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        <title>Frontiers in Aging | New and Recent Articles</title>
        <link>https://www.frontiersin.org/journals/aging</link>
        <description>RSS Feed for Frontiers in Aging | New and Recent Articles</description>
        <language>en-us</language>
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        <pubDate>2026-08-26T02:26:58.683+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1882462</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1882462</link>
        <title><![CDATA[Adaptive immune cells and kidney function in older adults: sex-specific associations in the health and retirement study (HRS)]]></title>
        <pubdate>2026-08-25T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Shannon M. Sullivan</author><author>Bibin Joseph</author><author>Shweta Sharma</author><author>Weihua Guan</author><author>Amy B. Karger</author><author>Jessica Faul</author><author>Bharat Thyagarajan</author>
        <description><![CDATA[BackgroundChronic kidney disease (CKD) is characterized by chronic inflammation and immune dysregulation. Aging of the adaptive immune system, marked by a shift from naïve to memory T-cell phenotypes, is associated with systemic “inflammaging”, but sex-specific associations between these immunophenotypes and kidney function in older adults remain poorly understood.MethodsWe analyzed cross-sectional data from 8,970 participants (aged ≥56 years) in the 2016 Health and Retirement Study (HRS) Venous Blood Study. Seventeen adaptive immune cell subsets were quantified using multiparameter flow cytometry. Kidney function was assessed using estimated glomerular filtration rate (eGFR, mL/min/1.73 m2) calculated from the 2021 race-free CKD-EPI creatinine-cystatin C equation. Survey-weighted linear regression models were adjusted for age, race/ethnicity, education, body-mass index (BMI), clinical comorbidities (diabetes, elevated blood pressure/hypertension), alcohol use, smoking status, and cytomegalovirus (CMV) serostatus. Sex-stratified analyses were conducted a priori, and sex interaction terms were evaluated to assess effect modification.ResultsFemales were older and more likely to be never smokers, CMV seropositive, and have lower eGFR, whereas males were more likely to use alcohol, smoke, have diabetes, elevated blood pressure/hypertension and higher educational attainment. In sex-stratified models, higher CD4+ T cells (β = 0.96, PFDR = 0.010), CD8+ naïve T cells (β = 0.87, PFDR = 0.026), Ratio of CD4+ to CD8+ T cells (β = 0.73, PFDR = 0.036), and lymphocytes (β = 2.42, PFDR<0.001) were associated with higher eGFR (higher kidney function) in females, while higher CD4+ effector memory T cells (Tem; β = −1.58, PFDR = 0.010), CD8+ effector T cells (Teff; β = −1.00, PFDR = 0.004), and CD8+ Tem (β = −1.40, PFDR = 0.002) were associated with lower eGFR (lower kidney function). In males, higher IgD + memory B cells (β = 1.01, PFDR = 0.005), IgD− memory B cells (β = 1.04, PFDR = 0.011), and lymphocytes (β = 2.08, PFDR<0.001) were associated with higher eGFR. Significant sex interaction was observed for CD8+ Tem (PFDR = 0.015), with a nominal interaction for CD8+ Teff (PFDR = 0.060). Associations were similar in sensitivity analyses and were not modified by CMV serostatus.ConclusionFindings suggest that CD8+ Tem and Teff T cells may serve as sex-specific biomarkers of renal vulnerability in postmenopausal females and underscore the need for longitudinal and mechanistic studies to clarify underlying pathways.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1888854</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1888854</link>
        <title><![CDATA[Repair and regeneration across the lifespan: an ontogenetic perspective]]></title>
        <pubdate>2026-08-24T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Hugo A. Barrera-Saldaña</author><author>Luis E. Fernández-Garza</author><author>Fernando Guillen-Silva</author><author>Oscar R. Fajardo-Ramirez</author><author>Rafael Francisco Iñigo Pavlovich</author><author>Fermín Valenzuela Gómez-Gallardo</author><author>David E. Rodriguez-Fuentes</author><author>Alexia Y. Avila-Villalobos</author><author>Silvia A. Barrera-Barrera</author><author>Rodrigo A. Somoza</author>
        <description><![CDATA[The capacity for tissue repair and regeneration undergoes a profound and progressive decline across the human lifespan, representing a fundamental driver of aging and chronic disease. This review establishes a comprehensive ontogenetic framework by mapping the continuous biological transition from the flawless, scarless regenerative plasticity of embryonic development to the irreversible fibrotic scarring and organ failure characteristic of senescence. We synthesize the hierarchical collapse of reparative networks across multiple biological scales. Importantly, this ontogenetic decline should not be interpreted as a purely degenerative trajectory but rather as a dynamic systems-level reprogramming in which evolutionary trade-offs prioritize tumor suppression, immune surveillance, and reproductive fitness over long-term regenerative fidelity. Recognizing this adaptive reallocation of biological resources reframes aging not simply as failure but as a predictable recalibration of repair hierarchies. At the molecular and cellular levels, the accumulation of genomic instability, unresolvable DNA damage, and mitochondrial dysfunction gradually overwhelms intracellular quality-control mechanisms. Concurrently, epigenetic drift and chronic, low-grade systemic inflammation (“inflammaging”) dismantle the stem cell niche, driving adult stem cell exhaustion and shifting wound healing away from functional tissue replacement toward maladaptive fibrosis. Furthermore, we examine divergent, organ-specific repair trajectories. By contrasting the severe regenerative restrictions of the adult central nervous system and myocardium with the persistent, yet exhaustible, resilience of the liver, we elucidate the unique intrinsic and microenvironmental barriers that impede structural and functional recovery. Finally, we evaluate the clinical paradigm shift from passive management of age-related degeneration to active restoration of tissue integrity. By integrating systemic geroscience—which addresses the global hallmarks of aging—with targeted bioengineering and in vivo epigenetic modulation, contemporary regenerative medicine seeks to recreate permissive, youthful microenvironments. Ultimately, mastering these ontogenetic principles holds unprecedented potential to reactivate endogenous repair pathways, mitigate multi-organ collapse, and significantly extend human functional healthspan.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1803413</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1803413</link>
