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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>2026-06-03T12:04:16.910+00:00</pubDate>
        <ttl>60</ttl>
        <item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1838730</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1838730</link>
        <title><![CDATA[The SIRT1–p53 axis drives a ferro-aging-like program and aggravates trophoblast dysfunction in preeclampsia]]></title>
        <pubdate>2026-06-03T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Rong Hu</author><author>Zhi Chen</author><author>Wei Bian</author><author>Jing Zhang</author><author>Xiaoqin Xu</author><author>Hui Xiong</author><author>Shaojian Xiang</author><author>Yubin Ding</author><author>Hongbo Qi</author><author>Huan Yang</author>
        <description><![CDATA[Preeclampsia (PE) is a pregnancy-specific syndrome driven by placental dysfunction, and premature placental senescence has increasingly been implicated in its pathogenesis. However, the upstream regulatory mechanisms remain poorly understood. Here, we found that placental SIRT1 expression was reduced in PE and was accompanied by senescence-associated features. In trophoblasts, SIRT1 knockdown enhanced senescence and senescence-associated secretory phenotype (SASP) release, while impairing proliferative capacity, migration, and invasion, whereas pharmacological activation of SIRT1 attenuated placental senescence and ameliorated PE-like manifestations in vivo. Mechanistically, iron chelation alleviated senescence, whereas senolytic intervention partially restored iron homeostasis, supporting a self-reinforcing interaction between iron dyshomeostasis and senescence. Collectively, these findings identify the SIRT1–p53 axis as an upstream regulator linking iron dyshomeostasis to placental senescence, support the existence of a ferro-aging-like pathogenic program in diseased placentas, and provide new insights into the molecular basis of placental dysfunction in PE.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1780273</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1780273</link>
        <title><![CDATA[Studying exercise-induced affect in older adults: how the circumplex model could enhance theoretical and practical advances in the field]]></title>
        <pubdate>2026-06-03T00:00:00Z</pubdate>
        <category>Hypothesis and Theory</category>
        <author>Attila Szabo</author><author>Celal Bulgay</author><author>Erzsébet Stephens-Sarlós</author><author>Róbert Járai</author><author>Angéla Somogyi</author><author>Szilvia Boros</author><author>Robert Podstawski</author><author>Ferenc Ihász</author><author>Roberto Ruíz-Barquín</author><author>Ricardo de la Vega</author>
        <description><![CDATA[Although decades of research show the health benefits of regular exercise in older adults, the affective mechanisms underlying these benefits remain poorly understood. In fact, research on exercise-induced affect has generally lacked a clear framework for explaining how specific exercise features influence emotional experiences in older adults. This theoretical paper addresses this critical gap by proposing the circumplex model of affect as a comprehensive approach to understanding how exercise modifies valence (pleasure–displeasure) and arousal (activation–deactivation) in older adults. Using interdisciplinary evidence, we explore how neurobiological mechanisms (e.g., BDNF-mediated neuroplasticity and oxidative stress regulation) and hormonal pathways may differently affect affective valence and arousal, the two main dimensions of the circumplex model, during aging. We also explore how key exercise variables, such as intensity, type, duration, and frequency, are linked to distinct affective profiles within the circumplex model, and how individual differences in cognition, health, and socioeconomic status influence these relationships. Our review of the literature reveals that heavy reliance on one-dimensional mood measures has masked important differences between emotional quality and activation level. We argue that using the circumplex approach allows for a clearer understanding of exercise affect links and moves the field beyond the vague claim that exercise improves mood. This circumplex theoretical framework could provide a stronger foundation for developing targeted, evidence-based exercise interventions to improve affective outcomes alongside physical health benefits in older adults.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1854915</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1854915</link>
        <title><![CDATA[The metabolic-epigenetic landscape of aging: interplay between histone acetylation, lactylation, and glycation]]></title>
        <pubdate>2026-06-03T00:00:00Z</pubdate>
        <category>Mini Review</category>
        <author>Olena Bolgova</author><author>Inna Shypilova</author><author>Volodymyr Mavrych</author>
