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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>2026-07-15T17:09:34.199+00:00</pubDate>
        <ttl>60</ttl>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1858763</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1858763</link>
        <title><![CDATA[Reframing brain aging: neuroinflammation as an interconnected network process]]></title>
        <pubdate>2026-07-15T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Ludmila Müller</author><author>Svetlana Di Benedetto</author><author>Viktor Müller</author>
        <description><![CDATA[Neuroinflammation has emerged as a central component of brain aging, shaping the balance between neural resilience and vulnerability to cognitive decline. Rather than representing a simple consequence of neuronal damage, neuroinflammatory processes are increasingly recognized as active regulators of synaptic integrity, neuronal survival, and circuit function. Under physiological conditions, neuroimmune signaling may contribute to tissue homeostasis, synaptic maintenance, and adaptive responses to cellular stress; however, persistent or dysregulated inflammatory activity may disrupt these functions, promoting network instability and increasing vulnerability to age-related pathology. These processes arise from complex interactions among neurons, glial cells, vascular elements, and peripheral immune signals that together form dynamic neuroimmune networks. Within the aging brain, microglia and astrocytes play key roles in coordinating immune surveillance, synaptic remodeling, and inflammatory signaling. Age-related alterations in glial function can disrupt homeostatic communication within neuron–glia networks, promoting persistent low-grade inflammation and altered synaptic regulation. Importantly, neuroinflammatory activity in the brain is strongly influenced by systemic factors, including peripheral immune aging, changes in blood–brain barrier integrity, and signals originating from the gut–brain axis. In this mini-review, we discuss brain aging from a network perspective, emphasizing how multiscale interactions between cellular and systemic processes shape neuroinflammatory trajectories across the lifespan. We further highlight emerging approaches—including multi-omics technologies, advanced neuroimaging, and systems-level analyses—that are enabling a more integrated understanding of neuroinflammatory dynamics. Viewing neuroinflammation as a network phenomenon may provide new insights into mechanisms of cognitive aging and identify potential targets for strategies aimed at preserving brain health.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1850689</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1850689</link>
        <title><![CDATA[Endothelial progenitor cells and circulating microRNAs as possible biomarkers for coronary artery disease]]></title>
        <pubdate>2026-07-15T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jakub Jozue Wojtacha</author><author>Jan Budzianowski</author><author>Magdalena Wojciech</author><author>Edyta Wawrzyniak-Gramacka</author><author>Barbara Morawin</author><author>Jarosław Hiczkiewicz</author><author>Agnieszka Zembron-Lacny</author>
        <description><![CDATA[IntroductionEndothelial cells and their precursors, i.e., endothelial progenitor cells (EPCs), along with other cell types such as smooth muscle cells and immune cells, release or sequester microRNAs (miRNAs) that actively participate in endothelial dysfunction, smooth muscle cell proliferation, vascular inflammation, and progression of atherosclerotic plaques, ultimately contributing to the transition from stable to acute coronary syndromes. The stability of circulating miRNAs has, for many years, attracted interest in their use as biomarkers in the diagnosis and monitoring of coronary artery disease (CAD).MethodsThe study was designed to assess the association of total circulating miRNAs with endothelial dysfunction and EPC-related parameters. The study was carried out in seventy-two patients with CAD (73.2 ± 5.6 years). They were compared with eighty healthy controls (HC) (70.9 ± 5.4 years).ResultsThe lipid-lipoprotein profile including triglycerides, total cholesterol, low-density lipoprotein (LDL), high-density lipoprotein (HDL), non-HDL and oxidized LDL as well as endothelium-specific variables such as nitric oxide, 3-nitrotyrosine, early EPCs and total EPCs were reduced in CAD patients (p <0.001). The lower levels of nitric oxide in CAD patients (77.60 ± 49.58 μmol/L) compared to HC (290.64 ± 151.93 μmol/L) confirmed the impairment of endothelial secretory function. Total circulating miRNA levels were three-fold higher in CAD (9.36 ± 1.48 ng/L) than in HC (3.22 ± 0.48 ng/L). For miRNA, the area under the curve (AUC) was 1.0 (sensitivity 100%, specificity 100%) with a cut-off value of 5.37 ng/L, indicating a strong discriminatory potential between CAD patients and healthy controls. However, the diagnostic performance of total circulating miRNAs (AUC = 1.0) was observed in a relatively small, single-centre cohort and should be considered exploratory, requiring confirmation in larger, independent studies.DiscussionOur study provides further evidence of complex interactions between EPCs and total circulating microRNAs in coronary artery disease. The findings suggest that circulating microRNAs, particularly in combination with EPC-related parameters, may represent promising biomarkers for clinical differentiation and characterization of endothelial dysfunction in CAD patients.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1880546</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1880546</link>
        <title><![CDATA[Transcriptome analysis of ageing in a long-lived seabird reveals sex-specific differences across age classes in immune and DNA repair pathways]]></title>
        <pubdate>2026-07-15T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Beatrice Berardi</author><author>Giacomo Dell'Omo</author><author>David Costantini</author>