        <title><![CDATA[Sexual health needs and challenges among ageing women in Sub-Saharan Africa: a systematic review]]></title>
        <pubdate>2026-08-21T00:00:00Z</pubdate>
        <category>Systematic Review</category>
        <author>Redson Mwandama</author><author>Yankho Henry Mdoka</author><author>Oudry Mulinde</author><author>Margubur Rahaman</author>
        <description><![CDATA[BackgroundThe global ageing population is growing rapidly, with Sub-Saharan Africa undergoing a significant demographic transition. Although research on general ageing-related health outcomes in the region, such as frailty, multimorbidity, and socioeconomic deprivation, has expanded in recent years, the sexual health needs of ageing women remain comparatively understudied and inadequately addressed. This systematic review synthesizes evidence regarding the sexual health needs, challenges, and reproductive health concerns of ageing women in Sub-Saharan Africa.MethodsScopus and PubMed databases were used to search, select, and review the publication records between 1 January 2000 and 26 May 2026. Sexual or reproductive health of women framed as ageing, older, elderly, menopausal, or postmenopausal in Sub-Saharan Africa studies were included. The PRISMA 2020 guidelines were followed for study selection and reporting. Data extraction and quality assessment were performed systematically.ResultsA total of 358 records identified across Scopus and PubMed, 34 studies met the eligibility criteria and were included in the review. Six themes were identified: patterns and predictors of sexual activity in later life; menopausal symptom burden and sexual dysfunction; the intersection of HIV status and reproductive ageing; socio-cultural norms and the culture of silence; contraceptive needs and fertility ambivalence; and health-seeking behaviour and systemic barriers. Ageing women encounter multiple intersecting challenges, including age-related physiological changes, socio-cultural marginalisation, and inadequate responses from health systems.ConclusionSexual health needs of ageing women in Sub-Saharan Africa remain largely overlooked in research, policy, and healthcare delivery. There is an urgent need for age-sensitive sexual and reproductive health services, training for healthcare providers, and policy frameworks that acknowledge and address the unique needs of this population. Future research should prioritise empirical studies that highlight the lived experiences of ageing women and evaluate interventions aimed at enhancing their sexual health and wellbeing.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1903105</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1903105</link>
        <title><![CDATA[PolyPIMuse significantly increases fall risk: comparison of three medication evaluation tools]]></title>
        <pubdate>2026-08-21T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>András Érszegi</author><author>Réka Viola</author><author>Bettina Vargáné Szabó</author><author>Zsófia Engi</author><author>Mária Matuz</author><author>Ria Benkő</author><author>Zoltán Pető</author><author>Dezső Csupor</author>
        <description><![CDATA[IntroductionFalls are a leading cause of injury and hospitalization in older adults, with pharmacotherapy identified as a modifiable risk factor. Tools for identifying potentially inappropriate medications (PIMs), such as the EU(7)PIM, PRISCUS, and FORTA lists, differ in methodology. However, their comparative performance in predicting fall risk has not been systematically evaluated. The aim of our work was to investigate the association between PIM use and fall risk among older adults and to analyze the correlations between PIM utilization based on three PIM lists (EU(7)PIM, PRISCUS, and FORTA C/D) and fall risk.MethodsIn a retrospective case -control study based on real-world data from Hungarian emergency and primary care settings, we analyzed fall-related emergency department visits (n=886) in individuals aged ≥65 years and matched them with a control group from general practices (n = 1364).ResultsUse of PIMs identified by all three lists was significantly associated with increased fall risk. (Use of 1 FORTA C/D active substance: AOR: 1.434; CI95%:1.120–1.838; p = 0.004; Use of 1 EU(7)PIM active substance: AOR: 1.201; CI95%: 0.907–1.591; p = 0.200; Use of 1 PRISCUS active substance: AOR: 1.390; CI95%:1.069–1.808; p = 0.014) Of the three lists, use of drugs on the PRISCUS list was most significantly associated with increased fall risk. (Use of 2 PRISCUS active substance: AOR: 1.557; CI95%:1.148–2.114; p = 0.004; Use of 3 PRISCUS active substance: AOR: 2.045; CI95%: 1.408–2.982; p = 0.000; Use of 4 PRISCUS active substance: AOR: 1.869; CI95%: 1.149–3.065; p = 0.012; Use of 5 PRISCUS active substance: AOR: 2.638; CI95%: 1.464–4.895; p = 0.002).DiscussionWe introduce the concept of “polyPIMuse” –the use of ≥5 PIM-listed drugs –which further elevated fall risk, particularly for PRISCUS and FORTA C/D lists. Despite methodological differences, all three PIM tools proved useful in predicting fall risk. Incorporating these tools into routine medication reviews may aid fall prevention strategies in geriatric care.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1910447</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1910447</link>
        <title><![CDATA[Collagen-induced restructuring of astrocytes and vessels in organotypic mouse brain slices]]></title>
        <pubdate>2026-08-20T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Eva Steiner</author><author>Valentin Wolfgang</author><author>Christian Humpel</author>