        <description><![CDATA[BackgroundThe aging epigenome is shaped by three mechanistically distinct histone post-translational modifications—acetylation, lactylation, and glycation—each driven by a different metabolic flux: mitochondrial oxidative phosphorylation, glycolytic lactate production, and reactive carbonyl stress, respectively. Understanding their interplay is central to a molecular physiology of epigenetic aging.ScopeThis mini review synthesizes current evidence on the mechanisms of histone acetylation, lactylation, and glycation in aging; their crosstalk and convergence on shared regulatory nodes; and their modulation by environmental, nutritional, and behavioral factors. Key controversies and research gaps are critically appraised.Key FindingsNAD + decline in aging disables the sirtuin deacetylase family, dysregulating the histone acetylation landscape and impairing autophagy, mitochondrial biogenesis, and DNA repair. Histone lactylation, written by p300 at H3K18 and related lysine residues, is context-dependent: physiological pulses during exercise and sleep are adaptive, while chronic accumulation in diabetic microglia drives neuroinflammation via TLR4/NF-κB, and excess in tumor cells enables senescence bypass. Histone glycation by methylglyoxal irreversibly displaces regulatory marks and inactivates sirtuin proteins; pharmacological induction of glyoxalase I and glycation-lowering interventions reduce this burden and extend healthspan. These three axes may converge on a unified metabolic-epigenetic collapse that we propose constitutes the cellular basis of an ‘aging’ metabolic memory.Controversies and GapsLactylation erasers remain uncharacterized; the pro-versus anti-senescence duality of H3K18la is unresolved; and genome-wide histone glycation mapping in human tissues is absent.ConclusionCombinatorial interventions targeting NAD + restoration, modulation of lactylation, and reduction of carbonyl stress offer the most evidence-based approach to slowing metabolic-epigenetic aging.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1840035</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1840035</link>
        <title><![CDATA[Homeodynamic Rejuvenation: an adaptive framework for resetting skin aging]]></title>
        <pubdate>2026-06-03T00:00:00Z</pubdate>
        <category>Perspective</category>
        <author>Anthony Brown</author><author>Carla Simonetto</author><author>Carlos López-Otín</author>
        <description><![CDATA[Skin aging reflects not only the accumulation of molecular damage, but also a progressive decline in the skin’s ability to restore equilibrium under continuous environmental stress. Classical models distinguishing intrinsic and extrinsic aging do not fully capture this dynamic process. In this article, we introduce Homeodynamic Rejuvenation as the restoration of functional competence and biological vitality, achieved not through reversal of visible signs of aging, but by re-establishing the skin’s ability to detect stress, coordinate adaptive responses, and recover efficiently following perturbation. Central to this framework is the concept of homeodynamic plasticity, which reflects the skin’s intrinsic capacity to dynamically sustain function under environmental and metabolic stress. By integrating principles of homeodynamics with exposome biology, this approach targets the reactivation of the cellular systems that govern stress sensing, repair, and recovery. Five core biological processes, namely, intracellular quality control, regenerative competence, metabolic resilience, cellular integrity, and structural integrity, underpin homeodynamic plasticity. Disruption or failure of one or more of these processes results in progressive functional decline, culminating in skin aging, of which dermatoporosis, a chronic cutaneous insufficiency syndrome, represents a terminal manifestation. These interconnected processes provide a coordinated basis for both restoring and assessing skin function. We propose that Homeodynamic Rejuvenation is best evaluated through dynamic perturbation–recovery kinetics, which quantify the skin’s ability to respond to and recover from stress. By linking these biological processes to measurable functional and clinical outcomes, Homeodynamic Rejuvenation offers a structured and translational framework for quantifying and restoring skin resilience.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1849207</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1849207</link>
        <title><![CDATA[Deep cervical lymphaticovenous anastomosis for Alzheimer’s disease: theoretical foundations, regulatory suspension, and translational challenges]]></title>
        <pubdate>2026-06-02T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Gang Li</author><author>Shusheng Jiao</author><author>Yi Zhou</author><author>Xiaofang Cheng</author>
        <description><![CDATA[Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by pathological changes in β-amyloid protein deposition, abnormal tau protein phosphorylation neurofibrillary tangles, and chronic neuroinflammation. Recent studies have shown that the glymphatic-meningeal-cervical lymphatic system pathway plays a crucial role in the clearance of intracranial metabolic waste. Dysfunction of this system may lead to a decrease in the clearance efficiency of Aβ and tau proteins. Deep cervical lymphaticovenous anastomosis (DCLVA) has been proposed as a novel surgical approach to enhance cervical lymphatic drainage, reduce Aβ/tau accumulation, and improve cognitive function in patients with AD. However, on 8 July 2025, the National Health Commission of China issued a notice prohibiting the clinical application of “deep cervical lymphaticovenous anastomosis” for the treatment of AD. This article provides a narrative review with critical appraisal of the theoretical basis, surgical mechanisms, and clinical evidence of DCLVA for AD. We objectively evaluate the strengths and limitations of current clinical studies, critically appraise the uncertainty of underlying physiology, and comprehensively analyze the potential risks, safety concerns, and translational obstacles that led to regulatory suspension. We further clarify unresolved scientific questions including pressure gradients, lymphatic contractility, reflux risk, anastomotic patency, and biomarker validation. By framing DCLVA within the context of its clinical prohibition, we provide clinicians and researchers with a balanced appraisal that acknowledges both the procedure’s potential and the substantial gaps that must be addressed before widespread application can be justified.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1837722</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1837722</link>
