11)], white matter [β (95% CI) = 1.54 (0.22, 2.86)], and multiple subregions, but not cognition. In participants with diabetes, hypomagnesemia was associated with lower volumes of multiple brain regions, which were not observed in participants without diabetes (P interaction<0.05). Limited or no interaction was detected for other potential modifiers, despite some variation in association direction or magnitude across subgroups. Conclusions Diabetes modified Mg’s association with brain volumes. Mg merits more attention among people with diabetes for preventing neurodegeneration.
{"title":"Associations of Serum Magnesium and Magnesium Intake with Brain Morphology and Cognitive Function in Puerto Rican Adults","authors":"Fan Chen, Yi Guan, Bang-Bon Koo, Tammy M Scott, Wenjun Li, Kelsey M Mangano, Mahdi Garelnabi, Rafeeque Bhadelia, Katherine L Tucker","doi":"10.1093/gerona/glaf241","DOIUrl":"https://doi.org/10.1093/gerona/glaf241","url":null,"abstract":"Background Magnesium’s (Mg) role in brain aging is under-studied. We examined associations of dietary and serum Mg with MRI and cognitive measures in a cohort with &gt;10 y follow-up. Methods Adults from the Boston Puerto Rican Health Study who underwent MRI (n = 218 with serum Mg, n = 198 with Mg intake) and cognitive testing (n = 1049 with serum Mg, n = 1363 with Mg intake) were included. Hypomagnesemia was defined as serum Mg &lt; 0.75 mmol/L, and adequate Mg intake as ≥ the Estimated Average Requirement (males : 350 mg/d, females : 265 mg/d). Multivariable linear regression and linear mixed-effects models were used to estimate associations of Mg with brain age gap (z-score), volumes (% of total intracranial volume), and cognitive scores (z-score). Effect modification by diabetes, hypertension, dyslipidemia, calcium: Mg intake ratio, or ApoE4 was evaluated. Results In the full sample, hypomagnesemia was not associated with brain MRI measures, but with global cognitive function [β (95% CI) = -0.058 (-0.11, -0.0020)], in fully adjusted models. Adequate Mg intake was associated with volumes of total gray matter [β (95% CI) = 2.83 (0.56, 5.11)], white matter [β (95% CI) = 1.54 (0.22, 2.86)], and multiple subregions, but not cognition. In participants with diabetes, hypomagnesemia was associated with lower volumes of multiple brain regions, which were not observed in participants without diabetes (P interaction&lt;0.05). Limited or no interaction was detected for other potential modifiers, despite some variation in association direction or magnitude across subgroups. Conclusions Diabetes modified Mg’s association with brain volumes. Mg merits more attention among people with diabetes for preventing neurodegeneration.","PeriodicalId":22892,"journal":{"name":"The Journals of Gerontology Series A: Biological Sciences and Medical Sciences","volume":"165 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145447437","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jingxin Zhou, Yingcheng He, Jiawei Wang, Jing Cao, Xiaoling Huang, Menglu Chen, Juan Ye
Background Malnutrition, characterized by degeneration of body composition due to reduced intake or inflammation, shares some common mechanisms with age-related macular degeneration (AMD), while their associations remain unexplored Methods This cohort study utilized data from the UK Biobank. Participants without pre-existing AMD and with complete malnutrition data were included. Cox regression was employed to evaluate the longitudinal association. An ElasticNet model was used to derive a metabolomic signature of malnutrition, which was subsequently assessed for association with AMD. Malnutrition and the metabolomic signature were further tested for associations with photoreceptor thinning. Structural equation modeling (SEM) was applied to delineate underlying mechanisms. Results A total of 444,681 participants (mean age: 56.4 ± 8.1 years; 45.8% male) were included, with 32,086 (7.2%) diagnosed with malnutrition at baseline. Over a median follow-up of 13.6 years, 10,009 AMD cases were identified. Malnutrition was associated with an increased risk of AMD (HR 1.221, 95% CI 1.144–1.304, P < 0.001). Metabolomic signature of malnutrition derived from 127 metabolites was significantly associated with AMD risk (per SD increase: HR 1.073, 95% CI 1.037–1.110, P < 0.001), and thinner photoreceptor layer (β = -0.214, 95% CI -0.314 to -0.114, P < 0.001). SEM revealed that malnutrition increased AMD risk partially through metabolomic changes induced photoreceptor thinning. Conclusions Malnutrition in middle-aged adults was significantly associated with increased risk of AMD, which was mediated by metabolomic alterations that impaired photoreceptor health.