        <description><![CDATA[IntroductionThe brain exhibits high plasticity and responds to many forms of external stimuli, such as trauma, seizures, drugs, and biomaterials. Collagen is a non-toxic biocompatible protein that participates in the plastic reformation of the brain. In this study, we explored whether collagen can reconstruct astrocytes and brain vessels by using microcontact printing on organotypic mouse brain slices.MethodsOrganotypic brain slices from postnatal days 8–10 were prepared and connected to collagen microcontact prints. After 2–6 weeks, glial fibrillary acidic protein–positive (GFAP+) astrocytes and laminin+ vessels were immunohistochemically stained.ResultsOur data show that (1) collagen restructures laminin+ vessels in the whole brain slice along 50-µm-wide collagen lanes. (2) This restructuring is linked to the reformation of GFAP+ astrocytes in the collagen–laminin lanes. (3) In contrast to 50 µm lanes, larger 400-µm collagen spots caused a marked depletion forming large holes in the brain slice accompanied with the cell death of GFAP+ astroglia. (4) Preliminary/exploratory data using live cell imaging may indicate that astroglia restructure before the vessels.DiscussionCollagen has the distinctive potential to induce plasticity and the restructuring of vessels and astrocytes, however, collagen may also lead to cell death under certain conditions.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1856979</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1856979</link>
        <title><![CDATA[A minimal three-arm oral regimen for healthspan: mechanistic alignment with transcriptomic signals from a large parental-lifespan GWAS]]></title>
        <pubdate>2026-08-19T00:00:00Z</pubdate>
        <category>Hypothesis and Theory</category>
        <author>Ngo Cheung</author>
        <description><![CDATA[A large genome-wide association study of parental lifespan was reported in 2019. A later transcriptome-wide association study (TWAS) based on those summary statistics identified a set of transcriptional programs associated with longer genetically predicted survival, including increased brain NAD + salvage, especially NMNAT2, reduced glucose-stimulated insulin secretion, a shift toward synaptic pruning with less broad plasticity, and a glial pattern characterized by relatively greater microglial and lower astrocytic signatures, with only weak pan-tissue senescence signals. Building on those directional findings, this short communication proposes a minimal three-arm oral regimen with unequal evidentiary weight: first, the Cheung Glutamatergic Regimen, consisting of low-dose dextromethorphan potentiated by a CYP2D6 inhibitor together with piracetam and L-glutamine, as an exploratory adjunct aimed at preserving residual functional connectivity; second, daily nicotinamide mononucleotide and N-acetylcysteine with pulsed senolytics for NAD + salvage and senescence modulation; and third, GLP-1 receptor agonism for metabolic reprogramming. The NAD+/senescence arm is the primary mechanistic anchor, GLP-1 receptor agonism provides secondary metabolic support, and the glutamatergic arm is exploratory. Each arm targets a separate node within the pruning-plasticity-metabolic triad. The regimen is fully oral, uses conservative dosing, and draws on prior therapeutic or human-exposure data, although the proposed combination has no established safety profile. Although direct combination data are lacking and the foundational TWAS remains a preprint, the components show plausible but uneven mechanistic alignment with the TWAS signals and may justify carefully designed, safety-focused pilot evaluation.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1898942</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1898942</link>
        <title><![CDATA[Editorial: Nutritional strategies for enhancing longevity and healthy aging]]></title>
        <pubdate>2026-08-18T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Pintu Choudhary</author><author>Pratik S. Gaikwad</author><author>Harsh B. Jadhav</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1734620</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1734620</link>
        <title><![CDATA[Baseline cognitive status and adherence are associated with cognitive change following language learning in older adults: an exploratory study]]></title>
        <pubdate>2026-08-17T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ladan Ghazi Saidi</author><author>Zoha Deldar</author><author>Ricardo Carrillo-Meza</author><author>Kiley Allgood</author><author>Alison Gansemer</author><author>Mariah Gentz</author><author>Amor Sofia Calderón-Hernández</author><author>Yunju Im</author><author>Cary R. Savage</author><author>Douglas H. Schultz</author>
        <description><![CDATA[IntroductionGiven cognitive benefits observed in lifelong bilinguals, a key question is whether L2 learning can boost cognition in later life.MethodsIn a pre–post intervention study, we assessed cognitive effects of learning a new language in older adults as measured by global cognition and domain-specific cognitive tests.Results and DiscussionWhile the MMSE, MoCA, and domain-specific measures (Stroop, Simon, nonword repetition, phonemic fluency, and semantic fluency) did not show significant whole-group pre-post change, a number of individual participants improved on all or some of these measures. Further, both linear regression and machine learning models indicated that participants with lower baseline scores on the MMSE, MoCA, phonemic fluency, and semantic fluency showed greater improvement in post-intervention measurements, reflecting greater cognitive gains, with phonemic fluency emerging as the best predictor of intervention outcome. A post hoc, adherence-sensitive analysis further indicated a +1.225-point MoCA advantage in completers relative to non-completers, consistent with an adherence-associated pattern. Machine learning analyses confirmed that cognitive gains were heterogeneous across participants and that the most responsive outcomes were reaction-time-based executive measures, particularly the Stroop task and Symbol Digit Substitution Test (SDST). Cluster analysis showed that the top improver profile combined lower baseline executive performance with markedly higher engagement and lesson completion.ConclusionThese results provide preliminary evidence that engagement in a structured and sustained L2-learning program may be associated with measurable pre–post cognitive changes in some older adults, especially when baseline performance leaves room for improvement. Further, high intervention adherence and engagement are critical to the extent of cognitive benefits derived from L2 learning interventions. Clinically, structured language learning programs that emphasize adherence, dose, and fidelity appear promising for older adults, especially those with emerging decline. These results are noteworthy, given the scarcity of effective options to improve cognitive health in aging, and the fact that L2 learning is low-cost and broadly accessible.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1929624</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1929624</link>