        <description><![CDATA[IntroductionSex differences in ageing rate and longevity are widespread across animals, but their molecular bases remain poorly understood. Ageing involves multiple hallmarks of functional decline, and experimental studies suggest sex-specific differences in gene expression, particularly in immune, metabolic, and mitochondrial pathways. Yet, transcriptional variation associated with sex and age in natural populations remains largely unexplored.MethodsHere, we present the first RNA-seq study of a free-living bird, the Scopoli’s shearwater (Calonectris diomedea), aimed at investigating sex differences in gene expression across age classes, comparing younger and older individuals of both sexes (16 males and 16 females).ResultsWe identified a sex-linked transcriptional signature involving genes associated with immune function, stress response, energetics, and development. Age-related reductions in energy metabolism were more pronounced in females, whereas the strongest sex-related differences were detected in immune function and genome stability pathways. Across age classes, males showed higher expression of genes involved in DNA repair and genome maintenance, while females displayed a shift from immune-related processes in early adulthood to stress-response pathways in late adulthood.DiscussionTogether, these findings reveal pronounced sex-biased transcriptional regulation across age classes, which we hypothesise is driven by the differentiation of sex-specific reproductive strategies during the egg-laying phase. Furthermore, our results indicate sustained investment in somatic maintenance into late adulthood, consistent with patterns typically observed in long-lived species.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1724246</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1724246</link>
        <title><![CDATA[Automated generation of personalized trajectories of aging phenotypes with DyViA-GAN]]></title>
        <pubdate>2026-07-15T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Saumyadipta Pyne</author><author>Deep Ray</author><author>Meghana Ray</author>
        <description><![CDATA[With a general increase in human lifespan, the need for technological advances to develop strategies for healthy aging has assumed great importance. In the present study, our goal is to predict the progression of selected aging phenotypes in a given healthy individual as they age past 65 years. Therefore, we developed a novel framework called dynamic views of aging with conditional generative adversarial networks (or DyViA-GAN) that can predict the plausible personalized trajectories of a selected aging phenotype conditioned on the available measurements of the phenotype at a few initial time instances and additional covariates. Given the prevalence of osteoporosis in the aging population, we selected the femoral neck bone mineral density (BMD) of a healthy individual as the phenotype of interest and baseline individual body mass index (BMI) as a covariate. We trained DyViA-GAN on a publicly available longitudinal dataset of a large cohort of mostly white women in the United States of age 65 years or above. It generated, for each individual, continuous phenotype trajectories, along with a corresponding region of acceptable predictions, for an age range of 66–89 years, for eight different combinations, both with and without involving the covariate. The prediction results were subjected to rigorous quality control and multiple comparative analyses. Our results clearly demonstrate the potential of generative deep learning frameworks in healthspan research.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1872170</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1872170</link>
        <title><![CDATA[Omega-3 fatty acids as modulators of advanced glycation end products in aging: mechanistic pathways and clinical implications - a narrative review]]></title>
        <pubdate>2026-07-14T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Anna Cortesi</author><author>Irene P. Tzanetakou</author><author>Konstantinos Giannakou</author><author>Aikaterini Bograkou-Tzanetakou</author><author>Elena Hadjimbei</author>
        <description><![CDATA[BackgroundAging is characterised by the progressive accumulation of advanced glycation end products (AGEs), formed through non-enzymatic glycation reactions between reducing sugars and proteins, lipids, or nucleic acids. AGEs contribute to tissue damage through irreversible protein cross-linking and receptor-mediated inflammatory signalling via the receptor for AGEs (RAGE). Elderly individuals are disproportionately affected due to cumulative oxidative stress, chronic low-grade inflammation (inflammaging), impaired renal and enzymatic clearance, and prolonged exposure to dietary AGEs. Omega-3 polyunsaturated fatty acids (PUFAs), particularly eicosapentaenoic acid (EPA) and docosahexaenoic acid (DHA), may modulate these pathways through anti-inflammatory, antioxidant, and metabolic mechanisms.ObjectivesTo synthesise available preclinical, in vitro, and clinical evidence on the mechanistic and therapeutic relationships between omega-3 PUFA supplementation and AGE formation, accumulation, and signalling, and to evaluate the effects of omega-3 supplementation on key age-related clinical outcomes in elderly populations, including cardiometabolic health, cognitive function, mental health, functional capacity, and quality of life.MethodsA narrative review was conducted using searches of PubMed, Scopus, and Web of Science. Eligible study designs included in vitro experiments, animal models, randomised controlled trials (RCTs), observational studies, and systematic reviews published in English. Evidence was synthesised thematically across mechanistic and clinical domains, with priority given to studies addressing AGE-related pathways and clinically relevant endpoints.ResultsPreclinical evidence demonstrates that omega-3 PUFAs attenuate oxidative stress and inflammatory signalling, partly through RAGE axis regulation and PPARγ activation. Clinical studies report reductions in circulating AGEs, RAGE, and pentosidine following supplementation, alongside upregulation of protective scavenger receptors such as AGER1. Omega-3 supplementation has also been associated with improvements in inflammatory markers, cardiometabolic risk, cognitive function, and physical capacity in older adults. However, RCT evidence assessing tissue-level AGE accumulation using non-invasive measures such as skin autofluorescence remains limited in elderly populations.ConclusionOmega-3 PUFAs demonstrate therapeutic potential in modulating AGE-related mechanisms and improving age-associated outcomes. Well-designed RCTs targeting tissue AGE accumulation and long-term endpoints in elderly cohorts are warranted.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1845642</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1845642</link>
        <title><![CDATA[Association between life’s essential 8 and activities of daily living disability in Chinese adults aged 80 years and older: a cross-sectional study from the CLHLS]]></title>
