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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>
        <generator>Frontiers Feed Generator,version:1</generator>
        <pubDate>2026-10-16T16:56:24.229+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1971981</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1971981</link>
        <title><![CDATA[Impaired autophagy and lysosome function in human fibroblast aging]]></title>
        <pubdate>2026-10-14T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Juan José Unzueta-Mendoza</author><author>Ian García-Aguirre</author><author>Mina Königsberg</author><author>Isabel Arrieta-Cruz</author><author>Solangy Lizcano-Meneses</author><author>Jonathan J. Magaña</author><author>Adriana Alarcón-Aguilar</author><author>Bulmaro Cisneros</author>
        <description><![CDATA[BackgroundHuman aging is characterized by a progressive, time-dependent deterioration in physiological and cognitive functioning. Aging is driven by an array of interconnected cellular hallmarks, including genomic instability, mitochondrial dysfunction, telomere attrition, epigenetic alteration and dysfunctional autophagy. Autophagy is a cytoprotective (cellular degradation and recycling) pathway that maintains homeostasis during starvation or stress, and whose activity is associated with extended lifespan. This multi-step process comprises autophagosome formation and maturation, autophagosome–lysosome fusion, and cargo degradation. Thus, analysis of autophagy flux is necessary to precisely design therapeutic interventions aimed at restoring autophagy in aging.MethodsThe autophagy flux was comprehensively analyzed in human skin fibroblasts from donors of different ages (20–96 years old), a cell system that retains age-associated cellular and molecular signatures. The subcellular localization and activity of the master transcription factor of autophagy and lysosome biogenesis, TFEB, was analyzed by confocal microscopy assays and transcriptional expression of TFEB target genes (RT-qPCR) respectively. The autophagy flux was evaluated by monitoring the autophagy markers LC3 and p62 by Western blotting and confocal microscopy analyses, using inhibitor drugs to block autophagy or lysosomal activity. Autophagosome maturation and autophagosome-lysosome fusion were analyzed by colocalizing LC3 with Sintaxin-17 and LC3 with the lysosomal protein LAMP1 respectively, using inhibitor drugs and confocal microscopy assays. The analysis of lysosomal morphology and function was evaluated by lysobrite dye staining and live-cell confocal microscopy analysis.ResultsThe initial stages of autophagy, including activation of TFEB, and autophagosome formation, remained apparently functional in fibroblast aging. In contrast, the rate of both autophagosome maturation and autophagosome-lysosome fusion, as well as the lysosomal function appears to be altered in aged fibroblasts. Specifically, enlarged dysfunctional lysosomes were identified as a hallmark of the fibroblasts of the 96-year-old donor. This lysosomal dysfunction may lead to a reduced ability to degrade canonical autophagy markers, LC3-II and p62, and the accumulation of lipofuscin.ConclusionOverall, the results provide evidence that autophagy flux is impaired at the late stages in aged fibroblasts, specifically in autophagosome maturation and autophagosome-lysosome fusion steps. Furthermore, it was demonstrated that this failure correlates with the presence of enlarged dysfunctional lysosomes. This study underscores the significance of enhancing lysosomal activity to counteract autophagy decline in aging.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1912337</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1912337</link>
        <title><![CDATA[Retinal neurodegeneration as accelerated ocular aging: a review of nutritional and metabolic supplements]]></title>
        <pubdate>2026-10-12T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Seyed Mohamadmehdi Moshtaghion</author><author>Maryam Shayan</author><author>Sarvesh Ramakrishnan</author><author>Andrew Ham</author><author>Ashkan Shafaei Gharehkoshan</author><author>Michael G. Morley</author><author>Nazlee Zebardast</author><author>Francisco Javier Díaz-Corrales</author><author>Enrique Rodríguez de la Rúa</author><author>Deeba Husain</author><author>Lucia Sobrin</author><author>Tobias Elze</author><author>David S. Friedman</author><author>Mohammad Eslami</author>
        <description><![CDATA[Retinal neurodegeneration is a major cause of irreversible vision loss and a shared feature of age-related macular degeneration (AMD), diabetic retinopathy (DR), and glaucoma (GL). Increasing evidence suggests that these conditions share important pathways with retinal aging, including mitochondrial dysfunction, metabolic insufficiency, redox imbalance, chronic low-grade inflammation, and progressive neuronal vulnerability. While antioxidant and micronutrient supplementation, most notably the Age-Related Eye Disease Study (AREDS) formulations, has demonstrated benefit in selected AMD populations, emerging metabolic and nutraceutical strategies targeting aging-related pathways are of unproven benefit. In this review, following a brief overview of the current landscape of investigated supplements, we synthesize preclinical and clinical evidence for a group of metabolic supplements, including nicotinamide adenine dinucleotide (NAD+) boosters, citicoline, pyruvate, and omega-3 fatty acids, that directly modulate mitochondrial bioenergetics, cellular redox state, membrane integrity, and neuroinflammatory signaling—pathways that are recognized hallmarks of biological aging and are particularly relevant to aging-related processes implicated in retinal neurodegeneration. Using a structured literature and clinical trial search, we summarize mechanistic insights and translational findings across AMD, DR, and glaucoma, emphasizing convergence on core pathways linking retinal neurodegeneration and ocular aging. Overall, current evidence supports biological plausibility and early functional or biomarker signals for these agents, particularly in glaucoma and diabetic retinal disease, although long-term efficacy remains unproven. Framing retinal disease at the intersection of neurodegeneration and aging biology, this review highlights metabolic supplementation as a promising but evolving strategy for preserving retinal function.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1920914</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1920914</link>
        <title><![CDATA[The impact of aging, sex, and exercise on brain mitochondria]]></title>
        <pubdate>2026-10-12T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Jianhua Zhang</author><author>Victor Darley-Usmar</author><author>Yun Li</author>
        <description><![CDATA[Mitochondrial function is essential for brain health. Its age-related decline impairs neuronal resilience and increases risk for the development of neurodegenerative diseases. As sex is an important biological variable in both physiological and pathological brain function, in this mini review, we highlight emerging evidence of sex differences in mitochondrial content and function in the brain and what is currently understood about how they change with age. Furthermore, as physical exercise is considered a key mitigating factor in brain injury and the development of neurodegenerative diseases, we review studies that address the effects of exercise on mitochondrial function in the brain, with particular attention to those that include data from both sexes. The current understanding of the effects of sex differences and exercise on brain mitochondrial function over the lifespan is limited, but nonetheless some interesting insights are emerging. We discuss the key knowledge gaps and offer some suggestions for further research. These include defining the extent and specificity of mitochondrial alterations with age in different species, brain regions and cell types, and their modification by exercise, which is both important for advancing aging biology and for designing intervention strategies to promote healthy aging, to mitigate age-dependent cognitive decline and treat neurodegenerative diseases.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1923192</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1923192</link>
        <title><![CDATA[Association of preoperative frailty and postoperative delirium with one-year mortality after surgery in older patients with hip fractures]]></title>
        <pubdate>2026-10-09T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Keqin Zhang</author><author>Peidong Zhang</author><author>Ling Chen</author><author>Housheng Wang</author><author>Wubin Chen</author><author>Yusheng Zhu</author><author>Dai Li</author><author>Wenbin Lu</author>
        <description><![CDATA[BackgroundWe aimed to evaluate the incidence of preoperative frailty and postoperative delirium (POD) and the association of preoperative frailty, POD with one-year mortality in older patients undergoing hip fracture surgery.MethodsPatients with hip fracture were identified from 2018 to 2023 in our hospital. The patients were categorized into four groups: patients without preoperative frailty who did not suffer from POD, patients without preoperative frailty who did suffer from POD, patients with preoperative frailty who did not suffer from POD, and patients with preoperative frailty who did suffer from POD. The primary outcome was one-year mortality after surgery. Multivariate landmark Cox regression analysis was used to assess the associations of preoperative frailty and POD with one-year mortality, and adjusted survival curves from the multivariate Cox model were plotted.ResultsOf 2,659 patients, 1,715 were included in the final analysis. The incidence of preoperative frailty was 24.0% (411/1715), and the POD rate was 16.9% (290/1715). Compared with older patients without preoperative frailty who did not suffer from POD (5.6%, 61/1088), the incidence of one-year mortality was significantly higher in patients without preoperative frailty who did suffer from POD (17.1%, 37/216), patients with preoperative frailty who did not suffer from POD (11.6%, 39/337), and patients with preoperative frailty who did suffer from POD (28.4%, 21/74). Preoperative no-frailty and POD (HR: 2.09, 95% CI: 1.36–3.21), frailty and no-POD (HR: 2.30, 95% CI: 1.51–3.50), and frailty with POD (HR: 3.95, 95% CI: 2.35–6.63) were all independently associated with one-year mortality after surgery in older patients with hip fracture.ConclusionPreoperative frailty and POD were each independently associated with increased one-year mortality. Patients with both conditions had the highest observed mortality risk after hip fracture surgery.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1847033</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1847033</link>
