Experimental gerontology最新文献

{"title":"Exploring how exercise frequency impacts muscle strength and balance in institutionalized older adults: Protocol for a randomized controlled trial","authors":"Filipe Rodrigues ,&nbsp;Bernardo Pereira ,&nbsp;Elisabete Silva ,&nbsp;Diogo Monteiro ,&nbsp;Raul Antunes","doi":"10.1016/j.exger.2025.112985","DOIUrl":"10.1016/j.exger.2025.112985","url":null,"abstract":"<div><div>This protocol for a randomized controlled trial aims to evaluate the impact of exercise frequency on muscle strength, balance, and fall risk among institutionalized older adults. Recognizing the unique physical and functional limitations of this population, the study will test whether two or three weekly sessions of multicomponent exercise yield differential outcomes. Sixty participants residing in nursing homes will be randomly assigned to one of two groups: a control group performing exercise twice weekly and an experimental group training three times weekly, over a 12-week intervention period. All sessions will follow international guidelines for older adults, incorporating aerobic, strength, balance, and flexibility training at light-to-moderate intensity. Primary outcomes include lower- and upper-body strength and dynamic balance; secondary outcomes comprise waist circumference, body mass index, and fall incidence. The program is designed with progressive adaptation and safety in mind, employing the Talk Test to regulate intensity and standardized measures to monitor physiological responses. The rationale stems from the gap in existing literature regarding optimal exercise frequency for institutionalized populations. While two sessions per week have been associated with functional improvements, it remains unclear whether an additional weekly session provides significant incremental benefits. By isolating frequency as the primary variable, the trial addresses the need to define the minimum effective dose of structured exercise for enhancing physical activity, functional capacity, and reducing fall risk. Results are expected to inform tailored physical activity guidelines and implementation strategies in long-term care settings, balancing clinical efficacy with feasibility and safety constraints typical of institutional environments.</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"213 ","pages":"Article 112985"},"PeriodicalIF":4.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145673237","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}

{"title":"Social isolation and intrinsic capacity decline in older adults: Mediating roles of sleep duration and pain","authors":"Wenhua Yu ,&nbsp;Yaru Zhou ,&nbsp;Xvyan Gao ,&nbsp;Jiayu Han ,&nbsp;Li Zhang ,&nbsp;Lina Ma","doi":"10.1016/j.exger.2025.112991","DOIUrl":"10.1016/j.exger.2025.112991","url":null,"abstract":"<div><h3>Background</h3><div>The decline of intrinsic capacity is a key determinant of healthy aging. While social isolation is recognized as a risk factor for functional deterioration in older adults, the pathways through which it influences intrinsic capacity, particularly via sleep duration and pain, remain underexplored.</div></div><div><h3>Objectives</h3><div>To evaluate the association between social isolation and intrinsic capacity in older adults, and to assess whether sleep duration and pain complaints mediate this relationship.</div></div><div><h3>Methods</h3><div>Data were obtained from the 2011 wave China Health and Retirement Longitudinal Study (CHARLS). Intrinsic capacity was assessed across five domains: locomotion, vitality, cognition, psychology, and sensory. Social isolation was measured using a composite index incorporating marital status, living arrangements, contact with children, and social participation. Logistic regression was used to examine the association between social isolation and intrinsic capacity. Mediation analyses were performed using multiple linear regression to estimate the mediating roles of sleep duration and pain complaints.</div></div><div><h3>Results</h3><div>Among 2451 participants, 1897 (77.4 %) exhibited decline in at least one intrinsic capacity domain. Prevalence of decline by domain was: locomotion (23.3 %), vitality (18.9 %), cognition (46.7 %), psychology (26.9 %), and sensory (44.2 %). 