        <title><![CDATA[Mesenchymal stem cell senescence as a potency brake: causes, consequences, and cures]]></title>
        <pubdate>2026-08-17T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Sen Zhou</author><author>Yu Xie</author><author>Yanjie Guo</author><author>Yufu Zhang</author><author>Yusi Liu</author>
        <description><![CDATA[Mesenchymal stem cells (MSCs) are widely investigated for regenerative medicine, tissue repair, immunomodulation, and selected cancer-related applications because of their multilineage differentiation potential, paracrine activity, immunoregulatory properties, and capacity to home to sites of injury. However, the therapeutic potential of MSCs depends not only on their tissue source or surface-marker expression but also on their functional state. MSC senescence is not a single phenotypic alteration; rather, it reflects the combined effects of persistent DNA damage response activation, disruption of mitochondrial and metabolic homeostasis, remodeling of epigenetic and secretory networks, and loss of proteostasis. Collectively, these changes drive MSCs toward reduced proliferative capacity, dysregulated paracrine signaling, impaired immunomodulatory activity, and diminished tissue-repair potential, thereby compromising cell-product potency and batch-to-batch consistency. This review summarizes the molecular mechanisms underlying MSC senescence, its source-specific functional consequences, and emerging rejuvenation strategies, with an emphasis on MSC quality control, potency assessment, and clinical translation.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1895104</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1895104</link>
        <title><![CDATA[Proteomics of aging: biomarkers for physiological systems and diseases]]></title>
        <pubdate>2026-08-14T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Ying Luo</author><author>Yu-Lin Xiao</author><author>Jie-Hua Chen</author><author>Hongjue Wang</author><author>Shuhong Luo</author><author>Hua Dong</author><author>Ruo-Pan Huang</author>
        <description><![CDATA[Aging is a progressive, multisystem process characterized by declining physiological resilience and increased susceptibility to chronic diseases. Recent advances in high-throughput proteomics have enabled comprehensive mapping of age-related changes across circulating proteins, revealing dynamic and non-linear trajectories that reflect biological rather than chronological aging. This review synthesizes current evidence on proteomic biomarkers across major physiological systems, including the immune, metabolic/endocrine, cardiovascular, musculoskeletal, and nervous systems, and highlights shared molecular signatures that underpin multisystem decline. Robust biomarkers such as IL-6, CRP, CXCL9/10, GDF15, IGF-1, VCAM-1, NT-proBNP, NfL, and GFAP consistently track inflammatory activation, mitochondrial and metabolic stress, extracellular matrix remodeling, and neuro-glial injury. Large population cohorts demonstrate that proteomic aging clocks, leveraging dozens to hundreds of circulating proteins, can predict frailty, multimorbidity, organ-specific biological age, and mortality with high accuracy. Emerging evidence suggests that a limited set of cross-system “protein aging modules”—including inflammatory cytokines, chemokines, complement proteins, and ECM-modifying enzymes—may serve as integrative readouts and potential regulators of aging biology. We discuss methodological advances, system-specific mechanisms, and translational applications of proteomic aging models. Together, these findings position proteomics as a powerful tool for quantifying biological age, identifying early disease risk, and guiding precision interventions to promote healthier aging.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1834323</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1834323</link>
        <title><![CDATA[From obesity to healthy longevity: a consensus-based clinical framework for diagnosis, staging, and treatment]]></title>
        <pubdate>2026-08-14T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Silvija Canecki-Varžić</author><author>Ines Bilić-Ćurčić</author><author>Maja Bakula</author><author>Tomislav Bulum</author><author>Maja Čavlović</author><author>Diana Delić-Brkljačić</author><author>Tamara Turk Wensveen</author><author>Daniela Fabris-Vitković</author><author>Dubravka Jurišić-Eržen</author><author>Sanja Klobučar</author><author>Kristina Kljajić</author><author>Mladen Krnić</author><author>Blaženka Miškić</author><author>Nataša Moser</author><author>Božidar Novoselović</author><author>Ivan Pećin</author><author>Tina Tičinović-Kurir</author><author>Jelena Vučak-Lončar</author><author>Marina Gradišer</author><author>Maja Cigrovski Berković</author><author>Gorana Mirošević</author><author>Kristina Selthofer-Relatić</author><author>Miro Bakula</author>
        <description><![CDATA[BackgroundObesity is a chronic, progressive, relapsing disease characterized by excess or dysfunctional adiposity that impairs health and contributes to multimorbidity, disability, and reduced life expectancy. Contemporary international frameworks recommend moving beyond BMI-only definitions toward disease-based diagnostic models that integrate adiposity, complications, and functional status. Croatia faces a high prevalence of obesity alongside constrained healthcare resources and limited reimbursement for modern pharmacotherapy, highlighting the need for nationally adapted clinical guidance.MethodsThis position statement was developed using a modified Delphi consensus process involving 23 multidisciplinary experts from academic and clinical institutions across Croatia. Consensus statements were derived from contemporary international guidelines, randomized controlled trials, and meta-analyses. Evidence quality and recommendation strength were graded using an adapted GRADE-based framework.ResultsThe document establishes a Croatia-specific framework for the diagnosis, staging, and management of obesity. Diagnosis requires confirmation of excess adiposity with evidence of clinical risk or dysfunction and integrates anthropometric measures with metabolic, mechanical, psychological, and functional domains. A staging system aligned with EASO and