Aging-Us最新文献

{"title":"Retraction of: Glypican-1-targeted and gemcitabine-loaded liposomes enhance tumor-suppressing effect on pancreatic cancer.","authors":"Yu Mu, Dezhi Wang, Liangyu Bie, Suxia Luo, Xiaoqian Mu, Yanqiu Zhao","doi":"10.18632/aging.206242","DOIUrl":"10.18632/aging.206242","url":null,"abstract":"","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"17 4","pages":"1075-1076"},"PeriodicalIF":3.9,"publicationDate":"2025-04-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12074819/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144043277","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary associations with reduced epigenetic age: a secondary data analysis of the methylation diet and lifestyle study.","authors":"Jamie L Villanueva, Alexandra Adorno Vita, Heather Zwickey, Kara Fitzgerald, Romilly Hodges, Benjamin Zimmerman, Ryan Bradley","doi":"10.18632/aging.206240","DOIUrl":"10.18632/aging.206240","url":null,"abstract":"<p><strong>Background: </strong>Aging is the primary risk factor for developing non-communicable chronic diseases, necessitating interventions targeting the aging process. Outcome measures of biological aging used in these interventions are mathematical algorithms applied to DNA methylation patterns, known as epigenetic clocks. The Methylation Diet and Lifestyle study was a pilot randomized controlled trial of a diet and lifestyle intervention that utilized epigenetic age as its primary outcome, measured using Horvath's clock. Significant reductions in epigenetic age post-intervention were observed but with notable variability.</p><p><strong>Purpose: </strong>This research aimed to identify dietary components associated with epigenetic age change across groups. Contributing factors to variability, such as weight changes and baseline differences in chronological and epigenetic age, were explored.</p><p><strong>Results: </strong>In hierarchical linear regression, foods investigated as polyphenolic modulators of DNA methylation (green tea, oolong tea, turmeric, rosemary, garlic, berries) categorized in the original study as methyl adaptogens showed significant linear associations with epigenetic age change (B = -1.24, CI = [-2.80, -0.87]), after controlling for baseline epigenetic age acceleration and weight changes. Although the intervention group lost significantly more weight than the control group, these changes were not associated with epigenetic age changes in the regression model. These findings suggest that consuming foods categorized as methyl adaptogens may reduce markers of epigenetic aging.</p>","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"17 4","pages":"994-1010"},"PeriodicalIF":3.9,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12074822/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144050792","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Frailty predicts adverse clinical outcomes in patients with moderate to severe chronic kidney disease.","authors":"Chiung-Ying Huang, Hsiao-Mei Tsao, Shu-Ling Liang, Tai-Shuan Lai, Yung-Ming Chen","doi":"10.18632/aging.206239","DOIUrl":"10.18632/aging.206239","url":null,"abstract":"<p><strong>Background and aim: </strong>Frailty predicts adverse clinical outcomes in older adults. Its prognoses in individuals with specific illnesses have not been fully explored. This study aimed to investigate the impact of frailty by using a semiautomated instrument in patients with advanced chronic kidney disease (CKD).</p><p><strong>Methods and results: </strong>In this prospective study, patients with CKD3b-5 before dialysis and aged ≥55 years with a clinical frailty scale of ≤5 were enrolled. Frailty was assessed by three commonly-used evaluation tools, i.e., Fried's frailty phenotype, Study of Osteoporotic Fractures (SOF) index, and Frailty index of 80 risk variables (FI80) incorporated in a semiautomated platform. Logistic regression, Kaplan-Meier analysis, and Cox proportional hazards models were used to analyze the predictors for frailty and the impact of frailty on composite outcomes of dialysis and overall death. Among 315 patients, the mean age was 73.1 years, and the estimated glomerular filtration rate was 22.2 ml/min/1.73 m². The prevalence of frailty was 6.2% by Fried's frailty phenotype, 0.6% by SOF index, and 26.7% by FI80. Logistic regression analysis