Idiopathic pulmonary fibrosis (IPF) is a paradigmatic aging-related lung disorder. In this retrospective cohort study, we evaluated 101 treatment-naïve patients at diagnosis (T0) and a subgroup (n = 31) after one year of antifibrotic therapy (T1). Analyses included leukocyte telomere length (LTL), DNA methylation age [DNAmAge assessed by Horvath, Levine (PhenoAge), Skin & Blood, Hannum, BLUP, Elastic Net (EN), and a 5-CpG panel], age acceleration (AgeAcc), and genetic susceptibility. At T1, LTL was independently predicted by baseline LTL (p = 0.0004) and treatment duration (p = 0.0056). Longitudinally, ΔLTL increased in nintedanib- versus pirfenidone-treated patients (p = 0.0402) and with treatment duration (p = 0.0233). DNAmAge modestly increased with chronological aging across all clocks, while AgeAcc remained stable, decreasing at follow-up (p = 0.0435) and higher in males (p = 0.0204). Genetic analyses on 17 IPF-associated SNPs confirmed enrichment of established risk variants, including MUC5B and DPP9, and identified an association between higher genetic burden and lower forced vital capacity (p = 0.0136). Extending this approach, genome-wide imputation enabled polygenic risk score (PRS) analysis, revealing significant case-control differences and discrimination (AUC up to 0.79), supporting a measurable polygenic contribution to disease susceptibility. These findings highlight the added value of integrating telomeric, epigenetic, and genome-wide genetic burden-captured through PRS-for improved risk stratification in IPF.

BACKGROUND:Soft tissue sarcomas (STSs) are rare malignancies with largely unknown etiology; the role of anthropometry and physical activity has been rarely explored. METHODS:We analyzed 2011-2019 data of an Italian, multicenter, hospital-based case-control study including 498 incident, histologically confirmed STS cases and 969 controls. Self-reported height, weight, and physical activity data were collected; hip and waist circumferences were measured in 76% of cases and 61% of controls. Odds ratios (ORs) and 95% confidence intervals (CIs) were estimated using multiple-adjusted logistic regression models. RESULTS:Compared with BMI < 25 kg/m 2 , the ORs for BMI one year prior to diagnosis/interview were 1.05 (95% CI: 0.80-1.37) for 25-29.9 kg/m 2 and 1.28 (95% CI: 0.90-1.83) for ≥30 kg/m 2 . The OR was increased for BMI 25-29.9 kg/m 2 at age 30; no association emerged for BMI at age 50 years. For waist circumference, the ORs were 1.93 (95% CI: 1.38-2.70) for >102 cm in males or >88 cm in females, and 3.54 (95% CI: 2.40-5.22) for the highest versus the lowest tertile. For waist-to-hip ratio, the ORs were 1.18 (95% CI: 0.81-1.71) for the intermediate, and 2.81 (95% CI: 1.95-4.03) for the highest tertile. Subjects reporting ≥5 h/week of total or intermediate/high intensity leisure-time physical activity at age 30-39 years had ORs of 0.63 (95% CI: 0.40-1.00) and 0.56 (95% CI: 0.32-1.00), respectively. CONCLUSION:These findings show a positive association between abdominal adiposity and STS risk, and an inverse association with regular leisure-time physical activity.

BACKGROUND:Soft-tissue sarcoma (STS) etiology is largely undefined. METHODS:We analyzed data from an Italian case-control study, including 498 incident, histologically confirmed STS cases and 969 hospital controls. Odds ratios (OR) of STS for self-reported personal medical history and family history of cancer were estimated using Firth penalized logistic regression models. RESULTS:STS risk was significantly increased with a history of burns [OR, 2.46; 95% confidence interval (CI), 1.10-5.47] and showed a nonsignificant excess with herpes zoster infection (OR, 2.31; 95% CI, 0.65-8.23). Hypertension (OR, 0.71; 95% CI, 0.53-0.94), hypercholesterolemia (OR, 0.66; 95% CI, 0.45-0.96), and tonsillectomy (OR, 0.69; 95% CI, 0.51-0.93) were more frequent among controls. No associations were observed for hepatitis, diabetes, immune-mediated diseases, fractures, surgeries other than tonsillectomy, tooth extraction, or blood transfusion. Family history of cancer showed no major associations, except for STS (0.6% of cases, 0.1% of controls, OR >7) and kidney cancer (OR, 4.69; 95% CI, 1.74-12.7). CONCLUSIONS:Our findings suggest a positive association with family history of STS although based on small numbers. Personal medical history and family history of other cancers had no major role; of interest are the suggestive associations of STS with a history of burns and herpes zoster. IMPACT:Further research is needed to replicate our findings and to explore potential underlying mechanisms.