        <title><![CDATA[Physiological amplitude: a systems-level framework for adaptive capacity in aging and metabolism]]></title>
        <pubdate>2026-06-02T00:00:00Z</pubdate>
        <category>Hypothesis and Theory</category>
        <author>Grazyna Sepczynska</author>
        <description><![CDATA[BackgroundAging is characterized by progressive loss of physiological complexity, inter-system coordination, and adaptive capacity. While mitochondrial dysfunction, metabolic inflexibility, impaired stress responses, and circadian dysregulation are well established, an integrative systems-level construct linking these processes remains lacking.ObjectiveTo introduce physiological amplitude as a unifying framework describing the bounded dynamic range of coordinated variability across interacting physiological systems.MethodsWe develop a conceptual, hypothesis-generating framework grounded in network physiology and systems biology, integrating mitochondrial function, metabolic flexibility, hormetic stress responses, and circadian regulation into a unified architecture of system-level adaptation.ResultsPhysiological amplitude is defined as the bounded dynamic range within which coordinated multiscale physiological dynamics are maintained. Aging is conceptualized as a progressive contraction of this accessible range across interconnected biological networks. This framework distinguishes physiological amplitude from variability and resilience by positioning it as a higher-order property emerging from constraint-defined interactions across physiological systems.ConclusionPhysiological amplitude provides an integrative framework for interpreting multiscale physiological dynamics and generates testable hypotheses for quantification using continuous monitoring and network-based analysis. As a candidate systems-level descriptor, it may support the development of integrative biomarkers of aging and metabolic decline, pending empirical validation.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1829442</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1829442</link>
        <title><![CDATA[Increased neurotoxic gliosis and blood-brain barrier dysregulation in canine cognitive dysfunction syndrome (CCD)]]></title>
        <pubdate>2026-06-02T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Sean W. Boland</author><author>Greta N. Coyner</author><author>Sydney J. Risen</author><author>Abdullatif Alsulami</author><author>Stephanie McGrath</author><author>Julie A. Moreno</author>
        <description><![CDATA[BackgroundAs Alzheimer’s Disease (AD) and related dementias (ADRD) prevalence is projected to double by 2050, the urgency for relevant models to study its pathology intensifies. Aging is the primary risk factor for AD development and influenced by a myriad of factors including neurotoxic glial activation and BBB degradation; however, historically AD models consist of transgenic mouse in-vivo and in-vitro methods. While this offers many strengths, it is limited in their ability to mimic aging induced AD pathology. Currently, canine cognitive dysfunction (CCD) syndrome is being investigated as it is a natural and spontaneous disease with similar pathologies to AD and other dementias. Our lab and many others have worked extensively to characterize CCD pathology. However, the role of microglial and astrocytic activation and the interplay between the blood-brain barrier (BBB) have not been investigated. This study aims to fill this gap in knowledge in CCD and in turn its relation to human AD. We hypothesize that CCD-afflicted canines will exhibit increased neurotoxic glial activation and BBB degradation.Methods/ResultsWe utilized immunohistochemistry (IHC), morphological analyses, and immunofluorescence to investigate CCD pathology comparing CCD negative and CCD positive dogs. In this study we see glial morphology consistent with those seen in neurotoxic glia in neurodegenerative disease, increased S100β/C3 astrocyte activation, decreased claudin-5 expression, and region-dependent perivascular AQP4 expression modulation in dogs with CCD, compared to those without CCD.ConclusionOur results further characterize glial and BBB roles in CCD pathogenesis and reinforces the strengths of modeling AD/ADRD in aging dogs.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1844227</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1844227</link>
        <title><![CDATA[Aging strong: an N = 1 mixed-methods study of long-term supervised high-intensity resistance training in a 71-year-old woman]]></title>
        <pubdate>2026-06-01T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Itai Har-Nir</author><author>Noam Manor</author><author>Jana Pelclova</author>