营养不良的特征是由于摄入减少或炎症引起的身体成分的退化，营养不良与年龄相关性黄斑变性（AMD）有一些共同的机制，但它们之间的关联尚不清楚。没有先前存在的AMD和有完整营养不良数据的参与者被纳入研究。采用Cox回归分析纵向相关性。使用ElasticNet模型得出营养不良的代谢组学特征，随后评估其与AMD的关联。营养不良和代谢组学特征进一步测试与光感受器变薄的关系。结构方程模型（SEM）被用于描述潜在的机制。结果共纳入444,681名参与者（平均年龄：56.4±8.1岁，45.8%为男性），其中32,086名（7.2%）在基线时被诊断为营养不良。在中位13.6年的随访中，发现了10,009例AMD病例。营养不良与AMD风险增加相关（HR 1.221, 95% CI 1.144-1.304, P < 0.001）。来自127种代谢物的营养不良代谢组学特征与AMD风险（每SD增加：HR 1.073, 95% CI 1.037-1.110, P < 0.001）和更薄的光感受器层（β = -0.214, 95% CI -0.314至-0.114,P < 0.001）显著相关。扫描电镜显示，营养不良增加AMD的风险部分是通过代谢组学变化引起的光感受器变薄。结论中年人营养不良与黄斑变性风险增加显著相关，黄斑变性与代谢组学改变介导的光感受器健康受损有关。
{"title":"Malnutrition and Age-Related Macular Degeneration: Mechanistic Insights from UK Biobank Metabolomic and Imaging Data","authors":"Jingxin Zhou, Yingcheng He, Jiawei Wang, Jing Cao, Xiaoling Huang, Menglu Chen, Juan Ye","doi":"10.1093/gerona/glaf229","DOIUrl":"https://doi.org/10.1093/gerona/glaf229","url":null,"abstract":"Background Malnutrition, characterized by degeneration of body composition due to reduced intake or inflammation, shares some common mechanisms with age-related macular degeneration (AMD), while their associations remain unexplored Methods This cohort study utilized data from the UK Biobank. Participants without pre-existing AMD and with complete malnutrition data were included. Cox regression was employed to evaluate the longitudinal association. An ElasticNet model was used to derive a metabolomic signature of malnutrition, which was subsequently assessed for association with AMD. Malnutrition and the metabolomic signature were further tested for associations with photoreceptor thinning. Structural equation modeling (SEM) was applied to delineate underlying mechanisms. Results A total of 444,681 participants (mean age: 56.4 ± 8.1 years; 45.8% male) were included, with 32,086 (7.2%) diagnosed with malnutrition at baseline. Over a median follow-up of 13.6 years, 10,009 AMD cases were identified. Malnutrition was associated with an increased risk of AMD (HR 1.221, 95% CI 1.144–1.304, P &lt; 0.001). Metabolomic signature of malnutrition derived from 127 metabolites was significantly associated with AMD risk (per SD increase: HR 1.073, 95% CI 1.037–1.110, P &lt; 0.001), and thinner photoreceptor layer (β = -0.214, 95% CI -0.314 to -0.114, P &lt; 0.001). SEM revealed that malnutrition increased AMD risk partially through metabolomic changes induced photoreceptor thinning. Conclusions Malnutrition in middle-aged adults was significantly associated with increased risk of AMD, which was mediated by metabolomic alterations that impaired photoreceptor health.","PeriodicalId":22892,"journal":{"name":"The Journals of Gerontology Series A: Biological Sciences and Medical Sciences","volume":"153 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145447438","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Sodiq Fakorede,Kai Cheng,Olubodun M Lateef,Okikiola Samuel Fakorede,Deqiang Wang,Dan Wang,Xia Liu
BACKGROUNDFalls are a leading cause of morbidity in older adults, with emerging evidence suggesting that systemic inflammation may contribute to this risk. C-reactive protein (CRP), a biomarker of inflammation, has been linked to various health issues, including declines in physical function. However, its direct influence on balance and fall risk remains uncertain. This study investigates the association between CRP levels and balance using observational data and Mendelian Randomization (MR) to explore its causal role in fall risk.METHODSWe analyzed data from the 2021-2023 National Health and Nutrition Examination Survey (NHANES), including 1,215 participants aged 60 and older. CRP levels were measured using immunoturbidimetric assays, and balance was assessed via the Modified Romberg Test. We used multivariable ordinal logistic regression models to evaluate the relationship between CRP and balance, adjusting for demographic, health, and lifestyle factors. Genetic instruments for CRP were derived from genome-wide association studies (GWAS), and MR analysis was performed using fall risk summary statistics (2,215 cases, 6,289 controls).RESULTSIn the NHANES cohort, higher CRP levels were associated with poorer balance (β = -0.201, p = 0.007). This association was stronger in males but not in females. MR analysis confirmed a causal link between elevated CRP and increased fall risk (OR = 1.13, p = 8.96 × 10-8), with no evidence of pleiotropy or heterogeneity.CONCLUSIONSour findings highlight CRP as a key factor influencing balance and a causal contributor to fall risk in older adults, suggesting that anti-inflammatory interventions may help reduce fall risk.