showed that age, but not CKD severity or proteinuria, was the most consistent predictor for frailty across the three evaluative tools. During an average follow-up period of 1.7 years, the incidences of kidney failure resulting in dialysis, overall death, or hospital admission were 10.5, 0.6, and 15.2 per 1,000 patient-month, respectively. Kaplan-Meier analysis revealed that frail patients identified by FI80 exhibited worse composite outcomes than their prefrail and robust counterparts (log-rank test, <i>P</i> = 0.01). Multivariate Cox models confirmed that frailty defined by FI80 predicted adverse composite outcomes (HR 3.51, 95% CI: 1.20, 10.22).</p><p><strong>Conclusions: </strong>Frailty is common among CKD patients, and its prevalence increases with age and disease advancement. The frailty status identified by the FI80 effectively predicted end-stage kidney disease or death in patients with advanced CKD.</p>","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"17 4","pages":"1060-1072"},"PeriodicalIF":3.9,"publicationDate":"2025-04-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12074821/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144010560","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of Factor Xa inhibitors on cardiovascular events in older patients with nonvalvular atrial fibrillation.","authors":"Masahiko Takahashi, Takeshi Morimoto, Ryu Tsushima, Yuya Sudo, Ai Sakamoto, Masahiro Sogo, Masatomo Ozaki, Keisuke Okawa","doi":"10.18632/aging.206238","DOIUrl":"10.18632/aging.206238","url":null,"abstract":"<p><strong>Background: </strong>Experimental studies have reported that Factor Xa inhibitors (Xa-Is) have positive effects on cardiac muscles and blood vessels via protease-activated receptor 2 inhibition, suggesting the preventive effects of Xa-Is on cardiovascular events. However, the clinical impact of Xa-Is on cardiovascular disease is unknown.</p><p><strong>Objectives: </strong>This study aimed to investigate the incidence of cardiovascular events among older patients with nonvalvular atrial fibrillation (NVAF) taking Xa-Is compared with those taking non-Xa-Is.</p><p><strong>Methods: </strong>We conducted a single-center historical cohort study of consecutive patients with NVAF who were aged ≥80 years and used oral anticoagulants. Xa-Is included rivaroxaban, apixaban, and edoxaban, and non-Xa-Is included dabigatran and warfarin. The outcome of cardiovascular events was defined as a composite outcome of congestive heart failure, arteriosclerotic disease, and cardiovascular death. We compared the 5-year incidence of cardiovascular events between patients taking Xa-Is and those taking non-Xa-Is.</p><p><strong>Results: </strong>Of 1705 patients aged ≥80 years who were diagnosed with AF, 1092 patients with NVAF were enrolled. Propensity score matching provided 445 patients in each group. The risks of cardiovascular events, congestive heart failure, arteriosclerotic disease, and cardiovascular death were significantly lower in the Xa-I group than in the non-Xa-I group (hazard ratio [95% confidence interval]: 0.43 [0.30-0.61], 0.44 [0.29-0.66], 0.47 [0.22-1.04], and 0.41 [0.23-0.75], respectively).</p><p><strong>Conclusions: </strong>Among patients with NVAF who were aged ≥80 years, the incidence of cardiovascular events was lower in the Xa-I users than in the non-Xa-I users.</p>","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"17 4","pages":"982-993"},"PeriodicalIF":3.9,"publicationDate":"2025-04-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12074823/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144060984","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pharmacological recapitulation of the lean phenotype induced by the lifespan-extending sulfur amino acid-restricted diet.","authors":"Naidu B Ommi, Dwight A L Mattocks, Karel Kalecký, Teodoro Bottiglieri, Sailendra N Nichenametla","doi":"10.18632/aging.206237","DOIUrl":"10.18632/aging.206237","url":null,"abstract":"<p><p>Sulfur amino acid restriction (SAAR), lowering the dietary concentration of sulfur amino acids methionine and cysteine, induces strong anti-obesity effects in rodents. Due to difficulties in formulating the SAAR diet for human consumption, its translation is challenging. Since our previous studies suggest a mechanistic role for low glutathione (GSH) in