877 participants (35.8 %) were identified as socially isolated. After adjustment for sociodemographic and health-related factors, social isolation was associated with increased odds of intrinsic capacity decline. Furthermore, social isolation was positively correlated with decline in intrinsic capacity, with both sleep duration and pain complaints serving as mediators in this relationship.</div></div><div><h3>Conclusions</h3><div>In this nationally representative sample of Chinese older adults, social isolation is associated with greater decline of intrinsic capacity, partially mediated through inadequate sleep duration and pain complaints. These findings suggest that interventions aimed at mitigating social isolation, along with integrated management of sleep and pain, may help preserve intrinsic capacity in aging populations.</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"213 ","pages":"Article 112991"},"PeriodicalIF":4.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145746209","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}

{"title":"Optimizing recovery after a hip fracture: Protocol of a randomized controlled trial to study the effects, costs, and cost-effectiveness of a combined protein and exercise intervention in older adults after a hip fracture (ProBUS study)","authors":"Emma Treijtel ,&nbsp;Hugo H. Wijnen ,&nbsp;Nienke M.S. Golüke ,&nbsp;Marian A.E. de van der Schueren ,&nbsp;Lisette C.P.G.M. de Groot ,&nbsp;Inge Groenendijk","doi":"10.1016/j.exger.2025.112999","DOIUrl":"10.1016/j.exger.2025.112999","url":null,"abstract":"<div><h3>Background</h3><div>Hip fractures are common among older adults and typically occur alongside accumulating comorbidities and age-related musculoskeletal decline. While nutritional or exercise interventions can support recovery, the effect of a combined approach during rehabilitation remains unclear. This study aims to evaluate the effects, costs, and cost-effectiveness of a high-protein diet plus exercise intervention on functional recovery after a hip fracture.</div></div><div><h3>Methods</h3><div>This randomized controlled trial will include 102 older adults (≥65 years) recovering in a rehabilitation centre after a hip fracture. Participants will be randomly assigned (1:1) to the intervention or control group, stratified by sex and hospital. The intervention group will receive weekly dietitian support to comply with a high-protein diet (≥1.2 g/kg body weight/day) and will participate in progressive resistance exercise training twice weekly for 3 months. The control group will receive usual care. Due to the nature of the intervention, participant and staff blinding is not feasible, but analyses will be performed blinded. Measurements will be performed in the first week after surgery, at rehabilitation discharge, and 3 months after baseline. The primary outcome is physical functioning using the Short Physical Performance Battery. Secondary outcomes include handgrip strength, muscle mass, bone density, quality of life, daily functioning, nutritional status, bone metabolism biomarkers, and costs.</div></div><div><h3>Discussion</h3><div>The intervention is expected to enhance recovery, attenuate postoperative bone and muscle loss, and improve quality of life. Implementation into standard care could improve efficiency and cost-effectiveness.</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"213 ","pages":"Article 112999"},"PeriodicalIF":4.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145800828","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}