        <pubdate>2026-07-10T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Jiaxin Huang</author><author>Bing Feng</author><author>Ge Chang</author><author>Chaoqun Geng</author><author>Weimin Bai</author><author>Jianchao Li</author>
        <description><![CDATA[BackgroundMaintaining functional independence is a major goal of healthy ageing in the oldest-old, yet evidence on the association between Life’s Essential 8 (LE8)and activities of daily living (ADL) disability in this population remains limited. We examined the associations between LE8 and ADL disability among Chinese adults aged ≥80 years.MethodsThis cross-sectional studyincluded 909 adults aged ≥80 years from the 2014 wave of the Chinese Longitudinal Healthy Longevity Survey biomarker sub-study. Cardiovascular health was assessed using the American Heart Association’s LE8framework. ADL disability was defined as at least one limitation across six basic activities, and disability severity was categorized as 0, 1, or ≥2 limitations. Multivariable logistic regression and proportional odds ordinal logistic regression were used to examine associations of LE8 with ADL disability and disability severity.ResultsIn the fully adjusted model, each 10-point higher LE8 score was associated with reduced odds of ADL disability [odds ratio (OR): 0.77, 95% confidence interval (CI): 0.62–0.95], and participants in the highest tertile had reduced odds than those in the lowest tertile (OR: 0.57, 95% CI: 0.34–0.95). Similar associations were observed for disability severity (per 10-point increase: OR: 0.77, 95% CI: 0.62–0.94). Restricted cubic spline analysis showed a significant overall association without strong evidence of nonlinearity. In component-level analyses, physical activity and diet showed the most prominent inverse associations with ADL disability.ConclusionHigher LE8 scores were associated with a lower ADL disability burden among Chinese adults aged ≥80 years. These fingdings support the potential value of LE8 as an integrated framework for characterizing functional vulnerability in the oldest-old.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1862298</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1862298</link>
        <title><![CDATA[Hip-hop dance participation and cognitive, gait, and muscle mass outcomes in community-dwelling older adults: a multi-site longitudinal study]]></title>
        <pubdate>2026-07-10T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Atsuko Miyazaki</author><author>Takashi Okuyama</author><author>Hayato Mori</author><author>Kazuhisa Sato</author><author>Sawako Ono</author><author>Atsushi Hiyama</author>
        <description><![CDATA[BackgroundDance-based interventions show promise for maintaining function in older adults, but long-term effects on body composition remain unclear. This study examined the effects of a hip-hop dance program on cognitive function, gait, and muscle mass over up to 3 years.MethodsThis multi-site longitudinal study included 102 community-dwelling older adults (mean age 74.2 years, 93% female) from six sites in Japan. The dance group (n = 74) participated in weekly hip-hop dance sessions and competed in the FIDA GOLD CUP, a competition for older adults. Controls (n = 28) maintained usual activities. Outcomes included cognitive function (MMSE, MoCA visuospatial), gait parameters, physical function, and body composition (SMI, segmental lean mass, BMI). Linear mixed models examined group × time interactions, and ANCOVA with permutation tests compared change scores in participants with complete data (n = 59).ResultsSignificant group × time interactions favoring the dance group were observed for MMSE (β = 0.58 points/year, p = 0.007) and MoCA visuospatial (β = 0.27/year, p = 0.023). Gait improved through temporal parameters: left contact time decreased (β = −0.018 s/year, p = 0.005) and gait speed increased (β = 0.065 m/s/year, p = 0.031), while stride length remained unchanged (p = 0.243). Right hip abduction strength (β = 1.22 kg/year, p = 0.016) and right single-leg stance time (β = 10.3 s/year, p = 0.026) improved. However, the dance group showed greater decline in skeletal muscle mass index (β = −0.064 kg/m2/year, p = 0.020) and leg segmental lean mass (left: β = −0.108 kg/year, p < 0.001; right: β = −0.088 kg/year, p = 0.004), while BMI remained unchanged (p = 0.949). ANCOVA confirmed these patterns for cognition, gait, and body composition outcomes.ConclusionHip-hop dance participation was associated with better preservation of cognitive function and more favorable gait-related change, characterized by enhanced temporal control rather than increased stride length. Specifically, reduced contact time and faster cadence suggest rhythm-based motor learning as the underlying mechanism. However, dance participation alone was not sufficient to prevent age-related muscle loss, indicating the need for combined interventions incorporating resistance training and adequate protein intake.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1875447</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1875447</link>
        <title><![CDATA[Predictive value of preoperative neutrophil-to-lymphocyte ratio for prognosis in aortic dissection patients without hypertension following TEVAR]]></title>
        <pubdate>2026-07-09T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Shun Yu</author><author>Xinghua Liu</author><author>Kunyu Guan</author><author>Liang Chen</author><author>Hao Zhang</author><author>Dengqun Sun</author><author>Yanjun Sun</author><author>Lixue Zhu</author><author>Lijun Weng</author><author>Biao Wu</author>