        <title><![CDATA[Age-associated remodeling of NK cell subsets, B cell subsets, and T cell surface markers in peripheral blood of healthy Chinese adults: a prospective multicolor flow cytometry study]]></title>
        <pubdate>2026-10-09T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Liyuan Zheng</author><author>Wei Cao</author><author>Yixuan Wang</author><author>Tengda Xu</author><author>Fada Wang</author><author>Leidan Zhang</author><author>Xinchao Liu</author><author>Taisheng Li</author>
        <description><![CDATA[BackgroundImmunosenescence refers to the structural and functional remodeling of the immune system that accompanies aging, and is closely linked to increased susceptibility to infection, diminished vaccine responses, and a higher burden of chronic disease. While flow cytometric profiling of peripheral blood lymphocyte subsets has become a key tool for characterizing immune aging, systematic age-related data on NK cell subsets (CD56hi/CD56dim/CD56neg three-way classification) and B cell subsets (IgD/CD27 four-way classification) in healthy Chinese adults remain scarce. Quantitative age trends for CD57 and TEMRA as markers of terminal T cell differentiation have also been incompletely described in this population.MethodsWe prospectively enrolled 146 healthy adults attending the annual health examination center of Peking Union Medical College Hospital (Panel 1: n = 103, age 20–82 years; Panel 2: n = 43, age 25–92 years, enriched for older participants). Panel 1 was a 12-color single-tube assay covering T cells (including CD57), NK cell trisubsets, and IgD/CD27-based B cell subsets. Panel 2 was a 12-color dual-tube assay focused on detailed T cell differentiation, incorporating CD45RA/CD62L, CD28, CD31, CD38, and HLA-DR. Spearman rank correlation, Kruskal–Wallis, and Mann-Whitney U tests were used for statistical analysis.ResultsIn Panel 1 (n = 103), ten parameters showed significant age correlations. CD4+CD57+ (r = +0.421, p < 0.001) and CD8+CD57+ (r = +0.338, p < 0.001) rose most strongly with age. Total NK frequency increased (r = +0.259, p = 0.008) while CD56hiCD16− regulatory NK cells declined (r = −0.263, p = 0.007) and NK PD-1 expression rose (r = +0.256, p = 0.009). IgD+CD27+ marginal zone-like B cells declined significantly in Panel 1 (r = −0.257, p = 0.009). Panel 2 (n = 43) revealed the strongest signals in CD8+ T cells: TEMRA accumulation (r = +0.532), CD28 loss (r = −0.552), and naive depletion (r = −0.534) all reached p < 0.001. CD4+ naive cells also declined significantly (r = −0.303, p = 0.048). Multivariate analysis confirmed that most associations were independent of sex.ConclusionThis study provides a comprehensive characterization of age-related immunophenotypic changes across NK cell subsets, IgD/CD27-defined B cell subsets, and multidimensional T cell markers in healthy Chinese adults, offering reference data for clinical immune assessment and vaccine response prediction.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1960201</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1960201</link>
        <title><![CDATA[OpenCap-based five-times sit-to-stand analysis in older Asian women with and without sarcopenia]]></title>
        <pubdate>2026-10-05T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jialiang Xu</author><author>Hejin Cai</author><author>Yan Wang</author><author>Zhengsheng Hu</author><author>Ming Zhang</author><author>Qitao Tan</author>
        <description><![CDATA[IntroductionSarcopenia‐related lower‐limb functional impairment is commonly assessed using five‐times sit‐to‐stand (5STS) completion time, which provides limited information about how performance differs within the task. This study examined two questions: the concurrent agreement of OpenCap‐derived lower‐limb kinematics with Vicon during repeated 5STS, and whether OpenCap‐derived kinematic and temporal measures distinguished healthy and sarcopenic older Asian women.MethodsTwenty‐four participants were classified as healthy (n = 12) or sarcopenic (n = 12) according to AWGS 2025 criteria and completed concurrent OpenCap and Vicon recordings. Agreement was assessed from participant‐level mean waveforms using RMSE and MAE for angular error magnitude, ICC(A,1) for absolute agreement, R2 for waveform similarity, and phase‐dependent bias.ResultsKnee flexion/extension showed the lowest absolute error and high agreement (RMSE = 1.84°, ICC(A,1) = 0.998). Hip flexion/extension also showed high agreement, although absolute error was larger (RMSE = 5.42°, ICC(A,1) = 0.970). Ankle agreement was more variable. Statistical parametric mapping identified localized reductions in hip and knee flexion in the sarcopenic group, while angular velocity waveforms did not differ significantly. Sarcopenic participants also showed longer total, ascent, and descent durations and greater repetition-related slowing, while repetition-duration variability did not differ significantly.DiscussionWithin this protocol, OpenCap showed strong participant‐level agreement for hip and knee kinematics and provided phase‐ and repetition‐specific descriptors of 5STS performance. The independent validity and incremental clinical value of the derived temporal measures require further evaluation.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1951042</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1951042</link>