Supplementary Materials S1 provides the questionnare used for data collection.

Supplementary Table S2 shows the distribution soft tissue sarcoma (STS) cases by histological type and controls, with odds ratios^ (OR) and corresponding 95% confidence intervals (CI), according to family history of any cancer and factors suggestively associated with STS risk in the main analysis.

Supplementary Table S1 shows Description of the 15 soft tissue sarcoma (STS) cases reporting history of burns.

Prolonged bed rest is a well-established human model of extreme physical inactivity, reproducing key features of accelerated aging, including muscle atrophy, metabolic dysregulation, low-grade inflammation, and oxidative stress (1,2). DNA methylation–based epigenetic clocks (DNAmAge) provide a sensitive tool to detect early biological aging responses to environmental stressors (3). DNAmAge was assessed in healthy subjects at baseline and after 21 days of bed rest, with paired analyses performed in the overall cohort and after sex stratification. In the whole sample, DNAmAge increased after bed rest compared with baseline. Sex-stratified analyses revealed a significant acceleration of DNAmAge in women, whereas no significant change was observed in men. The findings that will be presented strongly suggest that short-term bed rest triggers a sex-specific acceleration of epigenetic aging, with women showing greater sensitivity to muscle disuse. Sex- related differences in the biological response to unloading, including inflammatory, metabolic and mechanotransducive pathways, will be discussed as potential mechanisms underlying these epigenetic changes.

The growing global burden of type 2 diabetes (T2D) has prompted increasing attention to environmental factors that may contribute to its development. Among these, exposure to fine particulate matter (PM2.5) has emerged as a significant yet often overlooked risk factor. This systematic review conducted according to the PRISMA guidelines, provides a comprehensive and critical appraisal of the epidemiological evidence and discusses mechanisms linking PM2.5 exposure to the onset and progression of T2D. Long-term exposure to PM2.5 has been consistently associated with increased T2D risk in epidemiological studies, particularly among vulnerable groups such as individuals with obesity, metabolic syndrome, or advanced age. In addition, evidence from animal models suggests that acute exposure can exacerbate insulin resistance and impair glucose metabolism. Mechanistic studies highlight the roles of oxidative stress, systemic inflammation, endothelial dysfunction, and autonomic imbalance. Notably, recent findings implicate the transient receptor potential vanilloid 1 (TRPV1) in neurogenic inflammation and metabolic disruption, offering novel insights into how PM2.5 may influence glycemic control. Experimental evidence in humans indicates that traffic-related PM2.5, including diesel exhaust particles (DEPs), activates TRPV1, supporting its role as a molecular interface between environmental insults and metabolic disruption. Given its central role in neurogenic inflammation and metabolic regulation, TRPV1 has emerged as a promising therapeutic target. Preclinical studies have shown that pharmacological modulation of TRPV1 improves glucose tolerance and reduces inflammation. Currently, XEN-D0501, a TRPV1 antagonist, is undergoing clinical trials to assess its efficacy in regulating blood glucose and mitigating T2D-related inflammatory complications. These mechanistic insights are further supported by animal studies demonstrating that PM2.5 exposure induces metabolic dysfunction consistent with TRPV1 activation and inflammation-related pathways. Animal models corroborate human data, revealing that PM2.5 exposure promotes visceral adiposity, impairs hepatic insulin signaling, and triggers tissue-specific inflammation. Despite the strength of the overall evidence, heterogeneity in exposure assessment, driven by spatial and temporal variations in PM2.5 sources and composition, and in study design persists. Given the ubiquity of PM2.5 in urban environments, even modest increases in diabetes risk may translate into substantial public health burdens. Targeted policies to reduce air pollution, together with intensified research into biological susceptibility and prevention strategies, are essential. Addressing PM2.5 as a modifiable determinant of T2D represents a timely and actionable priority in environmental health.