{"title":"Disentangling the overlap between frailty and intrinsic capacity in older adults","authors":"Yuwei Qi ,&nbsp;Natasja M. van Schoor ,&nbsp;Laura A. Schaap ,&nbsp;Emiel O. Hoogendijk","doi":"10.1016/j.exger.2025.113006","DOIUrl":"10.1016/j.exger.2025.113006","url":null,"abstract":"<div><h3>Introduction</h3><div>It has been suggested that two prominent frameworks in geriatrics, frailty and intrinsic capacity (IC), represent two opposite ends of the same continuum. Frailty quantifies accumulated deficits and vulnerability, and IC measures an individual's capacities and functional reserves. This study investigates the overlap between frailty and IC in a large cohort of older adults.</div></div><div><h3>Methods</h3><div>We analysed 3246 participants aged 55+ from the Longitudinal Aging Study Amsterdam. Participants were categorised into four groups: neither frail nor low IC, low IC only, frail only, and both frail and low IC. Overlap was examined across age groups. Domain scores (vitality, sensory, cognition, psychology, locomotion) were compared between groups.</div></div><div><h3>Results</h3><div>Among 57–59 year olds, only 2.2 % were both frail and had low IC. This proportion increased with age, reaching 53.6 % at ages 87–89, while the “frail only” and “low IC only” groups declined. Overlap between frailty and domain scores showed that the “Neither” group consistently had the highest IC scores across all five domains, while the “Both” group consistently had the lowest scores.</div></div><div><h3>Conclusions</h3><div>In later life, being frail does not necessarily imply low IC, and vice versa. Frailty and low IC identify different groups in early older age, but the overlap between them becomes more pronounced with increasing age. Comprehensive assessment of ageing therefore requires measures that capture both vulnerability to decline and capacity.</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"213 ","pages":"Article 113006"},"PeriodicalIF":4.3,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145790653","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}

{"title":"Bidirectional associations between metabolic syndrome and epigenetic age acceleration: A 20-year longitudinal study in midlife adults","authors":"Hye-Young Park ,&nbsp;Kyeezu Kim","doi":"10.1016/j.exger.2025.113017","DOIUrl":"10.1016/j.exger.2025.113017","url":null,"abstract":"<div><h3>Introduction</h3><div>Metabolic syndrome (MetS) increases with age. Epigenetic alterations reflect lifelong biological and environmental influences on aging. MetS may contribute to epigenetic age acceleration (EAA) through inflammation and oxidative stress, while elevated EAA may, in turn, exacerbate metabolic dysfunction, but long-term evidence for this bidirectional association is limited.</div></div><div><h3>Methods</h3><div>We analyzed data from 1452 participants in the Korean Genome and Epidemiology Study at baseline (Wave 1), 10-year (Wave 5), and 20-year (Wave 10) follow-ups. MetS severity was defined by the number of diagnostic criteria, and DNA methylation-based EAA measures (PhenoAA, Grim2AA, DunedinPACE) at Wave 5 were included. Multivariable linear regression models examined the association between MetS and EAA both cross-sectionally (at Wave 5) and longitudinally (Wave 1 MetS – Wave 5 EAA and Wave 5 EAA – Wave 10 MetS). Mediation analysis examined whether EAA mediated the association between MetS severity across waves. All models were adjusted for chronological age, sex, smoking, drinking, physical activity, education, income, and body mass index.</div></div><div><h3>Results</h3><div>Cross-sectionally, all EAA measures were associated with higher MetS severity score (β ranged 0.37–1.26, all <em>P</em> &lt; 0.05). Longitudinally, earlier MetS severity was associated with EAA (Grim2AA: β = 0.25; DunedinPACE: β = 0.78, all <em>P</em> &lt; 0.05) and EAA was associated with later MetS severity (Grim2AA: β = 0.03; DunedinPACE: β = 0.01, all <em>P</em> &lt; 0.05). EAA partially mediated the association between earlier and later MetS severity (1.6–3.1 % mediation proportion, <em>P</em> &lt; 0.05).</div></div><div><h3>Conclusion</h3><div>Our findings suggest a bidirectional relationship between MetS and EAA, with biological aging potentially mediating metabolic deterioration. EAA may serve as both a marker and mediator of metabolic health, and a promising target for prevention and intervention.</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"214 ","pages":"Article 113017"},"PeriodicalIF":4.3,"publicationDate":"2025-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145879782","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}