SAAR-induced anti-obesity effects, we investigated if the pharmacological lowering of GSH recapitulates the lean phenotype in mice on a sulfur amino acid-replete diet. Male obese C57BL6/NTac mice were fed high-fat diets with 0.86% methionine (CD), 0.12% methionine (SAAR), SAAR diet supplemented with a GSH biosynthetic precursor, N-acetylcysteine in water (NAC), and CD supplemented with a GSH biosynthetic inhibitor, DL-buthionine-(S, R)-sulfoximine in water (BSO). The SAAR diet lowered hepatic GSH but increased Nrf2, Phgdh, and serine. These molecular changes culminated in lower hepatic lipid droplet frequency, epididymal fat depot weights, and body fat mass; NAC reversed all these changes. BSO mice exhibited all SAAR-induced changes, with two notable differences, i.e., a smaller effect size than that of the SAAR diet and a higher predilection for molecular changes in kidneys than in the liver. Metabolomics data indicate that BSO and the SAAR diet induce similar changes in the kidney. Unaltered plasma aspartate and alanine transaminases and cystatin-C indicate that long-term continuous administration of BSO is safe. Data demonstrate that BSO recapitulates the SAAR-induced anti-obesity effects and that GSH plays a mechanistic role. BSO dose-response studies in animals and pilot studies in humans to combat obesity are highly warranted.</p>","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"17 ","pages":"960-981"},"PeriodicalIF":3.9,"publicationDate":"2025-04-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12074818/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143813103","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Influence of rapamycin on safety and healthspan metrics after one year: PEARL trial results.","authors":"Mauricio Moel, Girish Harinath, Virginia Lee, Andy Nyquist, Stefanie L Morgan, Anar Isman, Sajad Zalzala","doi":"10.18632/aging.206235","DOIUrl":"10.18632/aging.206235","url":null,"abstract":"<p><strong>Design: </strong>This 48-week decentralized, double-blinded, randomized, placebo-controlled trial (NCT04488601) evaluated the long-term safety of intermittent low-dose rapamycin in a healthy, normative-aging human cohort. Participants received placebo, 5 mg or 10 mg compounded rapamycin weekly. The primary outcome measure was visceral adiposity (by DXA scan), secondary outcomes were blood biomarkers, and lean tissue and bone mineral content (by DXA scan). Established surveys were utilized to evaluate health and well-being. Safety was assessed through adverse events and blood biomarker monitoring.</p><p><strong>Results: </strong>Adverse and serious adverse events were similar across all groups. Visceral adiposity did not change significantly (η_p² = 0.001, <i>p</i> = 0.942), and changes in blood biomarkers remained within normal ranges. Lean tissue mass (η_p² = 0.202, <i>p</i> = 0.013) and self-reported pain (η_p² = 0.168, <i>p</i> = 0.015) improved significantly for women using 10 mg rapamycin. Self-reported emotional well-being (η_p² = 0.108, <i>p</i> = 0.023) and general health (η_p² = 0.166, <i>p</i> = 0.004) also improved for those using 5 mg rapamycin. No other significant effects were observed.</p><p><strong>Conclusions: </strong>Low-dose, intermittent rapamycin administration over 48 weeks is relatively safe in healthy, normative-aging adults, and was associated with significant improvements in lean tissue mass and pain in women. Future work will evaluate benefits of a broader range of rapamycin doses on healthspan metrics for longevity, and will aim to more comprehensively establish efficacy.</p>","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"17 ","pages":"908-936"},"PeriodicalIF":3.9,"publicationDate":"2025-04-04","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12074816/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143796664","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Decreased mitochondrial NAD+ in WRN deficient cells links to dysfunctional proliferation.","authors":"Sofie Lautrup, Shi-Qi Zhang, Shinichiro Funayama, Lisa Lirussi, Tina Visnovska, Hoi-Hung Cheung, Marc Niere, Yuyao Tian, Hilde Loge Nilsen, Geir Selbæk, Janna Saarela, Yoshiro Maezawa, Koutaro Yokote, Per Nilsson, Wai-Yee Chan, Hisaya Kato, Mathias Ziegler, Vilhelm A Bohr, Evandro F