As human life expectancy continues to rise, ageing and age-related diseases have become critical societal challenges, driving extensive research across genetics, molecular biology, biochemistry, and behavioral sciences. In this context, domestic dogs (Canis lupus familiaris) offer a unique model for ageing research due to their shared environmental exposures with humans, diverse genetic profiles, and relatively short lifespans. This review aims to identify potential biomarkers of ageing in dogs, facilitating a deeper understanding of age-related mechanisms and supporting the evaluation of interventions designed to promote healthy ageing. We present a research of peer-reviewed literature on age-related variations of various parameters across multiple biological systems, including epigenetic, telomere, immune, metabolic, and cognitive markers in dogs. Our findings highlight several robust biomarkers, such as DNA methylation-based epigenetic clocks, telomere attrition, CD4+/CD8+ T-cell ratio, hematological markers (e.g., globulin levels), and cognitive function scores. These biomarkers demonstrate strong parallels with human ageing processes, particularly concerning genomic and epigenetic alterations. However, challenges remain, including breed-specific variability, body size differences, and inconsistent evidence regarding inflammageing markers, such as pro-inflammatory cytokines. Despite these limitations, indicators of chronic inflammation (e.g., anemia of chronic disease and elevated globulins) are evident in older dogs. Future research directions include the standardization of biomarker protocols for dogs, the development of longitudinal studies to track dynamic age-related changes, and further exploration of emerging biomarkers, such as those related to microbiome composition and oxidative stress.

Background/Objectives: This retrospective multicenter study, conducted within the ORCHESTRA Project, investigated SARS-CoV-2 reinfections among 5777 healthcare workers (HCWs) from four University Hospitals (Modena, Verona, Padova and Trieste) in northern Italy, aiming to assess the risk of reinfection and its determinants, comparing the clinical characteristics of reinfections with those of first infections, and examining the impact of preventive measures and vaccination strategies. Methods: HCWs completed an online questionnaire between June and August 2022. The survey collected demographic, occupational, and clinical data, including information on first infections and reinfections. Statistical analyses were performed using SPSS 28.0, through bivariate and multivariate approaches. Results: Response rates were 41.8% for Modena, 39.5% for Verona, 17.9% for Padova, and 17.4% for Trieste. Among the respondents, 4.8% (n = 276) experienced 2 infections and 0.5% (n = 27) reported 3 infections, out of a total of 330 reinfection cases. Additionally, 43.0% (n = 2787) reported only one infection, while 51.5% were never infected. Reinfection rates increased across five study phases (based on the epidemiological context), likely due to the emergence of new SARS-CoV-2 variants. A booster vaccine dose significantly reduced reinfection risk. Higher reinfection risk was found among HCWs aged ≤30 years, those with chronic respiratory diseases, and those working in COVID-19 wards, particularly nurses and allied health professionals. Reinfections were associated with a lower frequency of symptoms both during the period of swab positivity and after a negative swab, as well as with a shorter duration of swab positivity. No significant differences in symptom duration were found between first infections and reinfections. Conclusions: Despite its limitations, the online questionnaire proved a useful tool. Natural infection and vaccination reduced both reinfection risk and symptom severity. Prior infections should be considered in planning vaccination schedules and prioritizing HCWs.