Lancet frameworks guides treatment intensity according to disease severity. Management is based on four pillars: lifestyle therapy, psychological support, pharmacotherapy, and metabolic/bariatric surgery. Pharmacological treatment is stage-based and comorbidity-driven, prioritizing agents with proven organ-protective effects. Special considerations are provided for older adults, emphasizing preservation of muscle mass, functional capacity, independence, and quality of life. Long-term structured follow-up is recommended for all patients, reflecting the chronic disease model of obesity.ConclusionThis position statement provides an evidence-based, nationally adapted clinical framework that aligns obesity management with modern chronic disease standards. By integrating disease staging, individualized therapy, and long-term care, it supports precision treatment across the lifespan and emphasizes obesity management as a key strategy for preventing complications, reducing disability, and promoting healthy longevity.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1780093</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1780093</link>
        <title><![CDATA[Intelligent health promotion system-based construction and implementation of exercise intervention for older adults with frailty and prefrailty]]></title>
        <pubdate>2026-08-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Mengya Liu</author><author>Li Zhang</author><author>Qin Huang</author><author>Xiaoli Zhu</author><author>Yu Wang</author><author>Lin Zhu</author>
        <description><![CDATA[BackgroundFrailty in the elderly population is increasing, and the development of high-quality clinical practice guidelines or consensuses can guide medical staff to better provide health services for frail elderly individuals. In recent years, scholars at home and abroad have actively explored exercise intervention management in elderly individuals with frailty or prefrailty. How to rapidly generalize interventions with “known and definite effects” for the community-dwelling frail elderly population is the core issue of the research on frailty. There is a lack of study regarding whether digital interventions can improve exercise adherence for older adults with frailty and prefrailty.ObjectiveIn accordance with the Comprehensive Framework for Implementation Research (CFIR), this study implemented scientific strategies for exercise interventions for elderly people with community frailty and prefrailty. Empirical research was conducted via the cloud platform of the home‒community integration system to provide a theoretical basis for improving the physical, psychological and social frailty of frail elderly people and reducing the incidence of adverse outcomes caused by frailty in the community.MethodsQualitative and quantitative research methods were fully integrated. Semistructured interviews were conducted with 64 older adults who designated family doctors and 44 community workers in the community to identify the regular exercise adherence of frail or prefrail older adults as well as the promoting and hindering factors of community workers in the implementation of scientific exercise interventions. Following the guidance of the Comprehensive Framework for Implementation Research (CFIR), scientific exercise intervention strategies for frail elderly people in the community were implemented. The control group received routine nursing, and the intervention group received a scientific nursing intervention. After 3 months of intervention, the effects of the strategy on implementation outcomes (feasibility, acceptability, fidelity, etc.), intervention outcomes (physical function, emotional state, social support, self-efficacy), process outcomes (skills or cognition), and resource utilization in older adults with frailty or prefrailty were evaluated.ResultsIn the qualitative interviews conducted with CFIR as the theoretical guiding framework, a total of 22 influencing factors, 12 promoting factors and 10 hindering factors in 4 areas were identified to construct scientific strategies for implementation。The implementation results revealed that the feasibility (P = 0.003), acceptability (P = 0.002) and fidelity (P = 0.001) of the intervention group were significantly better than those of the control group. The intervention results revealed that, compared with those in the control group, physical fitness (gait: P = 0.016; balance: P < 0.001; grip strength: P < 0.001; body fat percentage: P < 0.001), depression (P < 0.001), social support (P < 0.001), and self-efficacy (P < 0.001) significantly improved.ConclusionGuided by the implementation of the scientific theoretical framework, this study used a whole-process, systematic, diversified and scientific online and offline joint exercise implementation strategy, proving that the strategy can be used to create a safe, effective and sustainable exercise intervention for frail or prefrail elderly individuals in the community that effectively improves their physical fitness, depression, social support and self-efficacy, delays the progression of frailty, and reduces the incidence of adverse outcomes such as disability, falls, hospitalizations and even death.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1892852</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1892852</link>
        <title><![CDATA[Age-related differences in BMD response during three years of denosumab treatment]]></title>
        <pubdate>2026-08-13T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Koji Ishikawa</author><author>Tomoyuki Asada</author><author>William Richardson</author><author>Choiselle Marius</author><author>Mahoko Ishikawa</author><author>Tuyet Nguyen</author><author>Philip Varnadore</author><author>Soji Tani</author><author>Peter Passias</author><author>Benjamin Aaron Alman</author>