        <description><![CDATA[Older adults who engage in long-term, supervised high-intensity resistance training (HIRT) may preserve musculoskeletal function, independence, and psychological resources beyond typical age-related expectations. This N = 1 mixed-methods study characterized an upper-bound example of “aging strong” in a 71-year-old woman after eight consecutive years of structured HIRT. The participant completed three 60-min HIRT sessions per week emphasizing multi-joint lifts performed close to muscular failure, alongside high daily ambulatory activity and a protein-rich diet. A convergent assessment battery integrated dual-energy X-ray absorptiometry (DXA), one-repetition maximum tests, load–velocity and load–power profiling, functional performance tests (Short Physical Performance Battery, Timed Up and Go, 30-s chair stand, push-ups to failure), validated questionnaires of general self-efficacy and self-esteem, and a semi-structured interview analyzed using reflexive thematic analysis. DXA showed low whole-body fat (15.1%) and a high appendicular lean mass index (10.33 kg·m‐2), exceeding age-matched reference values and sarcopenia thresholds. Maximal strength was exceptional (bench- and leg-press one-repetition maximum of 1.05× and 3.85× body weight, respectively), and functional performance indicated minimal disability risk (Short Physical Performance Battery 12/12, Timed Up and Go 6.08 s, 30-s chair stand 21 repetitions). Load–velocity profiling revealed unusually slow minimal-velocity thresholds, causing standard group-based equations to underestimate measured one-repetition maximum by 11–28%, while load–power curves demonstrated high peak power at approximately 57% of one-repetition maximum in both exercises. Psychological assessments indicated high self-efficacy (35/40) and self-esteem (34/40), and qualitative themes highlighted strength as a foundation for resilience, emotional regulation, unwavering adherence, empowered body image, and training as a central life identity. Together, these integrated findings suggest that long-term, supervised HIRT may support a virtuous cycle in later life in which exceptional strength, power, favorable body composition, and functional independence are tightly linked with robust psychological resources and sustained adherence.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1826382</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1826382</link>
        <title><![CDATA[Gut microbiota-epigenetic interactions in systemic aging: mechanistic drivers for endocrine and reproductive network remodeling and therapeutic modulation]]></title>
        <pubdate>2026-06-01T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Christopher Birigwa</author><author>Qiang Tong</author><author>Bing Qu</author><author>Teng Zuo</author><author>Wenzheng Yuan</author><author>Jing Xiong</author><author>Jianfei Luo</author>
        <description><![CDATA[Researchers now see aging as a process shaped by the interactions among metabolism, epigenetics, and hormones. Recent studies suggest that gut microbes play an important role in this system by making metabolites that can affect gene expression and chromatin structure. Still, it is not fully clear how gut microbes and the body influence each other as we age, since both are constantly changing. This review brings together current research on how metabolites from gut microbes—such as short-chain fatty acids, bile acids, tryptophan derivatives, and polyamines—affect the body’s epigenetic machinery through processes such as DNA methylation, histone modifications, and chromatin remodeling. We examine evidence from cell studies, animal experiments, and human research to assess the strength of the links and distinguish direct effects on chromatin from indirect metabolic or gene-expression changes. We focus especially on endocrine and reproductive organs, such as the hypothalamus, pancreas, liver, fat tissue, and cells that support the gonads, where signals from gut microbes overlap with hormonal control and metabolism. In these tissues, microbial metabolites influence key pathways related to inflammation, mitochondria, and nutrient sensing, but there is still little direct evidence in humans. The review also points out differences between lab models and what is observed in patients, highlighting the need for further work to apply these findings in real-world settings. Interactions between gut microbes and epigenetics form a two-way link between metabolism, immunity, and aging of the endocrine system. While more evidence shows that microbial metabolites can shape gene activity and epigenetic patterns, most of what we know comes from animal studies rather than direct tests in people. Moving forward, researchers will need to use broad, long-term studies that combine different types of data to figure out cause and effect and which tissues are involved. Understanding this system better could help create new biomarkers and treatments to influence aging by targeting the microbiome and its effects on epigenetics.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1822206</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1822206</link>
        <title><![CDATA[Measurement properties of the SARC-T: test-retest reliability, agreement and minimal detectable change in older adults with sarcopenia]]></title>
        <pubdate>2026-05-29T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Blanca Pedauyé-Rueda</author><author>José Luis Maté-Muñoz</author><author>Juan Hernández-Lougedo</author><author>Cristian Solís-Mencía</author><author>Rebeca Bueno-Fermoso</author><author>Arturo Cano-Uceda</author><author>Cristina Ojedo-Martín</author><author>Pablo García-Fernández</author>