DNA methylation represents a crucial epigenetic mechanism orchestrating gene expression, cellular homeostasis, and the aging trajectory. Dysregulation of DNA methyltransferases (DNMTs)-the enzymes catalyzing this process-has been implicated in a wide spectrum of chronic conditions, including cancer, cardiovascular and metabolic disorders, and neurodegenerative diseases. Emerging evidence suggests that food-derived bioactive compounds can act as DNMT inhibitors, reshaping epigenetic landscapes. This systematic review, registered in PROSPERO (CRD42022320316), critically evaluated in vitro, in vivo animal, and ex vivo studies investigating the effects of dietary bioactives on DNMT expression and activity. A thorough search of PubMed up to 23 May, 2025, yielded 103 studies, of which 76 met the inclusion criteria. Eligible publications were original, peer-reviewed, and provided evidence from in vitro, in vivo animal, or ex vivo models. Frequently studied bioactives included epigallocatechin-3-gallate, curcumin, genistein, resveratrol, sulforaphane, and folate. Notably, nearly 90% of studies reported DNMT inhibition-often dose- and time-dependent. Approximately 21% defined minimal effective concentrations, predominantly for isolated compounds. Several studies described synergistic interactions between bioactives, and emerging data highlighted the gut microbiota's mediating role in epigenetic modulation. Despite promising outcomes, the predominance of preclinical evidence and variability in experimental protocols and dosing limit the immediate translational impact. Nonetheless, current findings underscore the promise of dietary DNMT modulators as foundational elements for precision nutrition strategies aimed at promoting healthy aging and mitigating age-associated disease risk. The potential application of DNA methylation age as a biomarker of biological aging has been increasingly supported by recent literature, reinforcing its relevance in future nutritional epigenetics research. Further well-designed clinical trials are warranted to assess long-term efficacy, safety, and bioavailability of these compounds and to validate their use in personalized epigenetic interventions using biological aging markers. This review was funded by the European Union-Next Generation EU, PNRR Project Age-It (DM 1557 11.10.2022), and the University of Padua SID Grant (2024DCTV1SIDPROGETTI-00194).

Aging is driven by fundamental mechanisms like oxidative stress, telomere shortening and changes in DNA methylation, which together prepare the ground for age-related diseases. Botanical extracts, rich in bioactive phytoconstituents, represent a promising resource for developing therapies that target these mechanisms to promote healthy aging. This study explores the geroprotective potential of Monarda didyma L. extract. In vitro analyses revealed the extract's strong antioxidant activity, ability to reduce telomere shortening, and capacity to protect against DNA damage, thereby decreasing cellular senescence and improving endothelial function. The randomized, double-blind clinical trial demonstrated that daily oral supplementation with the extract significantly improved leukocyte telomere length (LTL) and stabilized DNA methylation age (DNAmAge) in the intervention group, while the placebo group experienced accelerated epigenetic aging and hypermethylation of critical age-related genes (ELOVL2 and FHL2). The intervention group also reported enhanced quality of life, particularly in the physical domain, along with improved movement and quality sleep indices detected by questionnaire and wearable sensors. These compelling findings position Monarda didyma L. extract as a powerful candidate for future geroprotective therapies, with the potential to significantly impact healthy aging.

IntroductionThe long-term dynamics of T-cell immunity following SARS-CoV-2 vaccination, essential for durable protection, remain incompletely understood. This study, therefore, aimed to investigate the kinetics and persistence of spike-specific T-cell responses in vaccinated healthcare workers.MethodsWithin the framework of the ORCHESTRA Project, we conducted a longitudinal study on the kinetics and persistence of CD4+ and CD8+ T cell immunity in healthcare workers (n=305) from four hospitals and public health centers across two European countries who received either 2 or 3 doses of an mRNA vaccine, with or without prior SARS-CoV-2 infection. Specifically, the anti-spike adaptive immune cellular response was evaluated, focusing on its crosstalk with the B cell response as measured by serology. Circulating cellular adaptive immune cells were extensively analyzed using flow cytometry to assess pro-inflammatory cytokine production (TNF-α, IFN-γ, IL-2), functional activation (CD154), and memory differentiation (CD45RO).ResultsOur findings show that anti-spike T cell reactivity is not influenced by age, with the only exception of a weak positive correlation with spike-specific CD8+CD45RO+ T lymphocytes (Spearman’s rho = 0.34, p<0.001), and an equally weak negative correlation with CD8+TNF+ (Spearman’s rho = -0.23, p<0.01). Other variables, such as gender and job category, did not significantly impact the vaccine-induced, anti-spike T cell immune response.DiscussionNo distinct relationship between CD4+ and CD8+ T cell subsets was observed post-vaccination. However, specific dynamic changes in vaccine-induced T cells were identified showing clear dose- and time-dependence. Finally, the median level of CD8+CD154+ lymphocytes, indicative of activated T cells, was significantly associated with infection incidence and may represent a reliable predictive biomarker. This study provides evidence that the vaccine-induced anti-spike cellular immune response should be considered when making vaccination decisions, as it has predictive value for infection risk.