{"title":"Ginsenoside Rb1 attenuates arterial aging by reducing DNA damage in aged mice","authors":"Qi Si ,&nbsp;Lin Wu ,&nbsp;Ximei Zhang ,&nbsp;Guangyao Shi ,&nbsp;Yingying Zhao ,&nbsp;Yong Liu ,&nbsp;Baoshun Hao ,&nbsp;Shujie Yu ,&nbsp;Bin Zhou ,&nbsp;Yanling Zhang ,&nbsp;Xiaoxian Qian ,&nbsp;Dinghui Liu ,&nbsp;Jianrui Zheng","doi":"10.1016/j.exger.2025.113011","DOIUrl":"10.1016/j.exger.2025.113011","url":null,"abstract":"<div><h3>Objective</h3><div>Vascular aging is a critical risk factor for the development and progression of cardiovascular diseases. Age-related degenerative changes in vascular structure and function significantly promote the onset of various vascular disorders. Currently, the specific molecular mechanisms underlying age-associated vascular structural and functional decline have not been fully elucidated. Ginsenoside Rb1 (Rb1), as the primary active component of ginseng, has been confirmed to possess potential anti-aging properties. This study aims to investigate the protective effects of Rb1 on the aorta in aged mice and its underlying molecular mechanisms, thereby providing experimental evidence and theoretical support for the screening of natural anti-vascular aging drugs.</div></div><div><h3>Methods</h3><div>Naturally aged (72-week-old) male C57BL/6J mice were randomly divided into two groups (<em>n</em> = 5 per group) to receive intraperitoneal injections of either PBS (Old group) or 20 mg/kg Rb1 (Old + Rb1 group) for 6 weeks. Young mice (12-week-old, n = 5) served as controls. Aortic tissues were analyzed using histomorphology (hematoxylin and eosin, H&amp;E), nanoscale biomechanics (Atomic Force Microscopy, AFM), senescence biomarkers (P21 immunofluorescence, SA-β-gal staining), apoptosis (TUNEL assay), and DNA damage (γ-H2AX).</div></div><div><h3>Results</h3><div>Compared to the Old group, Rb1 significantly alleviated structural remodeling of the aging aorta, restoring smooth muscle cell alignment and extracellular matrix. AFM analysis showed that Rb1 ameliorated the aging-induced impairments in nanobiomechanical properties (including elasticity, viscosity, and surface topography) induced by aging. Furthermore, Rb1 treatment downregulated the expression of P21 in the aorta, reduced the positive area percentage of SA-β-gal positivity, and decreased the proportion of TUNEL-positive apoptotic cells, although none of these indicators were comparable to the levels observed in the Young control group. Notably, Rb1 significantly alleviates the elevation of γ-H2AX (a marker of DNA double-strand breaks) in the aging aorta.</div></div><div><h3>Conclusion</h3><div>This study demonstrates that Rb1 attenuates DNA damage, thus ameliorating structural remodeling and biomechanical function of the aging aorta, and delaying vascular aging and apoptosis. Our findings suggest that Rb1 counteracts age-related aortic impairment, potentially by targeting the DNA damage pathway, which highlights its therapeutic potential against vascular aging.</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"214 ","pages":"Article 113011"},"PeriodicalIF":4.3,"publicationDate":"2025-12-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145829423","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}

{"title":"Exploring senescence markers as potential drivers of osteoarthritis pain in aging adults","authors":"Muhammad Abbas ,&nbsp;Carlos J. Cruz ,&nbsp;Javier A. Tamargo ,&nbsp;Ania L. Lipat ,&nbsp;Rameesha Fareed ,&nbsp;Laurel Deaton ,&nbsp;Carson Gordon ,&nbsp;Alisa Johnson ,&nbsp;Blanka Sharma ,&nbsp;Christiaan Leeuwenburgh ,&nbsp;Kyle D. Allen ,&nbsp;Yenisel Cruz-Almeida","doi":"10.1016/j.exger.2025.112950","DOIUrl":"10.1016/j.exger.2025.112950","url":null,"abstract":"<div><div>Senescent cells (SnCs) contribute to various age-related diseases, such as osteoarthritis (OA), a degenerative joint condition that causes persistent pain and reduces physical functioning in older adults. The pathogenesis of OA includes subchondral bone remodeling, synovial inflammation, and cartilage breakdown. Cellular senescence, particularly the pro-inflammatory senescence-associated