        <title><![CDATA[A new blue zone? exceptional late-life survival in Bolotana, Sardinia]]></title>
        <pubdate>2026-10-05T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Giovanni Mario Pes</author><author>Steven N. Austad</author><author>Dan Buettner</author><author>Salvatore Pedde</author><author>Vittorio Romerio</author><author>Hiram Beltrán-Sánchez</author><author>S. Jay Olshansky</author>
        <description><![CDATA[BackgroundExceptional longevity in Sardinia has historically been associated with the original Sardinian Blue Zone. We investigated whether Bolotana, a small mountain municipality outside that area, exhibits a distinct late-life survival profile.MethodsUsing validated civil and parish records, we constructed sex-specific partial period life tables for 2021–2025. Late-life survival was defined as survival from age 70 onward and assessed through remaining life expectancy at age 70 (e70) and conditional survival from age 70 to 100 [S(70→100)]. Estimates were compared descriptively with Nuoro Province, Sardinia, and Italy, the original Sardinian Blue Zone, and published international benchmark. Statistical uncertainty was evaluated using parametric Poisson bootstrap. Sensitivity analyses included 2020–2025 and a period-matched 2015–2019 analysis.ResultsIn 2021–2025, e70 was 16.02 years in men (95% CI, 14.55–17.79) and 20.85 years in women (19.42–22.43); S(70–100) was 4.92% (1.58–12.76) and 13.83% (7.33–23.75), respectively. Female estimates (70–100) exceeded contemporary values for Nuoro Province, Sardinia, and Italy. Among international benchmarks, Bolotana women ranked second only to Hong Kong for both indicators, and S(70→100) was more than three times that of U.S. women. Inclusion of 2020 to address the potential effects of COVID-19 produced modest reductions, whereas the period-matched 2015–2019 analysis yielded a less pronounced late-life survival profile, particularly for survival to age 100.ConclusionBolotana exhibited a distinctive, predominantly female pattern of exceptional late-life survival and may be considered a candidate longevity blue zone. However, the magnitude of this advantage varied by calendar period. Longer observation and continued demographic validation, are required before Bolotana can be considered an established longevity blue zone.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1870661</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1870661</link>
        <title><![CDATA[Opportunities to enhance assisted living facility care quality through interprofessional collaborative practice]]></title>
        <pubdate>2026-10-02T00:00:00Z</pubdate>
        <category>Perspective</category>
        <author>David Hage</author><author>Rekha Pudur</author><author>Jan Golembiski</author>
        <description><![CDATA[Interprofessional Education (IPE) is increasingly recognized as a vital strategy for enhancing the quality of care in assisted living facility (ALF) settings. By fostering collaboration among healthcare professionals such as nurses, nurses’ aides, social workers, physicians, and administrators, IPE promotes a shared and more robust understanding of resident needs and care goals. This opinion article argues that greater integration of IPE and interprofessional collaborative practice (IPCP) into long-term care training programs can significantly improve communication, reduce errors, and enhance person-centered care. Assisted living communities face complex challenges, including managing chronic conditions, supporting cognitive issues, changes in resident acuity, and addressing psychosocial needs. IPCP equips staff with the skills to navigate these challenges collectively, leading to more coordinated and effective care. While barriers such as scheduling challenges and institutional silos frequently persist, the potential benefits of IPCP include broader integration of IPCP towards improved resident outcomes, resident and staff satisfaction, and operational efficiencies that warrant its broader adoption. This article calls for greater prioritization of IPCP in assisted living facility settings to enhance resident outcomes and staff collaboration.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1945744</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1945744</link>
        <title><![CDATA[Association between tooth retention and lower inflammatory dietary pattern in older adults]]></title>
        <pubdate>2026-10-02T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Lyzbeth B. Ortiz-Barrios</author><author>Paola Garcia-delaTorre</author><author>Berenice Rivera-Paredez</author><author>Sergio Sánchez-García</author><author>Berenice Palacios-González</author>