This study explores the role of inflammation and oxidative stress, hallmarks of COVID-19, in accelerating cellular biological aging. We investigated early molecular markers—DNA methylation age (DNAmAge) and telomere length (TL)—in blood leukocytes, nasal cells (NCs), and induced sputum (IS) one year post-infection in pauci- and asymptomatic healthcare workers (HCWs) infected during the first pandemic wave (February–May 2020), compared to COPD patients, model for “aged lung”. Data from questionnaires, Work Ability Index (WAI), blood analyses, autonomic cardiac balance assessments, heart rate variability (HRV), and pulmonary function tests were collected. Elevated leukocyte DNAmAge significantly correlated with advancing age, male sex, daytime work, and an aged phenotype characterized by chronic diseases, elevated LDL and glycemia levels, medications affecting HRV, and declines in lung function, WAI, lymphocyte count, hemoglobin levels, and HRV (p < 0.05). Increasing age, LDL levels, job positions involving intensive patient contact, and higher leukocyte counts collectively contributed to shortened leukocyte TL (p < 0.05). Notably, HCWs exhibited accelerated biological aging in IS cells compared to both blood leukocytes (p ≤ 0.05) and NCs (p < 0.001) and were biologically older than COPD patients (p < 0.05). These findings suggest the need to monitor aging in pauci- and asymptomatic COVID-19 survivors, who represent the majority of the general population.

Abstract Background Manipulations to decelerate biological aging and extend health span are major challenges for health given the social and healthcare costs of aging population. Excessive oxidative stress and inflammation are primary drivers in biological aging and age-related diseases. Didymin, a natural bioactive flavonoid and the major polyphenol of Monarda didyma L., has showed a crucial anti-inflammatory role. This clinical study aims to investigate the potential benefits of a 12-weeks supplementation of Monarda didyma L. extract on reducing / delaying the biological aging of a susceptible population of aging workers. Methods This is a randomized, placebo-controlled, double-blind, parallel design and monocentric clinical trial. Study population will comprise 80 participants, aged 45–65 years, randomly allocated to both Intervention group (supplementation of Monarda didyma L. extract) and placebo control group (placebo supplementation) for a 12-weeks period of treatment. All study participants, who will be enrolled at the Occupational Medicine Unit – Azienda Ospedale Università of Padova providing a written informed consent, will undergo clinical examination, an interview with structured questionnaires (demographic data, lifestyle, information quality of life and sleeping patterns) and collection of fasting blood for evaluation of indicators of biological aging as primary outcomes (DNA methylation age, telomere length, mitochondrial DNA copy number), as well as secondary outcomes including basic biochemistry and inflammation markers (emocrome, glycemia, insulin, total cholesterol, low and high density lipoproteins, triglycerides, creatinine, telomerase expression, C-reactive protein, interleukin6, aspartate transaminase, alanine transaminase, gamma-glutamyl transferase) and salivary sample for cortisol analysis. Clinical examination and sample collection, to assess primary and secondary outcomes, will be performed at enrollment and at the follow up after of this treatment. Tracking of additional parameters (heart rate, sleep, mobility) will be performed along the study period by using a wearable MiBand 7 watch and a daily diary to determine compliance and record effects on stress, well-being and health status. Discussion The success of this research could represent a turning point in the healthy aging research, leading to rejuvenation by means of a sustainable and safe intervention, accessible to everybody in order to extend health span. Trial registration: ClinicalTrials.gov PRS (NCT05399966), registration date: May 17, 2022.