        <description><![CDATA[BackgroundThe Sarcopenia Optoelectronic Chair-Rise Velocity Test (SARC-T) has been proposed as an instrumented chair-rise measure related to physical function in sarcopenia; however, its test-retest measurement properties have not been established. This study evaluated the test-retest reliability, agreement, measurement error and minimal detectable change at the 95% confidence level (MDC95) of the SARC-T in older adults with sarcopenia.MethodsAn observational methodological test-retest study was conducted in 55 institutionalized older adults with sarcopenia diagnosed according to EWGSOP2 criteria. The SARC-T was assessed in two sessions separated by 5 days under standardized conditions. The primary outcome was the best mean propulsive velocity recorded during the concentric phase. Test-retest reliability was assessed using ICC (3,1), Lin’s concordance correlation coefficient (CCC), standard error of measurement (SEM), MDC95, Bland–Altman analysis, and a linear mixed-effects model.ResultsTest-retest reliability was high (ICC = 0.93, 95% CI 0.88–0.96; CCC = 0.93, 95% CI 0.86–0.96). Measurement error was low (SEM = 0.017 m/s), and MDC95 was 0.05 m/s. Bland–Altman analysis showed a small but statistically significant mean bias of +0.008 m/s (p = 0.015), with 95% limits of agreement from −0.042 to +0.058 m/s, and additional analysis showed statistically significant proportional bias (slope = 0.161; p = 0.009). A small systematic session effect was also observed in the mixed-effects model (β = +0.008 m/s; 95% CI 0.002–0.018; p = 0.012).ConclusionUnder the standardized conditions of the present protocol, the SARC-T showed high test-retest reliability and low measurement error; however, the presence of statistically significant mean and proportional bias indicates that agreement is not fully uniform across the measurement range and should be interpreted with caution, particularly at the individual level. The MDC95 may help interpret whether longitudinal changes in mean propulsive velocity are likely to exceed measurement-related fluctuation. These findings should be considered within the context of this specific population of institutionalized older adults with sarcopenia.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1837212</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1837212</link>
        <title><![CDATA[Underuse of osteoporosis treatments before and after hip fracture: longitudinal findings from the Gruppo Italiano di Ortogeriatria (GIOG 2.0) study]]></title>
        <pubdate>2026-05-29T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Maria Cristina Ferrara</author><author>Wenxiang Guo</author><author>Eleonora Cucini</author><author>Alice Margherita Ornago</author><author>Elena Tassistro</author><author>Elena Pinardi</author><author>Alberto Finazzi</author><author>Paolo Mazzola</author><author>Chukwuma Okoye</author><author>Maria Grazia Valsecchi</author><author>Chiara Mussi</author><author>Giuseppe Sergi</author><author>Andrea Ungar</author><author>Raffaele Antonelli Incalzi</author><author>Stefano Volpato</author><author>Giuseppe Bellelli</author>
        <description><![CDATA[BackgroundOsteoporosis is a major cause of fragility fractures, with hip fracture (HF) representing the most severe complication in older adults. However, national data on osteoporosis treatment use before and after hip fracture in Italy are limited.MethodsThis multicenter prospective study included individuals aged ≥65 years admitted for HF between July 2019 and June 2024 at 12 orthogeriatric centers. Osteoporosis treatments (vitamin D, calcium, antiresorptive, anabolic, dual effect agents) were recorded at admission, discharge, and 120- and 365-day follow-ups. Patients were classified as “Never users” if untreated throughout the study period or “Ever users” if treated at least once. Multivariate logistic regression identified factors independently associated with lack of treatment.ResultsAmong 1,012 patients (median age 83 years; 77.2% female), 85.6% were untreated at admission; this proportion dropped to 34.4% at discharge but rose again to 50% at 1 year. Vitamin D and calcium were the predominant treatments, while antiresorptive, anabolic, and dual effect agents were underused. Overall, 22% of patients were classified as “Never users”. They were generally older, more often male, and had higher comorbidity, dementia, frailty, and mobility limitations. Only male sex was independently associated with lack of treatment (Odds Ratio 2.37, 95% Confidence Intervals 1.59–3.55).ConclusionDespite clinical guideline recommendations, osteoporosis treatment remains suboptimal among older HF patients in Italy, especially in male patients. Findings support the need for national programs and multidisciplinary strategies to reduce the treatment gap and improve long-term management.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1811330</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1811330</link>
        <title><![CDATA[The lifespan and healthspan extending effects of ellagic acid in Caenorhabditis elegans require an intact insulin/IGF-1 signaling pathway]]></title>
        <pubdate>2026-05-29T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Lipeng Xu</author><author>Jinze Li</author><author>Anran Li</author><author>Jixian Chen</author><author>Liping Wang</author><author>Yaming Shan</author><author>Xianbin Cheng</author>