背景：跌倒是老年人发病的主要原因，越来越多的证据表明，全身性炎症可能导致这种风险。c反应蛋白（CRP）是炎症的一种生物标志物，与各种健康问题有关，包括身体机能下降。然而，它对平衡和跌倒风险的直接影响仍不确定。本研究利用观察数据和孟德尔随机化（MR）研究CRP水平与平衡之间的关系，以探讨其在跌倒风险中的因果作用。方法我们分析了2021-2023年全国健康与营养调查（NHANES）的数据，包括1215名60岁及以上的参与者。采用免疫比浊法测定CRP水平，并通过改良Romberg试验评估平衡。我们使用多变量有序逻辑回归模型来评估CRP与平衡之间的关系，调整了人口统计学、健康和生活方式因素。CRP的遗传仪器来源于全基因组关联研究（GWAS）， MR分析采用跌倒风险汇总统计（2215例，6289例对照）。结果在NHANES队列中，较高的CRP水平与较差的平衡相关（β = -0.201, p = 0.007）。这种关联在男性中更强，而在女性中则不然。MR分析证实CRP升高与跌倒风险增加之间存在因果关系（OR = 1.13, p = 8.96 × 10-8），未发现多效性或异质性的证据。结论：研究结果表明，CRP是影响平衡的关键因素，是老年人跌倒风险的因果因素，提示抗炎干预可能有助于降低跌倒风险。
{"title":"Association of Systemic Inflammation with Balance and Falls in Older Adults: NHANES and Mendelian Randomization Study.","authors":"Sodiq Fakorede,Kai Cheng,Olubodun M Lateef,Okikiola Samuel Fakorede,Deqiang Wang,Dan Wang,Xia Liu","doi":"10.1093/gerona/glaf242","DOIUrl":"https://doi.org/10.1093/gerona/glaf242","url":null,"abstract":"BACKGROUNDFalls are a leading cause of morbidity in older adults, with emerging evidence suggesting that systemic inflammation may contribute to this risk. C-reactive protein (CRP), a biomarker of inflammation, has been linked to various health issues, including declines in physical function. However, its direct influence on balance and fall risk remains uncertain. This study investigates the association between CRP levels and balance using observational data and Mendelian Randomization (MR) to explore its causal role in fall risk.METHODSWe analyzed data from the 2021-2023 National Health and Nutrition Examination Survey (NHANES), including 1,215 participants aged 60 and older. CRP levels were measured using immunoturbidimetric assays, and balance was assessed via the Modified Romberg Test. We used multivariable ordinal logistic regression models to evaluate the relationship between CRP and balance, adjusting for demographic, health, and lifestyle factors. Genetic instruments for CRP were derived from genome-wide association studies (GWAS), and MR analysis was performed using fall risk summary statistics (2,215 cases, 6,289 controls).RESULTSIn the NHANES cohort, higher CRP levels were associated with poorer balance (β = -0.201, p = 0.007). This association was stronger in males but not in females. MR analysis confirmed a causal link between elevated CRP and increased fall risk (OR = 1.13, p = 8.96 × 10-8), with no evidence of pleiotropy or heterogeneity.CONCLUSIONSour findings highlight CRP as a key factor influencing balance and a causal contributor to fall risk in older adults, suggesting that anti-inflammatory interventions may help reduce fall risk.","PeriodicalId":22892,"journal":{"name":"The Journals of Gerontology Series A: Biological Sciences and Medical Sciences","volume":"64 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145411540","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Background To investigate the association of estimated glucose disposal rate (eGDR), a validated measure of insulin resistance (IR), with brain aging and dementia among diabetes-free people. Methods This study included 258,732 diabetes- and dementia-free adults aged ≥55 from UK Biobank, including 15,389 participants who underwent brain MRI scans. eGDR was assessed by a well-established formula. Brain age gap (BAG) was calculated as difference between machine learning-predicted brain age and chronological age. Dementia was ascertained based on medical records. Data were analyzed using Cox, Laplace, and linear regression. Results Over the follow-up, 7,063 participants developed dementia. The hazard ratios of dementia for eGDR quartiles 2-4 compared to eGDR quartile 1 were 0.88 (0.81, 0.96), 0.83 (0.76, 0.92), and 0.73 (0.66, 0.82), respectively. High eGDR was further associated with 1.31 (0.81, 1.80) years later onset of dementia. Those with high eGDR had 2.09 (1.74, 2.45) years younger brain age than chronological age. Among APOE ɛ4 carriers, those with high eGDR had 14% lower incidence of dementia and a 1.77-year gap between brain age and chronological age (P-for-interaction<0.001). Conclusion Higher eGDR is associated with prolonged onset of dementia and delayed brain aging among diabetes-free individuals, and could buffer genetic risk of APOE ɛ4.