IntroductionPrior investigations into post-COVID dysautonomia often lacked control groups or compared affected individuals solely to healthy volunteers. In addition, no data on the follow-up of patients with SARS-CoV-2-related autonomic imbalance are available.MethodsIn this study, we conducted a comprehensive clinical and functional follow-up on healthcare workers (HCWs) with former mild COVID-19 (group 1, n = 67), to delineate the trajectory of post-acute autonomic imbalance, we previously detected in a case–control study. Additionally, we assessed HCWs for which a test before SARS-CoV-2 infection was available (group 2, n = 29), who later contracted SARS-CoV-2, aiming to validate findings from our prior case–control investigation. We evaluated autonomic nervous system heart modulation by means of time and frequency domain heart rate variability analysis (HRV) in HCWs during health surveillance visits. Short-term electrocardiogram (ECG) recordings, were obtained at about 6, 13 months and both at 6 and 13 months from the negative SARS-CoV-2 naso-pharyngeal swab (NPS) for group 1 and at about 1-month from the negative NPS for group 2. HCWs who used drugs, had comorbidities that affected HRV, or were hospitalized with severe COVID-19 were excluded.ResultsGroup 1 was split into three subgroups clinically and functionally followed at, about 6 months (subgroup-A, n = 17), 13 months (subgroup-B, n = 37) and both at 6 and 13 months (subgroup-C, n = 13) from the negative SARS-CoV-2 NPS. In subgroup-A, at 6-month follow-up compared with baseline, the spectral components in the frequency domain HRV parameters, showed an increase in normalized high frequency power (nHF) (t = 2.99, p = 0.009), a decrease in the normalized low frequency power (nLF) (t = 2.98, p = 0.009) and in the LF/HF ratio (t = 3.13, p = 0.006). In subgroup B, the comparison of the spectral components in the frequency domain HRV parameters, at 13-month follow-up compared with baseline, showed an increase in nHF (t = 2.54, p = 0.02); a decrease in nLF (t = 2.62, p = 0.01) and in the LF/HF ratio (t = 4.00, p = 0.0003). In subgroup-C, at both 6 and 13-month follow-ups, the spectral components in the frequency domain HRV parameters were higher than baseline in nHF (t = 2.64, p = 0.02 and (t = 2.13, p = 0.05, respectively); lower in nLF (t = 2.64, p = 0.02 and (t = 2.13, p = 0.05, respectively), and in LF/HF (t = 1.92, p = 0.08 and (t = 2.43, p = 0.03, respectively). A significant proportion of HCWs reported persistent COVID-19 symptoms at both the 6 and 13-month follow-ups, seemingly unrelated to cardiac autonomic balance. In group 2 HCWs, at 1-month follow-up compared with baseline, the spectral components in the frequency domain HRV parameters, showed a decrease in nHF (t = 2.19, p = 0.04); an increase in nLF (t = 2.15, p = 0.04) and in LF/HF (t = 3.49, p = 0.002).ConclusionThese results are consistent with epidemiological data suggesting a higher risk of acute cardiovascular complications during the first 30 days after COVID-19. The SARS-CoV-2 associated autonomic imbalance in the post-acute phase after recovery of mild COVID-19 resolved 6 months after the first negative SARS-CoV-2 NPS. However, a significant proportion of HCWs reported long-term COVID-19 symptoms, which dot not seems to be related to cardiac autonomic balance. Future research should certainly further test whether autonomic imbalance has a role in the mechanisms of long-COVID syndrome.