        <description><![CDATA[BackgroundThe neutrophil-to-lymphocyte ratio (NLR) serves as a potential inflammatory biomarker for aortic dissection (AD), with elevated levels predicting adverse postoperative outcomes. Nevertheless, the prognostic significance of preoperative NLR in non-hypertensive AD patients receiving thoracic endovascular aortic repair (TEVAR) remains undefined.ObjectiveTo evaluate the predictive value of preoperative NLR for clinical prognosis in this specific cohort following TEVAR.MethodsThis study retrospectively analyzed 116 non-hypertensive AD patients undergoing TEVAR at our medical center (December 2014–December 2020). Receiver operating characteristic (ROC) curve analysis determined the optimal NLR cutoff, area under the curve (AUC), and 95% confidence interval (CI) for predicting the primary endpoint (all-cause mortality). Patients were stratified into low-NLR and high-NLR groups based on the cutoff. Survival differences were assessed using Kaplan-Meier analysis with log-rank testing. Associations between NLR and mortality risk were evaluated via univariate and multivariate Cox regression.ResultsThe cohort comprised 77.6% males, with 52.6% aged >55 years, 30.2% reporting smoking history, 13.8% alcohol use, and 14.7% comorbidities. Anatomical classification included Stanford type A (5.2%) and type B (94.8%); temporal classification was acute (12.1%), subacute (30.2%), and chronic (57.8%). Branch artery reconstruction was performed in 47.4% of patients. Postoperative outcomes included all-cause mortality (1.7%), dissection recurrence (3.4%), endoleak (6.0%), and secondary intervention (9.5%). NLR demonstrated strong predictive efficacy (cutoff: 7.69; sensitivity: 96.4%; specificity: 65.9%; AUC = 0.83, 95% CI: 0.76–0.90). The high-NLR group exhibited significantly reduced survival compared to the low-NLR group (P < 0.001). Univariate Cox regression identified high NLR (HR = 30.766, 95% CI: 4.177–226.611, P = 0.001) and branch reconstruction (HR = 2.335, 95% CI: 1.090–5.001, P = 0.029) as mortality risk factors. Multivariate analysis confirmed high NLR as an independent risk factor for all-cause death (HR = 2.033, 95% CI: 1.004–3.221).ConclusionPreoperative NLR elevation is significantly linked to decreased survival following TEVAR in AD patients with aortic dissection, and it may function as an independent predictor of all-cause mortality. This parameter may be used as a reliable prognostic marker for this specific patient group.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1873618</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1873618</link>
        <title><![CDATA[Comparative evaluation of deep learning models for three-class frailty assessment using gait metrics]]></title>
        <pubdate>2026-07-07T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Charmayne Mary Lee Hughes</author><author>Yan Zhang</author>
        <description><![CDATA[BackgroundFrailty assessment in older adults typically relies on subjective clinical tools that are time-consuming and require trained personnel, limiting their use in routine or large-scale screening. Wearable sensor-based gait analysis offers a promising objective alternative; however, comprehensive evaluations of deep learning models for multi-class frailty classification using structured gait metrics remain limited.MethodsThis study evaluates multiple deep learning architectures for three-class frailty classification using structured gait features derived from a single wearable inertial measurement unit (IMU). Four architectures (Transformer, ShapeFormer, InceptionTime, and LSTM-CNN) were evaluated using the publicly available GSTRIDE dataset, comprising 163 older adults (non-frail: n = 65, pre-frail: n = 77, frail: n = 21). Eleven clinically interpretable stride-level gait variables, extracted from a single IMU, were used as model input. A 10-fold participant-level cross-validation scheme, matching the default configuration of the original implementation (cv_seed = 1), was applied to ensure robust performance estimation and prevent data leakage.ResultsThe four architectures yielded comparable mean accuracy under a unified protocol (ShapeFormer 73.1% ± 10.6%, Transformer 72.6% ± 6.0%, InceptionTime 70.5% ± 9.5%, LSTM-CNN 65.9% ± 9.8%). A Friedman omnibus test on the per-fold scores did not reject the null of equal performance (borderline on accuracy and macro-F1 (p = 0.050 and 0.056 respectively), with no significant difference for macro-AUC [p = 0.840]), indicating that the apparent ranking is within sampling variability. Performance was higher for non-frail and pre-frail individuals, while classification of frail individuals remained challenging across all models.ConclusionMulti-class frailty classification using structured gait metrics from a single wearable sensor is feasible, though performance varies across models and frailty classes. Model stability and sensitivity to specific classes represent important trade-offs.SignificanceThese findings support the development of scalable, objective approaches to frailty assessment and underscore the importance of selecting models based on clinical priorities.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1864375</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1864375</link>
        <title><![CDATA[Sex-specific remodeling of proteasome complexes in lymph nodes of aged BTBR mice]]></title>
        <pubdate>2026-07-06T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Francesca Monittola</author><author>Michela Bruschi</author><author>Sofia Masini</author><author>Domenico Pio Losito</author><author>Mauro Magnani</author><author>Luigia Rossi</author><author>Alessandra Fraternale</author><author>Rita Crinelli</author>
        <description><![CDATA[Lymph node architecture and function are markedly altered with aging. We previously demonstrated that the lymph nodes of old C57BL/6 and BTBR male mice contain reduced levels of PA28αβ-capped proteasomes compared to young mice. Here, we examined aged BTBR females relative to aged males and found that proteasome remodeling occurs in a sex-specific manner. Specifically, old female exhibited higher immunoproteasome activity than old male, despite similar levels of proteasome and immunoproteasome subunit expression and proteasome complex assembly. In female mice activity was mostly driven by PA28αβ-capped 20S proteasomes that declined with age in males. These results highlight intriguing differences in proteasome assembly and activity between males and females providing evidence for sex-dependent changes in immunosenescence.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1797166</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1797166</link>
        <title><![CDATA[Aging and vaccines: impact of immunosenescence and inflammaging in vaccine response]]></title>
        <pubdate>2026-07-03T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Jalnar Albaloshi</author><author>Alhussain Alnakhli</author><author>Lamin B. Cham</author>