{"title":"Estimated glucose disposal rate is associated with brain aging and dementia among diabetes-free older adults","authors":"Jiao Wang, Shuqi Wang, Abigail Dove, Sakura Sakakibara, Stéphanie Paillard-Borg, Marc Guitart-Masip, Jirong Yue, Weili Xu","doi":"10.1093/gerona/glaf243","DOIUrl":"https://doi.org/10.1093/gerona/glaf243","url":null,"abstract":"Background To investigate the association of estimated glucose disposal rate (eGDR), a validated measure of insulin resistance (IR), with brain aging and dementia among diabetes-free people. Methods This study included 258,732 diabetes- and dementia-free adults aged ≥55 from UK Biobank, including 15,389 participants who underwent brain MRI scans. eGDR was assessed by a well-established formula. Brain age gap (BAG) was calculated as difference between machine learning-predicted brain age and chronological age. Dementia was ascertained based on medical records. Data were analyzed using Cox, Laplace, and linear regression. Results Over the follow-up, 7,063 participants developed dementia. The hazard ratios of dementia for eGDR quartiles 2-4 compared to eGDR quartile 1 were 0.88 (0.81, 0.96), 0.83 (0.76, 0.92), and 0.73 (0.66, 0.82), respectively. High eGDR was further associated with 1.31 (0.81, 1.80) years later onset of dementia. Those with high eGDR had 2.09 (1.74, 2.45) years younger brain age than chronological age. Among APOE ɛ4 carriers, those with high eGDR had 14% lower incidence of dementia and a 1.77-year gap between brain age and chronological age (P-for-interaction&lt;0.001). Conclusion Higher eGDR is associated with prolonged onset of dementia and delayed brain aging among diabetes-free individuals, and could buffer genetic risk of APOE ɛ4.","PeriodicalId":22892,"journal":{"name":"The Journals of Gerontology Series A: Biological Sciences and Medical Sciences","volume":"113 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-10-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145427434","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BACKGROUNDBased on data from the Global Burden of Disease (GBD) 2021, this study assessed the burden of falls from 1990 to 2021, with a focus on older adults (≥60 years), regional disparities, and projections to 2040.METHODSAge-standardized rates (ASRs) of incidence, prevalence, mortality, DALYs, YLDs, and YLLs were analyzed, along with estimated annual percentage changes (EAPC) and decomposition analysis to quantify the effects of aging and population growth. Age-specific risk factors were estimated via Population Attributable Fraction, and health disparities were examined using the Slope Index of Inequality and Socio-demographic Index (SDI)-linked concentration index. A Bayesian Age-Period-Cohort model projected burdens to 2040.RESULTSAlthough the all-age incidence ASR of falls declined, it increased in older adults from 1990 to 2021 [2021 incidence ASR, 5218.93 (95% UI 4056.57-6569.67) per 100,000; EAPCs, 0.49 (95% CI 0.07-0.91)] and was projected to rise further by 2040. Population aging accounted 59.36% for the increase in fall-related death numbers from 1990 to 2021. Low bone mineral density was a leading risk factor for fall-related mortality and DALYs in older adults. The absolute numbers of all burden measures increased in older adults from 1990 to 2021, and were expected to worsen further by 2040. Health inequalities persisted in older adults: lower-SDI regions had higher mortality despite lower incidence/prevalence, while higher-SDI regions showed the opposite.CONCLUSIONSThe public health challenge posed by falls are substantial in older adults. Enhanced preventive strategies alongside efforts to address socioeconomic disparities are needed.