        <description><![CDATA[IntroductionDenosumab increases bone mineral density and reduces fracture risk in patients with osteoporosis. However, whether BMD response to denosumab differs by age, particularly during longer term treatment, remains unclear. This study investigated the association between baseline age and BMD gain during 3 years of denosumab treatment in patients with osteoporosis.MethodsThis retrospective study included patients with osteoporosis who were treated with denosumab. DXA-based BMD and bone turnover markers were followed for up to 3 years. Percent BMD gain from baseline was evaluated. The longitudinal association between baseline age and %BMD gain was assessed using multivariable linear mixed effects models for the lumbar spine and total hip. Analyses were performed in the treatment naive cohort and the overall cohort according to prior osteoporosis treatment status.ResultsA total of 255 patients were included, of whom 110 were treatment naive. In multivariable linear mixed effects models, older baseline age was associated with smaller lumbar spine %BMD gain in the treatment naive cohort at both 1 and 3 years. Each 1 year increase in age was associated with a 0.187 percentage point lower lumbar spine %BMD gain at 1 year and a 0.293 percentage point lower gain at 3 years (1 year: β = −0.187, p = 0.006, 3 years: β = −0.293, p = 0.031). In contrast, baseline age was not significantly associated with total hip %BMD gain in the treatment naive cohort (1 year: β = −0.011, p = 0.826, 3 years: β = 0.028, p = 0.727). In the overall cohort, baseline age was not significantly associated with %BMD gain at either skeletal site.ConclusionOlder baseline age was associated with a modestly smaller lumbar spine BMD gain in treatment-naive patients, whereas no statistically significant age-related association was observed at the total hip. These findings indicate a modest, site-specific association between baseline age and BMD gain in treatment-naive patients.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1847451</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1847451</link>
        <title><![CDATA[Physical exercise for prevention of dementia study: a 48-month randomized controlled trial]]></title>
        <pubdate>2026-08-10T00:00:00Z</pubdate>
        <category>Clinical Trial</category>
        <author>Enzo Iuliano</author><author>Giovanni Fiorilli</author><author>Antonella Angiolillo</author><author>Graziamaria Corbi</author><author>Giulia Di Martino</author><author>Santina Ciccotelli</author><author>Carlo della Valle</author><author>Giuseppe Calcagno</author><author>Alessandra di Cagno</author><author>Alfonso Di Costanzo</author>
        <description><![CDATA[BackgroundAlthough multimodal exercise interventions are recognized for their potential to attenuate age-related cognitive decline, the current literature lacks longitudinal depth. Specifically, robust randomized evidence addressing the long-term efficacy of structured training protocols remains limited. This single-blind RCT involved 882 community-dwelling older adults categorized as healthy, having subjective memory complaints (SMCs), or having mild cognitive impairment (MCI).MethodsParticipants were randomized to an experimental group (EG), performing 48 months of supervised moderate-to-high-intensity multimodal training (aerobic, resistance, and stretching), or to a control group (CG), maintaining usual habits. The primary outcome was the 48-month change in Mini-Mental State Examination (MMSE) scores. Secondary outcomes were scores on eight neuropsychological tests assessed at 12, 24, 36, and 48 months. A linear mixed-effects model analysis with repeated measures (LMM) was used to evaluate significant differences between the CG and EG.ResultsIn the final analysis of 674 participants, healthy participants (between-group effect: p = 0.008; η2p = 0.007; time*group interaction: p < 0.001; η2p = 0.025) in the EG showed significantly higher MMSE scores than those in the CG. SMC participants in the EG also showed higher MMSE scores than those in the CG (between-group effect: p = 0.052; η2p = 0.004; time*group interaction: p < 0.001; η2p = 0.031), although the between-group difference only approached statistical significance. Similarly, healthy and SMC participants in the EG demonstrated significantly better performance in the secondary outcomes of memory, attention, and reasoning than those in the CG. The sample size of the MCI group was insufficient to allow for conclusive statistical analyses.ConclusionA 48-month multicomponent exercise program significantly improved cognitive performance in healthy and SMC older adults. Structured physical activity may effectively slow cognitive decline.Clinical Trial Registrationhttps://clinicaltrials.gov/study/NCT02236416. Identifier number: NCT02236416.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1875372</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1875372</link>
        <title><![CDATA[Sex differences in the pathogenesis of degenerative knee osteoarthritis: a comparative transcriptomics analysis]]></title>
        <pubdate>2026-08-06T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ayobami S. Ogunsola</author><author>Davis J. Brady</author><author>Jeffrey A. Foster</author><author>Marcel G. Brown</author><author>Molly A. Hartzler</author><author>Maxwell K. Langfitt</author><author>John S. Shields</author><author>Xue Ma</author>
        <description><![CDATA[IntroductionOsteoarthritis (OA) is one of the leading diseases worldwide and is expected to continue to rise in prevalence. Epidemiological studies on OA have long shown a sex discrepancy between males and females, with females consistently showing greater rates of OA. There are numerous theories about why this might be the case; however, the discrepancy is still poorly understood.MethodsIn this study, two cohorts of patients with Kellgren-Lawrence grade IV knee OA were grouped based on sex and analyzed to decipher transcriptomic differences. The first cohort was a GSE114007 public dataset from the NCBI Gene Expression Omnibus (GEO) database, while the second cohort was from our institution. For each cohort, differential gene expression analysis (DEG), principal component analysis (PCA), functional enrichment analyses (Kyoto Encyclopedia of Genes and Genomes, Gene Set Enrichment Analysis, and Gene Ontology), and protein-protein interaction (PPI) analysis were performed.ResultsIn the GSE114007 cohort, XIST gene was the sole significant DEG at the genome-wide level. In contrast, our local cohort showed 109 DEGs between males and females. Functional enrichment analyses in both the GSE114007 and local cohorts showed female upregulation of inflammatory pathways, while the local cohort also showed female increases in protein synthesis and metabolic pathways, with males showing greater enrichment of structural and tissue remodeling pathways. PPI analysis showed female upregulation of three clusters of interacting proteins related to protein synthesis and translation, energy metabolism, oxidative phosphorylation, cell communication, and tissue remodeling.DiscussionOur analyses suggest that the pathogenesis of OA in women may be related to inflammatory and metabolic mechanisms, whereas OA in men may be driven by structural pathways involved in stress and remodeling. Hence, sex specific therapeutic strategies may be necessary to effectively target the pathobiological mechanisms driving OA in males and females.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1800359</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1800359</link>