        <description><![CDATA[IntroductionTooth loss is highly prevalent among older adults and may compromise food selection, diet quality, and adherence to proinflammatory dietary patterns, thereby contributing to chronic inflammation and adverse health outcomes. This study investigated the association between tooth retention and the inflammatory potential of the diet among older adults.MethodsA cross-sectional analysis was conducted among 1,075 adults aged 60 years or older. According to the oral examination, participants were categorized as having ≥21, 11-20, 1-10, or no natural teeth, and as edentulous. The Dietary Inflammatory Index was constructed using a food-frequency questionnaire.ResultsIndividuals with more teeth were younger, possessed higher educational attainment, were less likely to smoke, and exhibited elevated Mini-Mental State Examination scores. After adjustment for potential confounders, older adults with 1–10 natural teeth had significantly higher odds of belonging to a more pro-inflammatory dietary category than those with 21–28 teeth (OR = 2.19; 95% CI: 1.44-3.33; p-value <0.001).ConclusionOur findings suggest that tooth retention is closely associated with the inflammatory potential of the diet in older adults and supports the integration of oral health into nutritional assessment and healthy aging strategies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1988532</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1988532</link>
        <title><![CDATA[Correction: Promoting healthy aging in a digital world: leveraging technology for enhanced elderly care and wellbeing]]></title>
        <pubdate>2026-09-30T00:00:00Z</pubdate>
        <category>Correction</category>
        <author>Patrizio Armeni</author><author>Irem Polat</author><author>Leonardo Maria De Rossi</author><author>Lorenzo Diaferia</author><author>Sara De Padova</author><author>Athena Gatti</author><author>Severino Meregalli</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1894052</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1894052</link>
        <title><![CDATA[Synovial fluid-derived extracellular vesicles modulate joint cell function in osteoarthritis]]></title>
        <pubdate>2026-09-30T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Alvaro Compañ</author><author>Vittoria Carrabs</author><author>María Luisa Ferrándiz</author><author>Antonio Silvestre</author><author>Ignacio Muñoz</author><author>María Carmen Carceller</author><author>María Isabel Guillén</author>
        <description><![CDATA[IntroductionOsteoarthritis (OA) is an age-related joint disease characterized by chronic inflammation and extracellular matrix degradation. Extracellular vesicles (EVs) in synovial fluid (SF) may modulate intercellular communication and influence disease progression.Material and methodsSF, cartilage, and synovial tissue were collected from knee OA patients (n = 68). SF-derived EVs (SF-EVs) were isolated by size exclusion chromatography and characterized by transmission electron microscopy (TEM), tunable resistive pulse sensing (qNano), and ELISA analysis of EV-associated markers (CD9, CD81, TSG101, and PDCD6IP) and the negative marker calnexin. In vitro experiments were performed using primary synoviocytes and chondrocytes stimulated with interleukin (IL)-1β in the presence or absence of SF-EVs. Inflammatory and catabolic markers were measured.ResultsSF-EVs (∼261 nm; ∼7 × 108 particles/mL) expressed canonical EV markers. In synoviocytes, SF-EVs reduced IL-1β-induced proliferation and decreased IL-6 and MMP-3 while increasing hyaluronic acid (HA). In chondrocytes, SF-EVs reduced IL-6 and MMP-13 and enhanced HA and IL-1Ra production, with sustained effects over time.ConclusionThese findings suggest that SF-EVs can modulate inflammatory and matrix-related responses in joint-resident cells under IL-1β-induced inflammatory conditions. Their distinct effects on synoviocytes and chondrocytes highlight the potential role of SF-EVs in regulating cell-specific responses within the osteoarthritic joint and warrant further investigation into their contribution to OA pathophysiology.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1890974</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1890974</link>
        <title><![CDATA[Comprehensive profiling of phenotypic features of memory T- and B-cells from birth to the onset of old age]]></title>
        <pubdate>2026-09-30T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Joaquim Pedro Brito-de-Sousa</author><author>Laise Rodrigues Reis</author><author>Ismael Artur da Costa-Rocha</author><author>Vanessa Peruhype-Magalhães</author><author>Christiane Costa-Pereira</author><author>Julia Pereira Martins</author><author>Lis Ribeiro do Valle Antonelli</author><author>Cristiana Couto Garcia</author><author>Angelica Oliveira Gomes</author><author>Jordana Grazziela Alves Coelho-dos-Reis</author><author>Ana Maria de Caetano Faria</author><author>Andréa Teixeira-Carvalho</author><author>Ana Carolina Campi-Azevedo</author><author>Karen Cecília de Lima Torres</author><author>Olindo Assis Martins-Filho</author>
        <description><![CDATA[IntroductionHuman aging is accompanied by profound and continuous remodeling of the immune system, characterized by rhythmic, stage-specific patterns. These features are characterized by waves of cellular differentiation, network reorganization, and functional recalibration, a phenomenon encompassed by the concept of immunobiography.MethodsThis study focuses on T- and B-cell memory immunophenotypes that shape adaptive immunity, including interferon-activated cells from healthy volunteers of both sexes, aged 9 months to 65 years, stratified into 12 consecutive age subgroups. Significant shifts were concentrated in intermediate age subgroups, particularly at 5–6 years, 10–19 years (the most pronounced), and 20–29 years.ResultsAlthough women exhibited an earlier onset of changes, men demonstrated greater lifelong variability in differentiated subsets, especially for early effector CD4+ cells. Additionally, other cell subsets showed variability, especially