{"title":"Global Burden of Falls 1990-2021: Aging Effect, Age-Stratified Risk Factors, and Projection to 2040 in Older Adults.","authors":"Huimin Chen,Huijing Liu,Yunfei Long,Dongdong Wu,Wei Du,Jing He,Shuhua Li,Xinxin Ma,Haibo Chen,Wen Su","doi":"10.1093/gerona/glaf238","DOIUrl":"https://doi.org/10.1093/gerona/glaf238","url":null,"abstract":"BACKGROUNDBased on data from the Global Burden of Disease (GBD) 2021, this study assessed the burden of falls from 1990 to 2021, with a focus on older adults (≥60 years), regional disparities, and projections to 2040.METHODSAge-standardized rates (ASRs) of incidence, prevalence, mortality, DALYs, YLDs, and YLLs were analyzed, along with estimated annual percentage changes (EAPC) and decomposition analysis to quantify the effects of aging and population growth. Age-specific risk factors were estimated via Population Attributable Fraction, and health disparities were examined using the Slope Index of Inequality and Socio-demographic Index (SDI)-linked concentration index. A Bayesian Age-Period-Cohort model projected burdens to 2040.RESULTSAlthough the all-age incidence ASR of falls declined, it increased in older adults from 1990 to 2021 [2021 incidence ASR, 5218.93 (95% UI 4056.57-6569.67) per 100,000; EAPCs, 0.49 (95% CI 0.07-0.91)] and was projected to rise further by 2040. Population aging accounted 59.36% for the increase in fall-related death numbers from 1990 to 2021. Low bone mineral density was a leading risk factor for fall-related mortality and DALYs in older adults. The absolute numbers of all burden measures increased in older adults from 1990 to 2021, and were expected to worsen further by 2040. Health inequalities persisted in older adults: lower-SDI regions had higher mortality despite lower incidence/prevalence, while higher-SDI regions showed the opposite.CONCLUSIONSThe public health challenge posed by falls are substantial in older adults. Enhanced preventive strategies alongside efforts to address socioeconomic disparities are needed.","PeriodicalId":22892,"journal":{"name":"The Journals of Gerontology Series A: Biological Sciences and Medical Sciences","volume":"52 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-10-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145374086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BACKGROUNDThe triglyceride-glucose (TyG) index, a practical and reliable indicator for insulin resistance, has been linked to an increased risk of dementia. However, the impact of its longitudinal changes on dementia risk remains unexplored.METHODSData were obtained from the Atherosclerosis Risk in Communities Study (ARIC). TyG index was calculated by combining triglyceride and fasting blood glucose levels. Longitudinal changes in TyG were evaluated using two indicators over two visits (median time interval: 2.9 years): the average TyG index and the difference in TyG index. Participants were stratified into tertiles based on these measures. Cox proportional hazard models were used to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs).RESULTSA total of 12,601 participants (54.9% female, mean age: 54.2 years) were included. During 264,735.5 person-years of follow-up, 2,460 (19.5%) participants developed incident dementia. Individuals in the highest tertile (T3) of the average TyG index had a 26% higher risk of dementia (HR: 1.26, 95% CI: 1.13-1.40, P-trend <0.001) compared to those in the lowest tertile (T1). Furthermore, independent of baseline levels, a greater increase in the TyG index between visit 1 and visit 2 was associated with an elevated dementia risk, with the HRT3 vs. T1 of 1.17 (95% CI: 1.05-1.29, P-trend = 0.003).CONCLUSIONSA higher level of average TyG index and difference in TyG index were both associated with a higher risk of dementia. These findings suggest that long-term monitoring of the TyG index may contribute to identifying individuals at elevated dementia risk.
{"title":"Longitudinal changes in triglyceride-glucose index and the risk of incident dementia: a prospective cohort study.","authors":"Tian Ge,Yihong Ding,Minqing Yan,Mengjia Zhao,Gulisiya Hailili,Minyu Wu,Jie Shen,Xiaoran Liu,Yuan Ma,Dan Zhou,Changzheng Yuan","doi":"10.1093/gerona/glaf237","DOIUrl":"https://doi.org/10.1093/gerona/glaf237","url":null,"abstract":"BACKGROUNDThe triglyceride-glucose (TyG) index, a practical and reliable indicator for insulin resistance, has been linked to an increased risk of dementia. However, the impact of its longitudinal changes on dementia risk remains unexplored.METHODSData were obtained from the Atherosclerosis Risk in Communities Study (ARIC). TyG index was calculated by combining triglyceride and fasting blood glucose levels. Longitudinal changes in TyG were evaluated using two indicators over two visits (median time interval: 2.9 years): the average TyG index and the difference in TyG index. Participants were stratified into tertiles based on these measures. Cox proportional hazard models were used to estimate the hazard ratios (HRs) and 95% confidence intervals (CIs).RESULTSA total of 12,601 participants (54.9% female, mean age: 54.2 years) were included. During 264,735.5 person-years of follow-up, 2,460 (19.5%) participants developed incident dementia. Individuals in the highest tertile (T3) of the average TyG index