secretory phenotype (SASP), may have a pivotal role in the progression of OA. SASP factors could exacerbate OA by releasing inflammatory cytokines, chemokines, and proteases, which sensitize nociceptors and accelerate degenerative joint processes, thereby contributing to the chronic pain experienced by OA patients. This contribution of SASPs in chronic pain may lead to mobility limitations and decreased independence of individuals. Thus, the interplay between SASP-driven inflammation and OA pathogenesis may be critical for understanding knee OA pain and functional impairment in older adults. Here, we aim to discuss the parallels between SASP-driven inflammation and OA pathophysiology, which could identify novel therapeutic targets for improving pain management and treatment outcomes in OA.</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"212 ","pages":"Article 112950"},"PeriodicalIF":4.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145427234","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}

{"title":"Research hotspots and trends in animal experiments on mild cognitive impairment","authors":"Qifang Liang ,&nbsp;Buping Liu ,&nbsp;Bingfeng Xing","doi":"10.1016/j.exger.2025.112944","DOIUrl":"10.1016/j.exger.2025.112944","url":null,"abstract":"<div><h3>Objective</h3><div>This study aimed to map the knowledge structure, evolutionary trends, and research frontiers in animal experiments on Mild Cognitive Impairment (MCI) from 2014 to 2025 using a bibliometric approach.</div></div><div><h3>Methods</h3><div>We retrieved 1520 relevant articles from the Web of Science Core Collection. CiteSpace software was employed to analyze publication trends, collaboration networks (countries, institutions, authors), keyword co-occurrence, clustering, and citation bursts. Metrics such as frequency, betweenness centrality, and burst strength were used to identify significant patterns.</div></div><div><h3>Results</h3><div>Annual publications peaked in 2017 before entering a plateau. The United States and China were the most productive countries, with the strongest collaborative link. Research focus has evolved from foundational pathology (Aβ, tau) to mechanisms like oxidative stress and, more recently, to neuroinflammation, the gut-brain axis, mitophagy, and exosomes, as indicated by strong citation bursts (e.g., neuroinflammation burst strength = 7.89). Keyword and cluster analysis confirmed this shift towards systems-level biology.</div></div><div><h3>Conclusion</h3><div>This analysis delineates the dynamic landscape of MCI animal research, highlighting a clear transition from molecular to systems biology. The identified hotspots and collaboration patterns offer valuable insights for guiding future research directions and fostering strategic partnerships in the field.</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"212 ","pages":"Article 112944"},"PeriodicalIF":4.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145427263","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}

{"title":"Dehydroepiandrosterone opposes cardiac aging via NFκB/IL-10/Sirt1/Nrf2 mediated pathway in aged rats","authors":"Yahya M. Naguib ,&nbsp;Mohamed S. Rizk ,&nbsp;Reda A. A. Abo-Elsoud","doi":"10.1016/j.exger.2025.112968","DOIUrl":"10.1016/j.exger.2025.112968","url":null,"abstract":"<div><h3>Background</h3><div>Cardiovascular aging is characterized by structural and functional deterioration of the heart, mediated by chronic inflammation, oxidative stress, and impaired cellular defense pathways. Dehydroepiandrosterone (DHEA), a steroid hormone with known anti-inflammatory and antioxidant properties, declines with age and may have therapeutic potential in ameliorating cardiac aging. The aim of the present study was to test the hypothesis that replenishing DHEA can counter the age dependent decline in cardiac functions. The possible underlying mechanisms were also tested.