in men, including early effector CD4+ and CD8+, interferon- mediated CD4+ and CD8+, central and effector memory CD4+, non-interferon-mediated CD4+, and naïve CD19+ B‐cells, predominantly between 10 and 39 years. Signature analyses confirmed sex-specific peaks occurring at distinct ages. Naïve cells displayed the highest overall connectivity, whereas B-cell network connectivity increased with age in women but decreased sharply in men after 20 years. Notably, the upregulation of immune memory cell subsets was accompanied by an increase in global connectivity.DiscussionOur findings indicate that immune memory remodeling across the human lifespan occurs in discrete, sex-dependent waves, probably shaped by cumulative antigen exposure and endocrine transitions. These trajectories may differentially balance adaptive immunity and inflammatory differentiation, potentially influencing long-term immune resilience and susceptibility to chronic inflammatory conditions.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1872955</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1872955</link>
        <title><![CDATA[Immune system ontogeny—a subtle evolution to perfection]]></title>
        <pubdate>2026-09-29T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Adriana Narcisa Munteanu</author><author>Mihaela Surcel</author><author>Elena Georgiana Dobre</author><author>Carolina Constantin</author><author>Monica Neagu</author>
        <description><![CDATA[It is well known that both innate and adaptive immune systems in newborns are immature, making them highly susceptible to infection. Additionally, pre-term newborns with hindered immune systems are more prone to increased mortality and morbidity. Newborns are capable of mounting adaptive immune responses, but their capability to develop long-lasting immunity is limited. Thus, the fetus and newborn’s immune system is considered “immature” due to functional disorders in immune response or suppression by regulatory cells. Aging is another factor that leads to impaired immune responses due to a state of chronic low-grade inflammation (inflammaging), which compromises defense against pathogens and malignancies and favors the onset of age-related disorders. However, in this complicated scenario, centenarians emerged as a paradigm shift due to their particular immune system that prevents inflammaging and enables them to achieve longevity. Therefore, the present review aims to provide an updated overview of immune response development through neonatal, infant, and adult life in order to highlight stage-specific mechanisms and uniquely regulated immune responses. Taken together, this information provides mechanistic insights that can be harnessed to develop age-adapted interventional strategies and prevent the onset of age-associated disorders in older adults.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1921485</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1921485</link>
        <title><![CDATA[New insight into Alzheimer’s disease: small molecule-Aβ in the brain transport and peripheral organ clearance]]></title>
        <pubdate>2026-09-29T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Tianci Ma</author><author>Yongyi Li</author><author>Yuting Ding</author><author>Shijie Liu</author><author>Chuanhao Gao</author><author>Xiang Li</author><author>Zhiqian Tong</author><author>Yan Lv</author>
        <description><![CDATA[Alzheimer’s disease (AD) represents one of the most prevalent neurodegenerative disorders without approved disease-modifying therapies. A major contributing factor is that, for decades, drug development has focused almost exclusively on repairing or removing lesions within the brain itself. Yet a growing body of work now points to AD as a systemic disorder, rooted in a breakdown of whole-body Aβ homeostasis. Nevertheless cerebral Aβ transport and peripheral Aβ clearance are commonly investigated as independent processes, and the coordinated interplay… remains insufficiently characterized. This review bridges the current research gap by systematically elaborating the full trafficking cascade of brain-derived Aβ from intracerebral drainage to peripheral elimination. Four major intracranial clearance pathways are comprehensively summarized, including the blood-brain barrier, blood-cerebrospinal fluid barrier, arachnoid granulation venous outflow, and meningeal lymphatic/glymphatic system. The peripheral clearance processes of circulating Aβ in the blood, liver, kidney, and gastrointestinal tract are further illustrated. A broad spectrum of emerging therapeutic strategies targeting Aβ transport and clearance is also reviewed, including specific pathway modulators, microglia regulators, Aβ aggregation inhibitors, natural multi-target compounds, ultrasound-mediated blood-brain barrier opening, and exosome-based intervention approaches. When we compare the relative contributions of central versus peripheral clearance, Comparative analysis of central and peripheral Aβ clearance indicates that the liver appears to dominate the peripheral elimination of Aβ, yet the real driver of cerebral Aβ deposition is not the failure of any single route, but rather the loss of synergy among multiple pathways. This mechanistic framework explains why purely brain-centric therapeutics are unlikely to correct a systemic Aβ imbalance. Instead, future translational efforts should give higher priority to combination regimens that simultaneously facilitate intracerebral drainage and bolster peripheral organ clearance. This review further discusses current hurdles and emerging opportunities in systemic AD drug discovery, with the aim of offering a unified conceptual framework-one that providing a unified conceptual framework for understanding AD pathogenesis and facilitating the exploration of novel therapeutic paradigms.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1792585</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1792585</link>