had a 26% higher risk of dementia (HR: 1.26, 95% CI: 1.13-1.40, P-trend <0.001) compared to those in the lowest tertile (T1). Furthermore, independent of baseline levels, a greater increase in the TyG index between visit 1 and visit 2 was associated with an elevated dementia risk, with the HRT3 vs. T1 of 1.17 (95% CI: 1.05-1.29, P-trend = 0.003).CONCLUSIONSA higher level of average TyG index and difference in TyG index were both associated with a higher risk of dementia. These findings suggest that long-term monitoring of the TyG index may contribute to identifying individuals at elevated dementia risk.","PeriodicalId":22892,"journal":{"name":"The Journals of Gerontology Series A: Biological Sciences and Medical Sciences","volume":"150 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145369474","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Jedd Pratt,Abadi Gebre,Carlos J Toro-Huamanchumo,Elsa Dent,Trent Bozanich,Wai E Lim,Elizabeth Byrnes,Julee McDonagh,Caleb Ferguson,Craig Sale,Kun Zhu,Carl Schultz,Richard L Prince,Joshua R Lewis,Marc Sim
Despite the nexus between cardiovascular health and frailty, the relevance of high-sensitivity cardiac troponin I (hs-cTnI), a biomarker of myocardial injury, to frailty is poorly understood. We examined whether hs-cTnI concentrations were associated with frailty in a well-characterised cohort of older women. A total of 1,151 community-dwelling women from the Perth Longitudinal Study of Aging Women (mean age±SD = 75.2 ± 2.7 years) were included. Frailty was operationalised using a validated Frailty Index (FI) of cumulative deficits, and a modified Fried phenotype. Plasma hs-cTnI were categorised into quartiles. Cross-sectional associations between hs-cTnI quartiles and frailty were assessed using multivariable-adjusted logistic regression models. A total of 235 (20.4%) women were classified as frail using the FI, while 74 (6.4%) were considered frail by Fried's phenotype. In a multivariable-adjusted model, compared to women in the lowest hs-cTnI quartile (Q1), those in Q3 and Q4 had 1.38 (95%CI 1.00-1.90) and 1.79 (1.20-2.67) greater odds for frailty when classified by the FI. When classified according to Fried's phenotype, women in Q2, Q3, and Q4 had 2.25 (1.10-4.09), 2.64 (1.19-5.21), and 2.44 (1.10-5.33) greater odds for frailty, compared to Q1. Associations remained largely unchanged when further adjusted for daily protein intake or systemic inflammation (lipocalin-2) and restricted to those with subclinical hs-cTnI levels (<15.6ng/L). Higher hs-cTnI levels are associated with greater odds for frailty, classified using a FI or Fried's phenotype, amongst older women. hs-cTnI may have applications beyond its typical use in cardiology, offering insight into the implications of underlying cardiovascular dysfunction relating to frailty.
{"title":"High-Sensitivity Cardiac Troponin I and Frailty: Associations with the Frailty Index and Fried Phenotype in Older Women.","authors":"Jedd Pratt,Abadi Gebre,Carlos J Toro-Huamanchumo,Elsa Dent,Trent Bozanich,Wai E Lim,Elizabeth Byrnes,Julee McDonagh,Caleb Ferguson,Craig Sale,Kun Zhu,Carl Schultz,Richard L Prince,Joshua R Lewis,Marc Sim","doi":"10.1093/gerona/glaf235","DOIUrl":"https://doi.org/10.1093/gerona/glaf235","url":null,"abstract":"Despite the nexus between cardiovascular health and frailty, the relevance of high-sensitivity cardiac troponin I (hs-cTnI), a biomarker of myocardial injury, to frailty is poorly understood. We examined whether hs-cTnI concentrations were associated with frailty in a well-characterised cohort of older women. A total of 1,151 community-dwelling women from the Perth Longitudinal Study of Aging Women (mean age±SD = 75.2 ± 2.7 years) were included. Frailty was operationalised using a validated Frailty Index (FI) of cumulative deficits, and a modified Fried phenotype. Plasma hs-cTnI were categorised into quartiles. Cross-sectional associations between hs-cTnI quartiles and frailty were assessed using multivariable-adjusted logistic regression models. A total of 235 (20.4%) women were classified as frail using the FI, while 74 (6.4%) were considered frail by Fried's phenotype. In a multivariable-adjusted model, compared to women in the lowest hs-cTnI quartile (Q1), those in Q3 and Q4 had 1.38 (95%CI 1.00-1.90) and 1.79 (1.20-2.67) greater odds for frailty when classified by the FI. When classified according to Fried's phenotype, women in Q2, Q3, and Q4 had 2.25 (1.10-4.09), 2.64 (1.19-5.21), and 2.44 (1.10-5.33) greater odds for frailty, compared to Q1. Associations remained largely unchanged when further adjusted for daily protein intake or systemic inflammation (lipocalin-2) and restricted to those with subclinical hs-cTnI levels (<15.6ng/L). Higher hs-cTnI levels are associated with greater odds for frailty, classified using a FI or Fried's phenotype, amongst older women. hs-cTnI may have applications beyond its typical use in cardiology, offering insight into the implications of underlying cardiovascular dysfunction relating to frailty.","PeriodicalId":22892,"journal":{"name":"The Journals of Gerontology Series A: Biological Sciences and Medical Sciences","volume":"28 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145369472","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Neuroinflammation is a