        <title><![CDATA[The relationship between sarcopenia detected in newly diagnosed lung cancer patients and serum levels of IL6, IGF-1 and myostatin]]></title>
        <pubdate>2026-08-06T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Kamil Süzer</author><author>Utku Oflazoglu</author><author>Leyla Demir</author><author>Sinan Unal</author><author>Zeynep Gulsum Guc</author><author>Yasar Yildiz</author><author>Furkan Oguzhan Karalar</author><author>Yuksel Kucukzeybek</author><author>Ahmet Alacacioglu</author>
        <description><![CDATA[AimSarcopenia can result from many factors, including cancer, and is a consequence of quantitative and qualitative deterioration in skeletal muscle mass. Although there are some hypothetical explanations for sarcopenia, the underlying mechanisms of this condition have not been clearly defined in cancer patients. In this study, we aimed to investigate the association between sarcopenia and serum levels of myostatin, insulin-like growth factor-1 (IGF-1), and interleukin-6 (IL-6) in patients with newly diagnosed lung cancer.Material and MethodThis cross-sectional prospective study included patients with newly diagnosed metastatic non-small cell lung cancer (NSCLC), who were categorized into two groups based on the presence or absence of sarcopenia. Body composition and muscle mass were evaluated using bioelectrical impedance analysis (BIA), and body mass index (BMI) was calculated. Handgrip strength was measured using a handheld dynamometer. Serum levels of myostatin, insulin-like growth factor-1 (IGF-1), and interleukin-6 (IL-6) were analyzed from fasting venous blood samples to assess their association with sarcopenia.ResultsA total of 69 patients were included in the study. The patients’ ages ranged from 49 to 75 years. Thirty-four of these patients were sarcopenic and thirty-five of them were non-sarcopenic. Eighty-seven percent (60) of the patients included in the study were male. While myostatin and IL-6 levels were higher in the sarcopenic patient group, IGF-1 mean levels were lower. In the non-sarcopenic patient group, the median levels of myostatin, IL-6, and IGF-1 were 11.82 ng/mL, 1.17 pg/mL and 23.51 ng/mL, respectively. In the sarcopenic patient group, the median levels of myostatin, IL-6, and IGF-1 were 16.76 ng/mL, 7.42 pg/mL and 12.82 ng/mL, respectively (p < 0.001, p < 0.01, and p < 0.001, respectively). Spearman’s correlation analysis between SMI (skeletal muscle mass index) and myostatin, IGF-1 and IL-6 levels showed a negative correlation of SMI with myostatin and IL-6, and a positive correlation with IGF-1 [(r = −0.436, p < 0.001) (r = −0.520, p < 0.001), (r = 0.219, p:0.071) respectively]. When a logistic regression model was constructed with sarcopenia status as the dependent variable and myostatin, IGF-1, IL-6, and ECOG performance parameters as independent variables, myostatin and IGF-1 were identified as independent predictors [OR: 1.332, CI: (1.128–1.574), p: 0.001; OR: 0.926, CI: (0.874–0.982), p: 0.01, respectively].ConclusionWe found a significant correlation between sarcopenia and myostatin, IGF-1 and IL-6 in patients with lung cancer. We suggest that myostatin, IGF-1, and potentially IL-6 may serve as reliable markers for sarcopenia in cancer patients. We believe that these findings may encourage future prospective studies investigating the potential relevance of myostatin, IGF-1 and IL-6 as markers of sarcopenia.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1851261</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1851261</link>
        <title><![CDATA[Artificial intelligence and machine learning in immunosenescence: from biomarker discovery to clinical translation]]></title>
        <pubdate>2026-08-06T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Xi Chen</author><author>Yan Han</author><author>Ruixuan Zhang</author><author>Xinyang Huang</author><author>Jinwu Liu</author><author>Hanxu Xie</author><author>Ling Teng</author><author>Chen Han</author><author>Ziqi He</author><author>Zimeng Yang</author><author>Shihan Huang</author><author>Jianhui Yan</author>
        <description><![CDATA[The global population is undergoing unprecedented aging, with immunosenescence established as a core upstream driver of nearly all age-related chronic diseases, imposing a massive global clinical burden. For decades, immunosenescence research has been mired in three persistent translational bottlenecks: inability to capture interindividual immune aging heterogeneity, failure to decode complex multi-layered biological regulatory networks, and inefficient therapeutic development pipelines. Artificial intelligence (AI) and machine learning (ML) have emerged as promising solutions to these bottlenecks, yet existing literature fails to systematically bridge AI technical advances with clinical immunology practice, and often does not distinguish proof-of-concept evidence from the steps needed for clinical use. This review provides a holistic, critical overview of AI/ML applications across the full translational spectrum of immunosenescence research, from mechanistic discovery, biomarker development, diagnostic innovation to therapeutic development and personalized medicine. We further analyze unresolved technical, ethical, and regulatory barriers to clinical translation, including underrecognized fundamental flaws in current model design. Emerging AI technologies to address these limitations are outlined, alongside a clinically realistic translational roadmap and key future research trends. This review fills critical gaps in existing literature, providing a rigorous framework to shift the field from “AI for AI’s sake” to clinical utility-focused research, ultimately advancing healthy aging interventions.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1815043</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1815043</link>
        <title><![CDATA[Ulcerative colitis (UC) in the elderly: diagnostic and therapeutic considerations]]></title>