        <description><![CDATA[Historically, effective vaccination has saved millions of lives and made an enormous contribution to addressing global public health threats. However, aging is an inevitable factor that negatively affects vaccine effectiveness and efficacy. With age, humans develop dysregulation of innate immune pathways, increased levels of proinflammatory markers, thymic involution, declines in T- and B-cell numbers and function, dysregulated metabolism, and epigenetic alterations. Immunosenescence, the gradual deterioration of host immunity with age, plays a critical role in susceptibility to infection, disease progression, and vaccine efficacy. Immunosenescence is often accompanied by inflammaging, an age-related increase in proinflammatory cytokine and chemokine levels. This multifactorial and dynamic process can lead to poor vaccine responses, potentially resulting in higher morbidity and mortality in older adults. Therefore, research focused on understanding the impact of immunosenescence and inflammaging on vaccine response will undoubtedly help optimize vaccine delivery among elderly individuals. In this review, we summarize the most recent knowledge on the multifactorial effects of age-induced immunosenescence and inflammaging and their role in vaccine efficacy against respiratory tract infections. The review further discusses strategic approaches such as IL-7 therapy, senolytic therapy, increasing telomerase activity, use of mTOR inhibitors, B cell therapy, development of broader vaccines and new adjuvants, and positive lifestyle changes, to enhance vaccine immunogenicity and efficacy in older adults. This could provide theoretical insights to improve vaccine effectiveness in the elderly and help address major global health issues.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1819415</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1819415</link>
        <title><![CDATA[Effects of a multicomponent exercise program on the gross and fine motor skills of healthy, sporting inactive older adults aged 60+]]></title>
        <pubdate>2026-07-03T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Anneke Schumacher</author><author>Marlene Krumpolt</author><author>Lucas Sannemann</author><author>Kerstin Witte</author>
        <description><![CDATA[This study aimed to assess the effectiveness of a multicomponent exercise program with integrated popular sports on the gross and fine motor coordination of healthy but sporting inactive adults aged 60 and above. Coordinative abilities are a key determinant of maintaining independence in later life. From February 2022 until December 2024 a 6-month pre-post intervention study with three measurement points: at baseline (t0), after 3 months (t1), and after completion of the intervention (t2) was conducted. The intervention groups started quarterly during the intervention period. In the intervention group (IG) a total of 161 older adults (68.23 ± 4.47 years; f = 107, m = 54) participated in a twice-weekly 90-min training program integrating popular sports. Gross motor skills were assessed using the Karlsruhe Health-Oriented Coordination Test (KHCT), and fine motor skills via the Motor Performance Series (MLS). Results were compared with an inactive control group (CGinactive: n = 32) and an active reference group of senior dancers (CGactive: n = 23), which was assessed cross-sectionally at baseline only. Compared to the CGinactive, the IG demonstrated significant improvements in six of the seven gross motor tasks and in two of the four fine motor tasks (group*time interaction: p < 0.05; Relative Treatment Effect = ΔRTE ≥0.12). Post-intervention, the IG’s performance approached that of the CGactive. The findings suggest that the low-threshold, multicomponent exercise program may improve coordinative abilities in previously inactive older adults. However, results should be interpreted with caution due to the non-randomized design and variability within the sample.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1849400</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1849400</link>
        <title><![CDATA[Effects of an 8-month intergenerational adapted taekwondo training on functional fitness in senior novice practitioners]]></title>
        <pubdate>2026-07-03T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Francesca Di Rocco</author><author>Andrea Perazzetti</author><author>Emanuel Festino</author><author>Olga Papale</author><author>Simone Ciaccioni</author><author>Philip X. Fuchs</author><author>Veronica Del Duca</author><author>Salvatore Chiodo</author><author>Laura Capranica</author><author>Cristina Cortis</author><author>Andrea Fusco</author>
        <description><![CDATA[BackgroundAging is commonly associated with declines in functional fitness that can be effectively attenuated through mid-to long-term, multifaceted physical activity. However, physical activity performed by older adults often aims to maintain, rather than improve, physical fitness. Martial arts are increasingly recognized as suitable multimodal interventions for older adults, as they integrate balance, flexibility, motor control, and cognitive engagement. Within this framework, taekwondo may represent a feasible activity to preserve and enhance functional fitness. Moreover, intergenerational approaches (combining younger and older participants in shared training sessions) may further support adherence, motivation, and social-cognitive stimulation. Despite this potential, long-term programs involving novice older adults remain largely unexplored. Therefore, this study aimed to evaluate the effect of an 8-month intergenerational adapted taekwondo training program for older novice practitioners.MethodsThis single-arm pre–post observational study used a volunteer convenience sample without a control group. Twenty-one seniors (14 females and 7 males: 63–83 years) participated twice-weekly 60-min taekwondo training for 8 months with one weekly session performed together with 21 children (6–13 years). The “American Alliance for Health, Physical Education, Recreation, and Dance” test battery was used to assess the seniors’ functional fitness before and after the intervention based on flexibility, upper-body strength, aerobic endurance, agility/dynamic balance, and coordination. Linear mixed-effects models for repeated measures examined time and sex effects.ResultsSignificant (p < 0.05) improvements were observed in aerobic endurance and coordination, with normative compliance increasing from 14.3% to 33.3% and from 66.7% to 95.2%, respectively. No significant changes were found in upper body strength, agility/dynamic, or flexibility, though males outperformed females in the Chair sit-and-reach and endurance tests.DiscussionDespite the limited sample size and the lack of a control group, which limit causal inference and generalizability, the program was associated with improvements in selected functional fitness domains, particularly aerobic endurance and coordination, whereas flexibility, agility/dynamic balance, and upper-body strength did not change significantly, suggesting that intergenerational adapted taekwondo may represent a feasible long-term physical activity option for novice older adults.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1872693</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1872693</link>