critical aspect of aging and neurodegenerative disorders, increasingly recognized for its significant role in the progression of cognitive impairments. Mitochondrial homeostasis is closely linked to cognitive function in the aging brain. However, it remains unclear whether exercise can safeguard cognitive function by enhancing mitochondrial homeostasis in the aged hippocampus affected by neuroinflammation. In this study, we established mouse models exhibiting memory impairment and neuroinflammation in the aged hippocampus to investigate whether exercise can reverse LPS-induced cognitive dysfunction in aged mice, reduce neuroinflammation, and simultaneously improve mitochondrial homeostasis in the hippocampus. Eighteen-month-old male ICR mice underwent eight weeks of moderate-intensity aerobic exercise. The exercise regimen enhanced memory function in LPS-injected aged mice, which was accompanied by reductions in inflammation, oxidative stress, and apoptosis in the aged hippocampus. Importantly, exercise improved mitochondrial homeostasis in the hippocampus of LPS-injected aged mice. Collectively, our results provide the first evidence that exercise can protect cognitive function in the context of neuroinflammation in the aged hippocampus, suggesting that this effect may be associated with the improvement of mitochondrial homeostasis.
{"title":"Exercise-induced alleviation of memory impairment in aged mice with neuroinflammation is linked with modulation of mitochondrial homeostasis in the hippocampus.","authors":"Peng-Da Li,Chong Han,Yuan-Yuan Qin,Zhi Jiang,Shan-Yao Pan,Bo Liao,Nan Wang,Xin-Han Cao,Gang Zhao,Jia-Qi Zhou,Zheng-Hong Qin,Yiqing Lu,Yaping Huai,Li Luo","doi":"10.1093/gerona/glaf233","DOIUrl":"https://doi.org/10.1093/gerona/glaf233","url":null,"abstract":"Neuroinflammation is a critical aspect of aging and neurodegenerative disorders, increasingly recognized for its significant role in the progression of cognitive impairments. Mitochondrial homeostasis is closely linked to cognitive function in the aging brain. However, it remains unclear whether exercise can safeguard cognitive function by enhancing mitochondrial homeostasis in the aged hippocampus affected by neuroinflammation. In this study, we established mouse models exhibiting memory impairment and neuroinflammation in the aged hippocampus to investigate whether exercise can reverse LPS-induced cognitive dysfunction in aged mice, reduce neuroinflammation, and simultaneously improve mitochondrial homeostasis in the hippocampus. Eighteen-month-old male ICR mice underwent eight weeks of moderate-intensity aerobic exercise. The exercise regimen enhanced memory function in LPS-injected aged mice, which was accompanied by reductions in inflammation, oxidative stress, and apoptosis in the aged hippocampus. Importantly, exercise improved mitochondrial homeostasis in the hippocampus of LPS-injected aged mice. Collectively, our results provide the first evidence that exercise can protect cognitive function in the context of neuroinflammation in the aged hippocampus, suggesting that this effect may be associated with the improvement of mitochondrial homeostasis.","PeriodicalId":22892,"journal":{"name":"The Journals of Gerontology Series A: Biological Sciences and Medical Sciences","volume":"50 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-10-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145357757","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Brooke A Vaughan,Graciela Muniz-Terrera,Janet E Simon,Dustin R Grooms,Brian C Clark,Christos Davatzikos,Guray Erus,Qu Tian,Luigi Ferrucci,Susan M Resnick,Eleanor M Simonsick
Muscle weakness and poor brain health both contribute to mobility limitations in older adults, but their respective contributions and interaction are not well-understood. This study examines the relationship between MRI-estimated brain-predicted age difference (brain-predicted age-chronological age), leg strength, and their interaction on mobility decline using Baltimore Longitudinal Study of Aging data (N = 645, 78.1 ± 7.54 years, 56% women). Partial Spearman correlations evaluated the relationships between leg strength, brain-predicted age difference (BPAD), gait speed, and time to complete 5 chair stands (5CS). Mixed-effects linear regression models examined associations of baseline BPAD, leg strength, and lifestyle factors with mobility change over time (5.74 ± 2.87 years). Logistic regression modeled predictors of success in a narrow course walking task. Leg strength significantly correlated with gait speed (r = 0.26, p < 0.001) and 5CS (r=-0.27, p < 0.001). BPAD was associated with decreased gait speed (β=-0.022, p = 0.011) and slower 5CS (β = 0.331, p = 0.012). Greater leg strength was associated with preserved gait speed (β = 0.023, p = 0.022) and faster 5CS (β=-0.552, p < 0.001). BPAD (OR = 0.712, 95% CI: 0.687, 0.940) and leg strength (OR = 0.805, 95% CI: 0.696, 0.964) predicted lower likelihood of narrow walk success. Interactions between BPAD and leg strength were not significant for any measure. These findings suggest accelerated brain aging and leg weakness independently contribute to mobility decline, highlighting the need for interventions targeting brain health and muscle strength to preserve mobility in aging populations.