        <title><![CDATA[Ultrasonographic evaluation of quadriceps femoris muscle mass in critically ill patients aged 60 years and older: a prospective observational study]]></title>
        <pubdate>2026-09-24T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Nestor-Julian Zarate-Herran</author><author>Johan-Sebastián Villada-Gómez</author><author>Nestor-David Caicedo</author><author>Diana-María Trejos-Gallego</author><author>Fernando Gomez</author>
        <description><![CDATA[Background and aimsMuscle wasting is a common complication in critically ill older adults admitted to intensive care units (ICU), with significant implications for morbidity and mortality. Ultrasound represents a promising bedside tool for assessing muscle mass changes. This study aimed to evaluate changes in quadriceps femoris muscle mass using ultrasonography at ICU admission and after 7 days of stay in patients aged 60 years and older.MethodsA prospective cohort study with repeated measurements was conducted between December 2024 and May 2025. Patients aged ≥60 years admitted to the ICU were included. Ultrasonographic measurements included rectus femoris cross-sectional area (RFCSA), bilateral quadriceps muscle thickness, and rectus femoris pennation angle at admission and day 7. Clinical characteristics, severity scores (APACHE II, SOFA), and functional status (Barthel index) were recorded. Statistical analysis included Wilcoxon signed-rank test and robust statistics.ResultsFifty patients were analyzed (60% male, median age 72.5 years). Significant muscle mass reductions were observed: RFCSA decreased by 16.2% (2.525–2.115 cm2, p < 0.001), right quadriceps thickness by 14.6% (2.012–1.719 cm, p < 0.001), left quadriceps thickness by 20.2% (2.049–1.635 cm, p < 0.001), and pennation angle by 18.2% (7.664°–6.270°, p < 0.001). ICU mortality was 30%. Multivariate analysis identified advanced age, female sex, hypoglycemic agent use, higher SOFA scores, and lower premorbid Barthel index as factors associated with greater muscle loss.ConclusionCritically ill older adults experience significant quadriceps muscle mass loss within the first week of ICU stay, as measured by bedside ultrasonography. These findings support the implementation of early muscle assessment and targeted interventions in this vulnerable population.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1858090</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1858090</link>
        <title><![CDATA[CaroRite™ for improving skin health and the visible signs of aging - a randomised, double-blind, placebo-controlled trial]]></title>
        <pubdate>2026-09-21T00:00:00Z</pubdate>
        <category>Clinical Trial</category>
        <author>Amanda Rao</author><author>Janice Pellow</author><author>David Briskey</author>
        <description><![CDATA[BackgroundThere is an increasing need to identify novel ingredients that can be safely utilized to enhance skin function and mitigate skin aging. Carotenoid supplementation shows promise in improving skin health and reducing signs of aging, owing to its antioxidant and anti-inflammatory properties.AimThis randomised, double-blind, placebo-controlled study aimed to investigate the efficacy of a carotenoid supplement, CaroRite™, on skin health and the visible signs of aging in healthy females.MethodsEighty female participants aged 40–55 years were recruited and randomised to receive either CaroRite™ (containing 28–30 mg mixed carotenoids) or a placebo. Participants were instructed to take one capsule daily for 12 weeks. Outcome measures included visible signs of aging (wrinkles, skin elasticity, hydration, sebum, pigmentation, pore size, and temperature), transepidermal water loss (TEWL), dermal thickness, skin carotenoid levels, dietary carotenoid intake, and safety.ResultsNo significant between-group differences were observed for visible signs of aging parameters (p > 0.05). At week 12, significant between-group differences from baseline were observed for TEWL (CaroRite™ −4.58 ± 9.43 vs. placebo 0.34 ± 6.73; p = 0.011) and dermal thickness (CaroRite™ 139.50 ± 220.21 μm vs. placebo 43.90 ± 225.97 μm; p = 0.036). Skin carotenoid levels increased by 48.1% in the active group (CaroRite™ +167.09 ± 117.23 vs. placebo 9.42 ± 47.16; p < 0.001), despite no significant differences in dietary carotenoid intake between groups.ConclusionDaily oral supplementation with CaroRite™ did not reduce the visible signs of ageing after 12 weeks, however notable improvements in skin carotenoid status, TEWL and dermal thickness was found. CaroRite™ demonstrated good bioavailability and was well tolerated. Overall, these findings support the use of CaroRite™ as part of a comprehensive approach to potentially improving skin health, particularly for enhancing skin carotenoid status and supporting underlying structural and barrier function.Clinical Trial RegistrationClinicalTrials.gov, Identifier NCT06878001.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1987600</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1987600</link>