Fang","doi":"10.18632/aging.206236","DOIUrl":"10.18632/aging.206236","url":null,"abstract":"<p><p>Werner syndrome (WS), caused by mutations in the RecQ helicase WERNER (<i>WRN</i>) gene, is a classical accelerated aging disease with patients suffering from several metabolic dysfunctions without a cure. While, as we previously reported, depleted NAD⁺ causes accumulation of damaged mitochondria, leading to compromised metabolism, how mitochondrial NAD⁺ changes in WS and the impact on WS pathologies were unknown. We show that loss of WRN increases senescence in mesenchymal stem cells (MSCs) likely related to dysregulation of metabolic and aging pathways. In line with this, NAD⁺ augmentation, via supplementation with nicotinamide riboside, reduces senescence and improves mitochondrial metabolic profiles in MSCs with <i>WRN</i> knockout (<i>WRN^-/-</i>) and in primary fibroblasts derived from WS patients compared to controls. Moreover, <i>WRN</i> deficiency results in decreased mitochondrial NAD⁺ (measured indirectly via mitochondrially-expressed PARP activity), and altered expression of key salvage pathway enzymes, including NMNAT1 and NAMPT; ChIP-seq data analysis unveils a potential co-regulatory axis between WRN and the NMNATs, likely important for chromatin stability and DNA metabolism. However, restoration of mitochondrial or cellular NAD⁺ is not sufficient to reinstall cellular proliferation in immortalized cells with siRNA-mediated knockdown of <i>WRN</i>, highlighting an indispensable role of WRN in proliferation even in an NAD⁺ affluent environment. Further cell and animal studies are needed to deepen our understanding of the underlying mechanisms, facilitating related drug development.</p>","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"null ","pages":"937-959"},"PeriodicalIF":3.9,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12074813/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143782113","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fisetin ameliorates vascular smooth muscle cell calcification via DUSP1-dependent p38 MAPK inhibition.","authors":"Mehdi Razazian, Sheyda Bahiraii, Azmat Sohail, Markus Mandl, Isratul Jannat, Georg Beilhack, Ioana Alesutan, Jakob Voelkl","doi":"10.18632/aging.206233","DOIUrl":"10.18632/aging.206233","url":null,"abstract":"<p><p>Medial vascular calcification is highly prevalent in advanced age and chronic kidney disease (CKD), where it is associated with increased risk for cardiovascular events and mortality. Vascular smooth muscle cells (VSMCs) actively regulate this process, which can be augmented by inflammation and cellular senescence. Thus, the present study investigated the impact of fisetin, a flavonol with anti-inflammatory and senolytic properties, on VSMC calcification. Fisetin treatment suppressed calcific marker expression and calcification of VSMCs as well as p38 MAPK phosphorylation induced by pro-calcific conditions. These effects were abolished by silencing of dual-specificity phosphatase 1 (DUSP1), a negative regulator of p38 MAPK activity. Moreover, knockdown of DUSP1 alone was sufficient to increase calcific marker expression in VSMCs, effects blunted by pharmacological p38 MAPK inhibition. Accordingly, DUSP1 knockdown aggravated calcification of VSMCs during pro-calcific conditions. In addition, fisetin ameliorated the effects of uremic conditions in VSMCs exposed to serum from dialysis patients. Fisetin also inhibited vascular calcification as well as calcific marker expression <i>ex vivo</i> in mouse aortic explants exposed to high phosphate and <i>in vivo</i> in a cholecalciferol overload mouse model. In conclusion, fisetin acts as a potent anti-calcific agent during VSMC calcification, an effect involving DUSP1-mediated regulation of p38 MAPK-dependent pro-calcific signaling.</p>","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"17 ","pages":"885-907"},"PeriodicalIF":3.9,"publicationDate":"2025-04-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12074812/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143782114","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Comprehensive genomic characterization of programmed cell death-related genes to predict drug resistance and prognosis for patients with multiple myeloma.","authors":"Yan Li, Fuxu Wang, Hongbo Zhao, Zhenwei Jia, Xiaoyan Liu, Guirong Cui, Tiejun Qin, Xiaoyang Kong","doi":"10.18632/aging.206234","DOIUrl":"10.18632/aging.206234","url":null,"abstract":"<p><strong>Background: </strong>Multiple myeloma (MM) is a cancer that is difficult to be diagnosed and treated. This study aimed to identify programmed cell death (PCD)-related molecular subtypes of MM and to assess their impact on patients' prognosis, immune status, and drug sensitivity.