        <description><![CDATA[IntroductionEllagic acid (EA) is a naturally occurring polyphenolic antioxidant speculated to influence aging, but its precise biological mechanisms remain poorly understood.MethodsUsing Caenorhabditis elegans as a model system, we investigated the anti-aging properties of EA. Lifespan assays were performed at multiple concentrations, and healthspan parameters including locomotor activity, lipofuscin accumulation, and reactive oxygen species (ROS) levels were assessed under thermal and oxidative stress. Genetic requirement was examined using loss-of-function mutants of daf-16, hsf-1, hlh-30, and skn-1. Gene expression was analyzed by qRT-PCR and reporter strains, and global transcriptional changes were mapped by RNA-sequencing.ResultsEA extended lifespan and preserved key healthspan features, including improved locomotor activity, reduced intestinal lipofuscin accumulation, and decreased ROS levels under stress conditions. The lifespan-extending effects of EA required daf-16, hsf-1, hlh-30, and skn-1, as EA failed to extend lifespan in these mutants. EA also enhanced the expression of downstream cytoprotective genes. Complementary RNA-sequencing revealed broader transcriptional remodeling, including metabolic pathways.DiscussionThese findings position EA as a modulator of a coordinated transcriptional network—rather than a single pathway—involving the insulin/IGF-1 signaling pathway and interconnected stress-response networks to promote longevity and stress resistance.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1811756</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1811756</link>
        <title><![CDATA[Strategies of oral hygiene care for healthy aging: insights from elderly care in Taiwan]]></title>
        <pubdate>2026-05-29T00:00:00Z</pubdate>
        <category>Opinion</category>
        <author>Ming-Kuo Chen</author><author>Patrick Pang</author><author>Yi-Huang Shih</author><author>Ting Liu</author><author>Huiwen Zou</author>
        <description></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1844391</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1844391</link>
        <title><![CDATA[CD21+CD11c+ B cells predicting handgrip strength decline in older adults]]></title>
        <pubdate>2026-05-29T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Diego Mabe-Castro</author><author>Matías Mabe-Castro</author><author>Lindybeth Sarmiento Varón</author><author>Marcelo A. Navarrete</author><author>Matías Castillo-Aguilar</author><author>Cristian Núñez-Espinosa</author>
        <description><![CDATA[BackgroundPreserving physical function is central to healthy aging, and declines in handgrip strength are strong predictors of frailty, disability, and mortality. Although immunosenescence has been implicated in age-related functional decline, the contribution of specific B-cell subsets to longitudinal changes in muscle strength remains poorly understood.ObjectiveTo examine whether baseline B-cell phenotypes are associated with 1-year changes in handgrip strength in community-dwelling older adults.MethodsSixty-two adults aged ≥60 years from the Magallanes Region, Chile, underwent baseline and 1-year follow-up assessments of handgrip strength and body composition. Peripheral B-cell subsets were characterized by flow cytometry, identifying CD45+CD19+ lymphocytes and classifying subsets according to CD21 and CD11c expression. Associations between baseline B-cell subsets and 1-year change in handgrip strength were evaluated using robust linear regression adjusted for age, sex, and change in muscle mass.ResultsParticipants showed a significant 1-year decline in handgrip strength (mean change: −2.02 kg), whereas muscle mass remained stable. Higher baseline frequencies of CD19+CD21+CD11c+ B cells were independently associated with greater decline in handgrip strength over 12 months (βstd = −0.31, CI95% [-0.60, −0.03], p = 0.031). No other B-cell subset was associated with changes in handgrip strength or muscle mass.ConclusionBaseline levels of CD19+CD21+CD11c+ B cells were associated with a subsequent decline in handgrip strength in community-dwelling older adults, independent of change in muscle mass. These findings support a potential link between B-cell phenotypes and functional decline, warranting further investigation in larger cohorts.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1822042</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1822042</link>
        <title><![CDATA[Cognitive decline, and quality of life: evidence from community-dwelling older adults in the United Arab Emirates]]></title>
        <pubdate>2026-05-29T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Wegdan Bani Issa</author><author>Dana N. Abdelrahim</author><author>Hadia Radwan</author><author>Manal Awad</author><author>Farah Naja</author><author>Roba Saqan</author><author>Tamer Shousha</author><author>Heba Khalil</author><author>Ayat Nashwan</author><author>Adam Ibrahim</author><author>Hajar Ibrahim</author><author>Latifa Alsaad</author><author>Heba Hijazi</author><author>Alham Al-Sharman</author><author>Rachel Rossiter</author><author>Jassim Alhammadi</author><author>Mohamad Alameddine</author>
        <description><![CDATA[BackgroundCognitive function and quality of life (QoL) are closely linked in older adults, with accumulating evidence suggesting that cognitive performance is an important determinant of overall perceived QoL in older adults.ObjectivesTo examine cognitive function and its association with multidimensional QOL among adults aged ≥60 years in the United Arab Emirates (UAE) and identify sociodemographic and lifestyle correlates.MethodsA cross-sectional study of 606 community-dwelling older adults from the UAE (55.4% male; mean age 67.2 ± 5.8 years) assessed cognitive function (MoCA) and QOL (OPQoL-Brief). Associations were analyzed using correlation and multiple linear regression (p < 0.05) between the sociodemographic factors and cognitive function (MOCA) to QOL.ResultsParticipants aged 60–87 years were predominantly Emirati (84.2%), married (77.6%), and living with family (96.7%). Cognitive impairment was present in 69.3% (40.9% mild, 24.8% moderate, 3.6% severe), with the lowest abstraction scores. Mean QOL was 4.21 ± 0.51/5, lowest in social engagement. Cognitive impairment independently predicted lower QOL (β = 0.138; 95%CI: 0.043–0.232; p = 0.001), along with female sex, older age, lower education or income, unmarried status, living alone, and low physical activity.ConclusionCognitive function is a key determinant of QOL, supporting integrated, person-centered aging strategies in the UAE.]]></description>