        <title><![CDATA[Editorial: Biomarkers and aging: new insights for precision medicine]]></title>
        <pubdate>2026-09-21T00:00:00Z</pubdate>
        <category>Editorial</category>
        <author>Oluwafemi Gabriel Oluwole</author><author>Paulo Adriano Schwingel</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1992402</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1992402</link>
        <title><![CDATA[Correction: Cognitive and behavioral benefits of newspaper reading in community‐dwelling older adults: a feasibility randomized controlled trial]]></title>
        <pubdate>2026-09-21T00:00:00Z</pubdate>
        <category>Correction</category>
        <author>Mamoru Sato</author><author>Sawako Negoto</author><author>Shinya Nakano</author><author>Chihoko Urata</author><author>Tetsuya Ioji</author><author>Hideya Kodama</author><author>Emi Yoshimura</author><author>Yukinori Tasaki</author><author>Shinichiro Goroku</author><author>Kiichiro Morita</author><author>Yoshihisa Shoji</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1866906</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1866906</link>
        <title><![CDATA[Unraveling skeletal muscle senescence in an in vitro cell culture model]]></title>
        <pubdate>2026-09-18T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Kayo Moreira Bagri</author><author>Morgana Teixeira Lima Castelo-Branco</author><author>Claudia Mermelstein</author>
        <description><![CDATA[IntroductionSkeletal muscles are crucial for voluntary movement, posture, breathing, joint stability, and therefore are essential for maintaining overall health and quality of life. Aging, sarcopenia, cancer, immobilization, and several muscle pathologies can have an impact on muscle function, and muscle cell senescence is associated with these conditions.MethodsHere we aimed to develop a primary cell culture model to study skeletal muscle cell senescence. We induced cell cycle arrest in cultured embryonic chick muscle cells using a low concentration of cytosine arabinoside (Ara-C) for 9 days.ResultsOur results show that Ara-C was able to induce several cellular senescence-associated bone fide characteristics, including reduced cell proliferation, increased β-galactosidase expression, increased reactive oxygen species production (ROS), increased p53 and p21 expression, increased muscle fibroblast cell size and nuclei numbers, increased lysosomal activity, decreased muscle differentiation (decreased muscle fiber size and decreased desmin expression), and increased secretion of IL-6, TNFα and TGFβ. Interestingly, inhibition of fibroblast growth factor receptor recovers the AraC-induced senescent phenotype in myogenic cells.ConclusionThis new experimental model could be used to deepen our understanding of the molecules and signaling pathways associated with the initiation and establishment of skeletal muscle senescence. Furthermore, this model could be used to test new drugs and therapeutic interventions aiming the amelioration of senescence-associated conditions.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1870256</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1870256</link>
        <title><![CDATA[Association of smoking cessation with late-life frailty risk: the Singapore Chinese health study]]></title>
        <pubdate>2026-09-17T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ainsley Ryan Yan Bin Lee</author><author>Huiqi Li</author><author>Kevin Yiqiang Chua</author><author>Woon-Puay Koh</author>
        <description><![CDATA[ObjectiveTo examine whether smoking cessation, in terms of duration and age at quitting, was associated with late-life physical frailty.DesignProspective population-based cohort study.SettingChinese living in Singapore.ParticipantsWe analyzed data from 4,574 men (mean baseline age 52.7 years, range 45–65 years) enrolled in the Singapore Chinese Health Study.MeasurementsParticipants self-reported smoking behaviors at four time-points over a 20-year follow-up. Physical frailty was assessed in late life (mean age 73.6 years, range 65–88 years) using a modified Cardiovascular Health Study phenotype, incorporating weakness, slowness, exhaustion and weight loss. Multivariable logistic regression was used to estimate odds ratios (OR) and 95% confidence intervals (CI) for association with frailty.ResultsPersistent smokers had higher odds of frailty compared to never smokers (OR: 1.34; 95% CI: 1.01–1.76). Those who had quit smoking within 10 years before frailty assessment also had increased odds (OR = 1.33; 95% CI: 0.86–2.01), albeit not statistically significant. The OR (95% CI) was attenuated to 1.08 (0.76–1.51) for those quitting 10–20 years and 0.97 (0.59–1.55) for those quitting >40 years. Those who quit smoking by age 60 years had similar odds relative to never smokers: OR was 1.05 (0.74–1.48) for quitting at ages 50–60 years and further reduced to 0.86 (0.57–1.25) for quitting at ages <40 years.ConclusionWhile persistent smoking was associated with increased odds of late-life physical frailty, smoking cessation for at least 10 years, or before the age of 60 years, could mitigate this risk substantially.]]></description>
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