</p><p><strong>Methods: </strong>We used the ConsensusClusterPlus method to classify molecular subtypes with prognostically relevant PCD genes from the MM patients screened. A prognostic model and a nomogram were established applying one-way COX regression analysis and LASSO Cox regression analysis. MM patients' sensitivity to chemotherapeutic agents was predicted for at-risk populations.</p><p><strong>Results: </strong>Six molecular subtypes were classified employing PCD-related genes, notably, three of them had a higher tendency for immune escape and two of them were correlated with a worse prognosis of MM. Furthermore, the C3 subtype had activated pathways such as oxidative phosphorylation and DNA repair, while the C2 and C4 subtypes had activated pathways related to apoptosis. The Risk score showed that the nomogram can correctly predict the OS for MM patients, in particular, patients in the high-risk group had low overall survival (OS). Pharmacovigilance analyses revealed that patients in the high-risk and low-risk groups had greater IC₅₀ values for the drugs SB505124_1194 and AZD7762_1022, respectively.</p><p><strong>Conclusions: </strong>A 12-gene Risk score model developed with PCD-related genes can accurately predict the survival for MM patients. Our study provided potential targets and strategies for individualized treatment of MM.</p>","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"17 ","pages":"1043-1059"},"PeriodicalIF":3.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12074814/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143774975","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Examining frailty phenotypes of community-dwelling older adults in Taiwan using the falls risk for older people in the community - Taiwan version (Tw-FROP-Com).","authors":"Ya-Mei Tzeng, Senyeong Kao, Wun-Sin Chen, Shueh-Fen Chen, Shan-Ru Li, Yu-Lung Chiu, Yu-Tien Chang, Yaw-Wen Chang","doi":"10.18632/aging.206231","DOIUrl":"10.18632/aging.206231","url":null,"abstract":"<p><strong>Background: </strong>Falls are the second leading cause of accidental injury-related deaths among Taiwanese adults aged 65 and older. This study examined the association between Fried frailty phenotypes and fall risk in this population.</p><p><strong>Materials and methods: </strong>A cross-sectional study was conducted in Keelung City with 375 participants from an Elderly Fall Prevention Program. Frailty was assessed using the modified Fried criteria: weakness, slowness, exhaustion, low physical activity, and unintentional weight loss. Participants with 0-2 criteria were classified as non-frail, and those with 3 or more as frail. Fall risk was evaluated using the Taiwan version of the Falls Risk for Older People in the Community (Tw-FROP-Com), a 28-item tool scoring 0-60 across 13 risk factors.</p><p><strong>Results: </strong>Participants had a mean age of 75.4 ± 6.8 years; 76.0% were female, 18.7% were frail, and 32.7% had fallen in the past year. Those with a fall history had higher rates of weakness (56.7%), slowness (49.6%), and frailty (26.1%). Regression analysis showed that weakness (β = 0.64), slowness (β = 0.21), exhaustion (β = 1.28), unintentional weight loss (β = 3.99), and low physical activity (β = 0.88) were significantly associated with increased fall risk. Frailty explained over 50% of fall risk variance, with unintentional weight loss as the strongest predictor.</p><p><strong>Conclusion: </strong>Unintentional weight loss is the most significant predictor of fall risk among frailty traits. Individual frailty components better predict fall risk than composite frailty measures.</p>","PeriodicalId":55547,"journal":{"name":"Aging-Us","volume":"17 ","pages":"1011-1025"},"PeriodicalIF":3.9,"publicationDate":"2025-04-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12074817/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143774982","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}