        <pubdate>2026-08-04T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Łucja Wróbel</author><author>Ewa Małecka-Wojciesko</author>
        <description><![CDATA[Ulcerative colitis (UC) demonstrates a bimodal incidence distribution, with a significant second peak and the highest prevalence observed in individuals aged ≥60 years. The pathogenesis of elderly UC involves immunosenescence—manifested by Th17/Treg imbalance and the accumulation of cells with a pro-inflammatory senescence-associated secretory phenotype (SASP)—alongside age-related dysbiosis, increased intestinal permeability, and mitochondrial dysfunction that impairs mucosal regeneration. Clinically, older patients more frequently present with left-sided colitis, characterized by anemia and weight loss, while abdominal pain is less common. Managing geriatric UC is challenging due to inadequate colonoscopy preparation and complex differential diagnosis (e.g., colorectal cancer, ischemic colitis). Furthermore, older adults face a fivefold increased risk of Clostridioides difficile infection and a sharply rising risk of colorectal cancer if diagnosed after 70 years of age. While 5-aminosalicylic acid remains the first-line therapy, it requires renal monitoring. Conversely, steroids increase infection and osteoporosis risks, thiopurines are restricted due to myelotoxicity and malignancy risks, and among biologics, vedolizumab offers better safety than anti-TNF agents. Ultimately, managing UC in older adults requires a comprehensive, multidisciplinary approach that accounts for multimorbidity, polypharmacy, nutritional status, and mental health to optimize pharmacotherapy and mitigate high-risk surgical interventions.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1793208</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1793208</link>
        <title><![CDATA[Promoting physical activity and physical functioning among residents in nursing homes – lessons learnt by the PROGRESS project]]></title>
        <pubdate>2026-08-03T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Vera Belkin</author><author>Berit K. Labott</author><author>Claudia Voelcker-Rehage</author>
        <description><![CDATA[IntroductionNursing home residents show high sedentary behavior and limited physical functioning, while structural constraints hinder sustainable prevention. This study examined how group-based physical exercise and environmental interventions, such as activity-promoting materials and interior design, can be integrated into everyday care to promote a physical activity–promoting culture in nursing homes and identified key organizational and individual determinants of sustainable implementation.MethodsPROGRESS was a participatory, cluster-randomized cross-over trial conducted in seven nursing homes in the Münster area in Germany. Residents received two of four guided or non-guided exercise (n = 62) and/or environmental interventions (e.g., activity posters, a seated bike ergometer, walking brochures/routes; n = 65). Data from attendance logs, participatory workshops, and a follow-up questionnaire at t4 (the fourth and final measurement time point, approximately 50 weeks after baseline assessment; n = 73) were analyzed using descriptive statistics and structured content analysis for open-ended feedback. Based on these findings, the PROGRESS pyramid was developed as a framework for sustainable implementation of physical activity into everyday care.ResultsOf the 73 participants, 90.4% attended at least one guided intervention session. Participation was highest in the exercise intervention, with most residents reporting weekly engagement. In contrast, engagement with environmental interventions was more variable and strongly dependent on staff support, with 63.0% of residents reporting no independent use of physical activity opportunities. Comparisons between self-reported participation and attendance records revealed substantial discrepancies, particularly for environmental interventions. Overall satisfaction with the project was high (mean = 2.7 ± 2.5 on a 0 = happy to 10 = angry scale). Most participants supported continuation of the interventions (86.0%), and 64.0% reported perceived personal benefits. Organizational and individual determinants jointly shaped participation.ConclusionIn order to promote physical activity and functioning sustainably in nursing homes, it is necessary to address organizational conditions and individual needs in a coordinated manner. The PROGRESS pyramid translates these findings into a practical framework comprising organizational and communicational foundations, resident participation, education, and staff qualification to guide the long-term integration of exercise and environmental interventions into daily routine.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1886928</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1886928</link>
        <title><![CDATA[Guided positional stabilization: a hypothesis on the role of targeted interfaces in enhancing upright stability among frail older adults]]></title>
        <pubdate>2026-08-03T00:00:00Z</pubdate>
        <category>Hypothesis and Theory</category>
        <author>Mayur Bhatt</author><author>Harikrashna Bhatt</author>
        <description><![CDATA[Elderly adults are at a higher risk of falls due to many reasons including issues in balance, coordination and overall sensory responsiveness. Falls ultimately threaten health and result in the fear of falling this causes restricted mobility and further decrease in health. Although there are traditional interventions such as railings, walkers or balance therapy which aim to reduce falls, they often function on compensatory mechanisms with little for postural regulation. We hypothesize that Guided Positional Stabilization (GZ) which use light strategically situated contact interfaces, can improve upright stability in frail elderly individuals by stimulating proprioceptive and tactile pathways. GZ is not a support aid rather a neurosensory framework that engages the nervous system in reactive and anticipatory balance corrections. Learning from concepts in biomechanics, neuroscience and geriatrics, this article presents the design requirements, theory, and possible clinical applications of GZ in fall prevention. We also put forward a pilot research agenda for testing the effectiveness of GZ in real world environments.]]></description>
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