        <title><![CDATA[Weight-adjusted-waist index, inflammation, and cognitive performance in older adults: a cross-sectional analysis from the Hordaland Health Study]]></title>
        <pubdate>2026-07-01T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ingrid Revheim</author><author>Lasse M. Giil</author><author>Ole Martin Steihaug</author><author>Hanne Rosendahl-Riise</author><author>Bård Erik Bogen</author><author>Ragnhild Eide Skogseth</author>
        <description><![CDATA[IntroductionObesity has been associated with reduced cognitive function, potentially through inflammatory and neuroinflammatory mechanisms. The weight-adjusted waist index (WWI) is a novel anthropometric measure capturing central adiposity. However, its association with cognitive performance has been scarcely studied, and it remains unclear whether inflammation influences this relationship. This study aims to examine the association between WWI and cognitive performance, and whether this association is explained by inflammatory markers.MethodsWWI was calculated as waist circumference divided by the square root of body weight (cm/√kg). Cognitive performance was assessed using a test battery comprising the Controlled Oral Word Association test (COWAT; verbal fluency), the Kendrick Object Learning Test (KOLT; memory), and a modified Digit Symbol Test (m-DST; processing speed). Inflammatory markers included C-reactive protein and the kynurenine-to-tryptophan ratio. Multivariable linear regression analyses were used to assess associations between WWI and cognitive test scores per standard deviation, and to evaluate potential attenuation by inflammatory markers.ResultsA total of 2,066 community-dwelling older adults (55% women; median age 71 years [IQR 70–72]) from the Hordaland Health Study (1997–99) with complete data on WWI and cognitive tests were included in the cross-sectional analyses. Higher WWI was associated with lower cognitive performance across all tests: COWAT (ß −0.06 [95% CI −0.10, −0.02]), KOLT (ß −0.06 [95% CI −0.11, −0.02]), and m-DST (ß −0.09 [95% CI −0.12, −0.04]). Adjustment for inflammatory markers did not attenuate these associations. Body mass index, waist circumference, body fat percentage, and lean mass index were not significantly associated with cognitive performance.ConclusionHigher WWI, reflecting greater central adiposity, was associated with lower performance across multiple cognitive domains. Inflammatory markers did not attenuate this relationship. Other anthropometric and body composition measures were not associated with cognitive performance. These findings suggest that central adiposity relative to body weight may be more relevant for cognitive health than overall body adiposity in older adults.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1804033</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1804033</link>
        <title><![CDATA[Handgrip strength across clinical conditions and health-related outcomes in older adults: a scoping review]]></title>
        <pubdate>2026-06-30T00:00:00Z</pubdate>
        <category>Review</category>
        <author>José Julián Bernal-Sánchez</author><author>Duber Esteban Uzuriaga-Fori</author><author>Sharon Estefany Rivera-Viveros</author><author>Zharick Marcela Viafara-Carabali</author><author>Esther Cecilia Wilches-Luna</author><author>Diana Yazmín Perafan-Gonzalez</author>
        <description><![CDATA[Background and AimHandgrip strength (HGS) is a simple, non-invasive, and widely used measure of muscle function that has been examined in relation to several health-related outcomes in older adults. This scoping review aimed to map the extent, range, and nature of the evidence on the relationship between HGS and clinical conditions or health-related outcomes in older adults and aging-related populations, with particular attention to population characteristics, outcome classification, and HGS measurement protocols.MethodsThis scoping review was reported in accordance with the PRISMA-ScR checklist. Observational studies, including cross-sectional, cohort, longitudinal, and panel designs, were eligible when they examined HGS in relation to clinical conditions or health-related outcomes in older adults or aging-related populations. Searches were conducted in ScienceDirect, Scopus, Web of Science, LILACS, SciELO, and MEDLINE via PubMed, with SpringerLink used as a supplementary publisher platform. Articles published in English, Spanish, or Portuguese were considered. Study selection, data charting, and methodological appraisal were performed using structured forms. Findings were synthesized descriptively by study characteristics, health-related domain, HGS measurement protocol, and HGS operationalization.ResultsThe search identified 890 records, and 18 studies comprising 243,334 participants were included in the final synthesis. Ten studies were cross-sectional, whereas eight used longitudinal, cohort, or panel designs. Neurocognitive and mental health outcomes were the most frequently examined domain, followed by musculoskeletal conditions or syndromes, functional outcomes, quality of life, frailty, comorbidity burden, and cardiovascular risk. HGS measurement varied across studies in terms of dynamometer type, hand assessed, number of attempts, summary value, cut-off points, and analytical operationalization. Lower HGS or HGS-related parameters were reported across studies in relation to poorer health-related outcomes, although study design, population heterogeneity, and differences in HGS protocols limited direct comparability.ConclusionThis review shows that HGS has been studied across multiple aging-related health domains, particularly neurocognitive and musculoskeletal outcomes. However, the predominance of observational designs and heterogeneity in HGS measurement and outcome definitions limit causal interpretation. Further longitudinal studies using standardized HGS protocols and consistent outcome definitions are needed.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1866981</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1866981</link>
        <title><![CDATA[Heterogeneous leukocyte telomere trajectories and inflammatory resolution 12 months after mild COVID-19: an exploratory cohort study]]></title>