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        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1822261</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1822261</link>
        <title><![CDATA[Sex-specific differences in vascular circulation and metabolic regulation associated with aging and cardiovascular health problems]]></title>
        <pubdate>2026-05-28T00:00:00Z</pubdate>
        <category>Brief Research Report</category>
        <author>Andrzej Marcinek</author><author>Joanna Katarzynska</author><author>Jerzy Gebicki</author>
        <description><![CDATA[The Flow Mediated Skin Fluorescence–Post-Occlusive Reactive Hyperemia (FMSF–PORH) technique proves that the skin can serve as an easily accessible and sensitive model for monitoring systemic redox changes in the NADH/NAD+ balance. The three most important diagnostic parameters of the method are related to the response to transient ischemia. Hyperemic Response (HRmax) characterizes the hyperemia phase and reflects the rapid increase in macrocirculatory blood flow after occlusion of the brachial artery. Hypoxia Sensitivity (HS) characterizes the reperfusion phase, by assessing the activation of myogenic microcirculatory oscillations. Ischemic Response (IRmax) is related to the ischemia phase and reflects the adaptation of cellular metabolism to ischemia. All three FMSF–PORH parameters depend on health condition and age. Sex-specific differences in the FMSF–PORH parameters are not seen in young healthy individuals, but appear with cardiovascular health problems and/or advanced age. Females compared to males have a significantly lower the IRmax parameter, characterizing metabolic (mitochondrial) regulation. In contrast, the HRmax parameter, characterizing macrocirculation, is higher in females than in males. All parameters slowly deteriorate with age and cardiovascular health problems. The results of this study highlight the need for a sex-specific perspective on vascular and metabolic health, as well as differentiated preventive healthcare strategies.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1791384</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1791384</link>
        <title><![CDATA[Physical exercise therapy as an anti-aging strategy for osteosarcopenia: a narrative review]]></title>
        <pubdate>2026-05-28T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Ting ting Liu</author><author>Pengwei Zhang</author><author>Wan tao Dong</author><author>Yan long Gong</author><author>Zhi jie Fang</author><author>Ning Li</author><author>Xin Ma</author>
        <description><![CDATA[With global population aging accelerating, osteosarcopenia—the coexistence of sarcopenia and osteoporosis—has become a critical health challenge leading to frailty, falls, and disability in the elderly. This syndrome is closely linked to chronic inflammation, metabolic imbalance, and cellular aging. Physical exercise therapy, as a non-pharmacological intervention, shows unique advantages in preventing musculoskeletal degeneration and restoring metabolic homeostasis. Evidence indicates that regular aerobic and resistance exercise promotes osteogenesis and muscle protein synthesis while inhibiting bone and muscle loss through mechanical loading, regulation of myokines and osteokines, and energy metabolism remodeling. Key molecular pathways include activation of the SIRT1/AMPK/PGC-1α axis, modulation of mTOR signaling, and suppression of inflammatory cytokines such as IL-6 and TNF-α, which collectively enhance mitochondrial function and reduce oxidative stress. Moreover, physical exercise strengthens muscle–bone crosstalk via factors like irisin, myostatin, osteocalcin, and sclerostin, exerting systemic anti-aging effects. Future studies should emphasize personalized physical exercise prescriptions combined with biomarker monitoring and smart technologies to achieve sustainable musculoskeletal health and promote healthy aging.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1839065</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1839065</link>
        <title><![CDATA[Tobacco, biological aging and epigenetic resilience: the Andorran paradox]]></title>
        <pubdate>2026-05-26T00:00:00Z</pubdate>
        <category>Perspective</category>
        <author>Pooja Reddy</author><author>Dhairya Nanavaty</author><author>Pradeepkumar Devarakonda</author><author>Pedro Moreno</author>