</div></div><div><h3>Methods</h3><div>Thirty male Wistar rats were divided into three groups: control, aged, and aged treated with DHEA (30 mg/kg/day via intraperitoneal injection for 4 weeks). Cardiovascular parameters (SBP, DBP, HR), biomarkers of myocardial insult (troponin I, CK-MB, myoglobin, LDH, and GP-BB), cardiac performance (lactic acid and treadmill endurance test), markers for inflammation (NFκB and IL-10) and oxidative stress (MDA and TAC), and the gene expression of NFκB, IL-10, Sirt1 and Nrf2 were assessed.</div></div><div><h3>Results</h3><div>Aging was associated with significant increases in SBP, DBP, HR, serum levels of myocardial injury markers, lactic acid, NFκB and MDA, and cardiac muscle NFκB gene expression. Aging was also associated with reduced cardiovascular endurance, serum levels of IL-10 and TAC, as well as cardiac muscle IL-10 Sirt1 and Nrf2 gene expression. Administration of DHEA significantly improved all affected parameters compared to untreated aged rats. Nevertheless, control-comparable values were not achieved. Notably, DHEA downregulated cardiac muscle NFκB while it upregulated IL-10, Sirt1, and Nrf2 gene expression, suggesting a possible common anti-inflammatory/antioxidant pathway.</div></div><div><h3>Conclusion</h3><div>DHEA supplementation in aged rats mitigated cardiovascular aging by improving hemodynamic parameters, reducing myocardial injury, demoting inflammation, enhancing antioxidant capacity, and activating key protective genes. Our findings support a potential therapeutic value of DHEA in modulating age-dependent decline in cardiac functions through a possible NFκB/IL-10/Sirt1/Nrf2 pathway.</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"212 ","pages":"Article 112968"},"PeriodicalIF":4.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145531069","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}

{"title":"Neurodegeneration and glial activation related blood biomarkers in Alzheimer's disease: A systematic review and an updated meta- analysis","authors":"Rasoul Ebrahimi ,&nbsp;Amir Abbas Salehi Amniyeh Khozani ,&nbsp;Mohammad Mahdi Masouri ,&nbsp;Mojtaba Seifi ,&nbsp;Anahita Hashempoor ,&nbsp;Sana Mohammad Soltani ,&nbsp;Shokoofe Noori","doi":"10.1016/j.exger.2025.112960","DOIUrl":"10.1016/j.exger.2025.112960","url":null,"abstract":"<div><h3>Background and objectives</h3><div>This systematic review and meta-analysis aims to evaluate blood biomarkers associated with neurodegeneration and glial activation, specifically GFAP, NfL, YKL-40, MCP-1, neurogranin, GAP-43, S100B, and NSE, in individuals diagnosed with Alzheimer's Disease (AD).</div></div><div><h3>Methods</h3><div>PubMed and Web of Science were searched until February 20, 2025, without restrictions on language, time, or study design, to identify studies reporting blood levels of the biomarkers in individuals along the AD continuum (including those with MCI and AD dementia) and cognitively unimpaired (CU) controls. Pooled effect sizes were calculated using the Hedges' g method with a random-effects model.</div></div><div><h3>Results</h3><div>A total of 3684 studies were identified, with 144 meeting inclusion criteria (AD continuum <em>n</em> = 42,587, CU <em>n</em> = 30,000). Compared with CU individuals, patients on the AD continuum showed higher levels of NfL (SMD = 0.82, 95 % CI 0.67–0.96, <em>p</em> &lt; 0.05), GFAP (SMD = 1.57, 95 % CI 1.26–1.88, p &lt; 0.05), and YKL-40 (SMD = 1.39, 95 % CI 0.56–2.21, p &lt; 0.05). Both biomarkers were significantly elevated in more advanced stages of the disease, particularly in AD dementia compared with mild cognitive impairment (MCI) (GFAP SMD = 0.79, 95 % CI 0.55–1.03, <em>p</em> &lt; 0.05; YKL-40 SMD = 0.98, 95 % CI 0.17–1.79, <em>p</em> = 0.02). No significant differences were found for MCP-1, neurogranin, S100B, or NSE.</div></div><div><h3>Discussion</h3><div>Our findings suggest that these biomarkers reflect AD-related pathology. Limitations include the lack of cultural and linguistic diversity in the study populations. Future research should focus on biomarker-defined AD populations for further validation</div></div>","PeriodicalId":94003,"journal":{"name":"Experimental gerontology","volume":"212 ","pages":"Article 112960"},"PeriodicalIF":4.3,"publicationDate":"2025-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145534151","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}