肌肉无力和大脑健康状况不佳都是老年人行动能力受限的原因，但它们各自的作用和相互作用尚不清楚。本研究利用巴尔的摩老龄化纵向研究数据（N = 645, 78.1±7.54岁，56%女性），研究mri估计的脑预测年龄差异（脑预测年龄-实足年龄）、腿部力量及其与活动能力下降的相互作用之间的关系。部分Spearman相关性评估了腿部力量、脑预测年龄差异（BPAD）、步态速度和完成5个椅子站立（5CS）的时间之间的关系。混合效应线性回归模型检验了基线BPAD、腿部力量和生活方式因素随时间（5.74±2.87年）与活动能力变化的关系。逻辑回归模型预测在狭窄路线步行任务的成功。腿部力量与步态速度（r= 0.26, p < 0.001）和5CS （r=-0.27, p < 0.001）显著相关。BPAD与步态速度降低（β=-0.022, p = 0.011）和5CS减慢（β= 0.331, p = 0.012）相关。更大的腿部力量与保持的步态速度（β= 0.023, p = 0.022）和更快的5CS （β=-0.552, p < 0.001）相关。BPAD （OR = 0.712, 95% CI: 0.687, 0.940）和腿部力量（OR = 0.805, 95% CI: 0.696, 0.964）预测狭窄行走成功的可能性较低。BPAD和腿部力量之间的相互作用在任何测量中都不显著。这些发现表明，加速的大脑老化和腿部无力分别导致了活动能力下降，强调了针对大脑健康和肌肉力量的干预措施的必要性，以保持老年人的活动能力。
{"title":"The Predictive Power of Brain-Predicted Age and Leg Strength on Mobility Decline in Aging: Findings from the Baltimore Longitudinal Study of Aging.","authors":"Brooke A Vaughan,Graciela Muniz-Terrera,Janet E Simon,Dustin R Grooms,Brian C Clark,Christos Davatzikos,Guray Erus,Qu Tian,Luigi Ferrucci,Susan M Resnick,Eleanor M Simonsick","doi":"10.1093/gerona/glaf222","DOIUrl":"https://doi.org/10.1093/gerona/glaf222","url":null,"abstract":"Muscle weakness and poor brain health both contribute to mobility limitations in older adults, but their respective contributions and interaction are not well-understood. This study examines the relationship between MRI-estimated brain-predicted age difference (brain-predicted age-chronological age), leg strength, and their interaction on mobility decline using Baltimore Longitudinal Study of Aging data (N = 645, 78.1 ± 7.54 years, 56% women). Partial Spearman correlations evaluated the relationships between leg strength, brain-predicted age difference (BPAD), gait speed, and time to complete 5 chair stands (5CS). Mixed-effects linear regression models examined associations of baseline BPAD, leg strength, and lifestyle factors with mobility change over time (5.74 ± 2.87 years). Logistic regression modeled predictors of success in a narrow course walking task. Leg strength significantly correlated with gait speed (r = 0.26, p < 0.001) and 5CS (r=-0.27, p < 0.001). BPAD was associated with decreased gait speed (β=-0.022, p = 0.011) and slower 5CS (β = 0.331, p = 0.012). Greater leg strength was associated with preserved gait speed (β = 0.023, p = 0.022) and faster 5CS (β=-0.552, p < 0.001). BPAD (OR = 0.712, 95% CI: 0.687, 0.940) and leg strength (OR = 0.805, 95% CI: 0.696, 0.964) predicted lower likelihood of narrow walk success. Interactions between BPAD and leg strength were not significant for any measure. These findings suggest accelerated brain aging and leg weakness independently contribute to mobility decline, highlighting the need for interventions targeting brain health and muscle strength to preserve mobility in aging populations.","PeriodicalId":22892,"journal":{"name":"The Journals of Gerontology Series A: Biological Sciences and Medical Sciences","volume":"81 1","pages":""},"PeriodicalIF":0.0,"publicationDate":"2025-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145351706","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
京公网安备 11010802042870号
京ICP备2023020795号-1
扫码关注我们
求助内容：
应助结果提醒方式：