        <description><![CDATA[Longevity is not solely determined by the absence of risk factors but often reflects the balance between harmful exposures and protective adaptations. We introduce the framework of epigenetic resilience as a counterbalancing mechanism by which favorable environmental and lifestyle factors can potentially offset detrimental influences such as tobacco use. Tobacco is a well-established accelerator of biological aging through adverse epigenetic reprogramming, yet populations such as Andorra paradoxically exhibit both high smoking prevalence and some of the longest life expectancies worldwide. This observation underscores the potential role of resilience factors—including diet, physical activity, psychosocial cohesion, and environmental context—that may buffer or counteract the negative epigenetic imprints of smoking. By highlighting this paradox, we emphasize the importance of understanding how protective influences reshape DNA methylation landscapes to sustain healthspan despite harmful exposures. Recognizing and enhancing epigenetic resilience might offer a path toward targeted interventions that could mitigate the consequences of tobacco and other stressors, ultimately informing strategies to promote healthy aging at both individual and population levels.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1832962</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1832962</link>
        <title><![CDATA[An overview of current research on exercise interventions in aging and aging-related disease]]></title>
        <pubdate>2026-05-26T00:00:00Z</pubdate>
        <category>Review</category>
        <author>Arad Jain</author><author>Campbell Johnston</author><author>Yiyu Zhang</author><author>Janice Oh</author><author>Carolyn Tsung</author><author>Eric Kent</author><author>Hongji Zhang</author>
        <description><![CDATA[Global declines in physical activity have contributed to an acceleration in immune aging, characterized by systemic inflammation (inflammaging) and impaired immune regulation (immunosenescence). This narrative review provides an overview of the evidence in both preclinical and clinical models supporting exercise as a critical intervention to counteract immune aging and its related diseases. Regular physical activity modulates systemic inflammation, reduces neutrophil extracellular trap (NET) formation, and promotes favorable shifts in immune cell populations, including T cell and natural killer (NK) cell subsets. Exercise interventions have been associated not only with maintaining immune health but also in mitigating autoimmune disease progression, improving metabolic regulation, enhancing tumor immune surveillance, and reducing neuroinflammation. Emerging studies highlight the role of exercise in promoting vascular normalization within the tumor microenvironment, alleviating tumor hypoxia and acidosis, and restoring T and NK cell function. In the elderly, appropriately prescribed multimodal exercise regimens may lower infection risk without clear evidence of immunodepression, supporting exercise as a potentially safe and effective strategy for immune rejuvenation. Furthermore, novel mechanistic insights, including the modulation of NET burden, IGF-1 signaling, kynurenine metabolism, and microbiome composition, suggest that exercise influences key biological pathways underlying age-related immune decline. While exercise offers broad clinical benefits, future research should prioritize mechanistic studies to optimize exercise prescriptions and inform the development of exercise-mimetic therapeutics. Taken together, investigating the exercise regimens employed in these studies remains a promising intervention for promoting healthy immune aging and improving resilience against chronic inflammatory, metabolic, infectious, and malignant diseases.]]></description>
      </item><item>
        <guid isPermaLink="true">https://www.frontiersin.org/articles/10.3389/fragi.2026.1770257</guid>
        <link>https://www.frontiersin.org/articles/10.3389/fragi.2026.1770257</link>
        <title><![CDATA[Inflammatory biomarkers and sarcopenia in older adults]]></title>
        <pubdate>2026-05-25T00:00:00Z</pubdate>
        <category>Original Research</category>
        <author>Ahalya Kanakan</author><author>Anup Singh</author><author>Sarita Kumari</author><author>Surendra Pratap Mishra</author>
        <description><![CDATA[Chronic inflammation contributes to the pathogenesis of sarcopenia in older adults. This study aimed to evaluate the correlation between inflammatory biomarkers such as C-reactive protein (CRP), tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), and the anabolic hormone insulin-like growth factor-1 (IGF-1) with sarcopenia. A hospital-based case-control study was conducted among patients aged ≥60 years attending the Geriatric Medicine outpatient clinic. Participants were screened using the SARC-F tool and sarcopenia diagnosis was confirmed according to the Asian Working Group for Sarcopenia (AWGS) criteria. Serum levels of CRP, IL-6, TNF-α, and IGF-1 were measured using enzyme-linked immunosorbent assay (ELISA) in 30 sarcopenic cases and 30 age- and sex-matched controls. Group differences were assessed using independent samples t-test or Mann–Whitney U test, and correlations were evaluated using Spearman’s rank correlation coefficient. The mean ages of cases and controls were 67.6 ± 7.5 and 66.1 ± 6.2 years, respectively; females comprised 56.7% of cases and 46.7% of controls. Mean CRP (5.58 ± 2.47 mg/L vs. 2.98 ± 3.00 mg/L; p = 0.001) and TNF-α levels (176.66 ± 163.10 pg/mL vs. 45.10 ± 89.14 pg/mL; p < 0.001) were significantly higher in sarcopenic cases compared to controls. No statistically significant differences were found for IL-6 or IGF-1 levels. Increased CRP and TNF-α levels are associated with sarcopenia in older adults, suggesting a role of systemic inflammation in its pathogenesis. IGF-1, an anabolic hormone known to be influenced by inflammation, did not differ significantly between groups. Larger studies with rigorous exclusion of confounders are needed to validate these findings and clarify the role of inflammatory processes in sarcopenia.]]></description>
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