        <pubdate>2026-06-30T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Daiane Renata dos Santos</author><author>Daniela Valadão Freitas Rosa</author><author>Arnaldo Santos Leite</author><author>Carolina Coimbra Marinho</author><author>Maria Aparecida Camargos Bicalho</author><author>Marco Aurelio Romano-Silva</author><author>Débora Marques de Miranda</author><author>Alexandre Guimarães de Almeida Barros</author>
        <description><![CDATA[BackgroundThe longitudinal interplay between leukocyte telomere length (LTL) and persistent immune activation after mild SARS-CoV-2 infection remains incompletely characterized.MethodsIn this exploratory observational study, 51 adults (76.5% female; mean age 39.0 ± 9.7 years) with RT-PCR-confirmed mild COVID-19 had blood sampled in the acute symptomatic phase and at 12 months. Relative LTL was quantified by qPCR (Cawthon T/S method, 36B4 reference). A 45-analyte multiplex bead-based immunoassay quantified circulating cytokines, chemokines and growth factors. Paired changes were assessed with Wilcoxon signed-rank tests; cross-sectional and longitudinal associations between immune mediators and LTL were evaluated by Spearman correlation with Benjamini–Hochberg false discovery rate (FDR) control and by multivariable linear regression adjusted for baseline LTL, age, sex and comorbidity burden.ResultsForty-eight participants had paired LTL data. Group-level T/S ratio increased modestly between the acute phase and 12 months (mean Δ = +0.0094; Wilcoxon p = 0.041; Cohen’s d_z = 0.31), but interindividual trajectories were markedly heterogeneous (52% increased, 33% decreased, 15% unchanged). Twenty of 45 cytokines decreased significantly between timepoints (FDR <0.05), consistent with systemic resolution of acute inflammation. Among residual immune mediators at 12 months, hepatocyte growth factor (HGF) was inversely associated with the LTL trajectory (Spearman ρ = −0.48; p = 0.0005; FDR = 0.024). This association persisted in a multivariable model adjusted for baseline LTL, age, sex and comorbidity count (β = −0.040; 95% CI −0.061 to −0.018; p = 0.0006), and the model explained 43% of variance in T/S1. Cytokines previously highlighted in similar cohorts (IL-7, IL-9, IL-17A, EGF) showed univariable correlations that did not survive FDR correction.ConclusionTwelve months after mild SARS-CoV-2 infection, leukocyte telomere trajectories are highly individual, while most acute-phase inflammatory mediators have resolved. Residual circulating HGF, a pleiotropic factor recognized as a component of the senescence-associated secretory phenotype but also involved in tissue repair, endothelial activation, and metabolic signaling, was the only mediator robustly associated with the longitudinal LTL trajectory after multiple-testing correction and may identify a subgroup with persistent tissue-remodeling or senescence-associated activity. This association is interpreted as exploratory and hypothesis-generating rather than as a validated biomarker. Given the absence of an uninfected control group, modest sample size, and qPCR-based LTL quantification, these findings should be interpreted as hypothesis-generating.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1776669</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1776669</link>
        <title><![CDATA[Mechanistic redundancy and hierarchy of aging mechanisms: implications for strategies to extend healthspan and biomarker integration]]></title>
        <pubdate>2026-06-29T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Maria Shvedova</author>
        <description><![CDATA[Aging involves a network of interrelated biological processes that differ in causality and impact. This review proposes a hierarchical framework of primary, secondary, and tertiary drivers of human aging while emphasizing the extensive feedback loops and mechanistic redundancy. Primary mechanisms include molecular damage, particularly genomic and mitochondrial DNA damage, and mutation accumulation that cumulatively result in genomic instability, and telomere attrition, which represents a separate primary driver. Although rarely recognized as an independent aging mechanism, female sex hormone decline, particularly the abrupt loss of sex steroid signaling at menopause and earlier perimenopausal changes, may constitute a primary sex-specific driver of human aging as an evolved process that amplifies molecular and physiological deterioration. Mechanisms acting as both primary and secondary include damage to molecules other than DNA including protein damage with loss of proteostasis and lipid damage, which may arise directly from molecular insults or emerge as downstream consequences of DNA damage and other primary mechanisms, while also feeding back to accelerate upstream deterioration. Secondary mechanisms comprise cellular senescence, impaired macroautophagy, deregulated nutrient sensing, epigenetic alterations, mitochondrial dysfunction, and altered intercellular communication. These processes emerge downstream of initial damage and further reciprocally reinforce it. Tertiary mechanisms of aging comprise stem cell exhaustion, chronic inflammation, and dysbiosis, which represent the system-level deterioration exacerbating molecular dysfunction. This hierarchical network-based model suggests that many hallmarks of aging may represent manifestations of redundant upstream molecular insults. This review focuses on primary mechanisms as the causative drivers of aging and proposes that the strategy to extend healthspan may require preventive approaches targeting distinct redundant primary mechanisms. Complex preventive interventions that simultaneously reduce molecular damage, slow telomere attrition, and compensate for estrogen depletion may delay the initiation and amplification of secondary and tertiary aging mechanisms. This framework supports coordinated multi-target strategies for healthspan extension and underscores the need for validated biomarkers that reflect these upstream processes as part of an integrated preventive approach.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1791524</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1791524</link>
        <title><![CDATA[Impact of biopsychosocial frailty trends on survival and quality of life of older adults: a secondary analysis of data from a community-based active monitoring program]]></title>
        <pubdate>2026-06-26T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Giuseppe Liotta</author><author>Olga Madaro</author><author>Clara Donnoli</author><author>Fabio Riccardi</author><author>Giulia Picardo</author><author>Fausto Ciccacci</author><author>Michele Bisogno</author><author>Paola Scarcella</author>
        <description><![CDATA[BackgroundAdvancing age frequently brings about a complex condition known as biopsychosocial frailty, which significantly impacts an older adult’s survival and quality of life. This research investigates how changes in frailty levels affect mortality, hospitalization, and institutionalization, utilizing data from the “Long Live the Elderly!” program, a community-based initiative focused on proactive monitoring.MethodsA secondary analysis was conducted on data from 6,802 older adults participating in the LLE program across six Italian cities. Frailty was assessed using the Short Functional Geriatric Evaluation, which encompasses physical, psychological, and socio-economic dimensions. Trends in frailty were analyzed over an average follow-up period of 4.6 years, with survival outcomes evaluated using Cox proportional hazard models.ResultsAt baseline, 40.0% of participants were robust, 25.9% pre-frail, 27.4% frail, and 6.7% very frail. Frailty levels deteriorated in 36.9% of participants, while 11.2% experienced improvement. Higher frailty levels were significantly associated with increased mortality, hospitalization, and institutionalization. However, individuals whose frailty remained stable or improved showed significantly lower mortality rates compared to those whose frailty declined. Socio-economic enhancements were linked to better frailty outcomes, while psychophysical deterioration was the primary driver of declines.ConclusionFrailty is a dynamic condition that may improve or worsen over time. Stabilizing or improving frailty trajectories was associated with reduced mortality, hospitalization, and institutionalization, supporting the relevance of multidimensional frailty monitoring in community settings These findings can support the importance of proactive multidimensional frailty monitoring in aging populations.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1872180</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1872180</link>
        <title><![CDATA[From molecular damage to regulatory constraint: epigenetic and metabolic limits of cellular plasticity in aging]]></title>
        <pubdate>2026-06-26T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Antoni R. Godlewski</author><author>Tomasz Dziaman</author>
        <description><![CDATA[Aging is most often portrayed as the progressive buildup of molecular damage, yet this conventional view leaves much unexplained. Over time, cells and tissues appear to lose the regulatory flexibility that allows them to adapt, repair, and reconfigure their functional states. Genomic instability, metabolic imbalance, mitochondrial dysfunction, and proteostatic decline converge on aging, but their effects focus on chromatin organization, transcriptional coordination, and signaling networks that maintain cellular identity. In this review, we propose that aging can be usefully viewed as a progressive restriction of epigenetic and regulatory plasticity, rather than as the simple accumulation of lesions. Pathways such as Wnt signaling, TET-dependent DNA demethylation, and metabolic sensors including AMPK, mTOR, and sirtuins create an interconnected landscape that links environmental and metabolic conditions with long-term cellular behavior. As this landscape becomes increasingly rigid and constrained, cells retain viability but lose their capacity for dynamic responses, stabilizing in low-plasticity states that include cellular senescence. Framing aging as a shift from adaptive plasticity toward regulatory rigidity offers a possible integrative lens on classical hallmarks and epigenetic aging signatures, without replacing existing models. Rather than targeting individual hallmarks in isolation, future approaches may need to complement hallmark-focused strategies by restoring dynamic balance within epigenetic and signaling networks that preserve tissue-level homeostasis and regenerative potential, thereby suggesting specific, testable predictions for interventions acting on metabolic–epigenetic axes.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1802482</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1802482</link>
        <title><![CDATA[Employed cancer survivors develop a peer-support intervention to improve social connections: a participatory design study]]></title>
        <pubdate>2026-06-26T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Alicia G. Dugan</author><author>Keith M. Bellizzi</author><author>Hannah L. Austin</author><author>Sara Namazi</author><author>Jennifer M. Cavallari</author>
        <description><![CDATA[IntroductionAmong the 4.3 million working-age breast cancer survivors in the U.S., employment offers financial stability, purpose, and normalcy. However, many face barriers that hinder workforce participation, including social disconnection. Using a participatory intervention design approach that directly engages survivors, this study aimed to identify root causes of disconnection and prioritize solutions to support psychosocial wellbeing and work retention.MethodsThis study recruited six employed breast cancer survivors for a design team that used the Intervention Design and Analysis Scorecard’s (IDEAS) Steps 1-5 to develop and prioritize intervention options. The team, facilitated by university researchers, met for seven 1-h sessions. Qualitative data from IDEAS worksheets and meeting notes were analyzed.ResultsSurvivors identified three causes of social disconnection: (1) changes in self-concept and worldview, (2) symptom-related social withdrawal, and (3) unsupportive responses from others. The team developed and evaluated three intervention models, considering scope, effectiveness, resources, and barriers. An intervention including written materials, a website, a peer-led support group, and a social media forum, was prioritized as the most feasible and impactful option. A follow-up study will pilot-test the intervention to assess effects on wellbeing and work outcomes.DiscussionThe team prioritized a multi-component intervention to foster connection and work engagement primarily targeting individual and interpersonal factors rather than workplace-level factors, likely reflecting the absence of a common employer. Findings highlight social connection as a modifiable target and support further intervention development and pilot-testing, with attention to accessibility and relevance across diverse survivor populations through cultural, economic, and structural adaptations.]]></description>
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