Sarcopenia, a musculoskeletal disease characterized by the progressive loss of skeletal muscle mass, strength, and physical performance, presents significant challenges to global public health due to its adverse effects on mobility, morbidity, mortality, and healthcare costs. This comprehensive review explores the intricate connections between sarcopenia and low birth weight (LBW), emphasizing the developmental origins of health and disease (DOHaD) hypothesis, inflammatory processes (inflammaging), mitochondrial dysfunction, circadian rhythm disruptions, epigenetic mechanisms, and genetic variations revealed through genome-wide studies (GWAS). A systematic search strategy was developed using PubMed to identify relevant English-language publications on sarcopenia, LBW, DOHaD, inflammaging, mitochondrial dysfunction, circadian disruption, epigenetic mechanisms, and GWAS. The publications consist of 46.2% reviews, 21.2% cohort studies, 4.8% systematic reviews, 1.9% cross-sectional studies, 13.4% animal studies, 4.8% genome-wide studies, 5.8% epigenome-wide studies, and 1.9% book chapters. The review identified key factors contributing to sarcopenia development, including the DOHaD hypothesis, LBW impact on muscle mass, inflammaging, mitochondrial dysfunction, the influence of clock genes, the role of epigenetic mechanisms, and genetic variations revealed through GWAS. The DOHaD theory suggests that LBW induces epigenetic alterations during foetal development, impacting long-term health outcomes, including the early onset of sarcopenia. LBW correlates with reduced muscle mass, grip strength, and lean body mass in adulthood, increasing the risk of sarcopenia. Chronic inflammation (inflammaging) and mitochondrial dysfunction contribute to sarcopenia, with LBW linked to increased oxidative stress and dysfunction. Disrupted circadian rhythms, regulated by genes such as BMAL1 and CLOCK, are associated with both LBW and sarcopenia, impacting lipid metabolism, muscle mass, and the ageing process. Early-life exposures, including LBW, induce epigenetic modifications like DNA methylation (DNAm) and histone changes, playing a pivotal role in sarcopenia development. Genome-wide studies have identified candidate genes and variants associated with lean body mass, muscle weakness, and sarcopenia, providing insights into genetic factors contributing to the disorder. LBW emerges as a potential early predictor of sarcopenia development, reflecting the impact of intrauterine exposures on long-term health outcomes. Understanding the complex interplay between LBW with inflammaging, mitochondrial dysfunction, circadian disruption, and epigenetic factors is essential for elucidating the pathogenesis of sarcopenia and developing targeted interventions. Future research on GWAS and the underlying mechanisms of LBW-associated sarcopenia is warranted to inform preventive strategies and improve public health outcomes.

The growing phenomenon of population aging is redefining demographic dynamics, intensifying age-related conditions, especially dementia, projected to triple by 2050 with an enormous global economic burden. This study investigates visual arts-mediated Cognitive Activation Therapy (CAT) as a non-pharmacological CAT intervention targets both biological aging [leukocyte telomere length (LTL), DNA methylation age (DNAmAge)] and cognitive functionality. Aligning with a broader trend of integrating non-pharmacological approaches into dementia care. The longitudinal study involved 20 patients with mild to moderate neurocognitive disorders. Cognitive and functional assessments, and biological aging markers -i.e., LTL and DNAmAge- were analyzed before and after CAT intervention. Change in LTL was positively correlated with days of treatment (p =0.0518). LTL significantly elongated after intervention (p =0.0269), especially in men (p =0.0142), correlating with younger age (p =0.0357), and higher education (p =0.0008). DNAmAge remained instead stable post-treatment. Cognitive and functional improvements were observed for Copy of complex geometric figure, Progressive Silhouettes, Position Discrimination, Communication Activities of Daily Living—Second edition, Direct Functional Status (p < 0.0001) and Object decision (p =0.0594), but no correlations were found between LTL and cognitive gains. Visual arts-mediated CAT effectively mitigates cellular aging, especially in men, by elongating LTL. These findings underscore the potential of non-pharmacological interventions in enhancing cognitive and functional status and general well-being in dementia care. Further research with larger and longer-term studies is essential for validation.

Population aging is one of the most important demographic transformations of our time. Increasing the “health span”—the proportion of life spent in good health—is a global priority. Biological aging comprises molecular and cellular modifications over many years, which culminate in gradual physiological decline across multiple organ systems and predispose to age-related illnesses. Cardiovascular disease is a major cause of ill health and premature death in older people. The rate at which biological aging occurs varies across individuals of the same age and is influenced by a wide range of genetic and environmental exposures. The authors review the hallmarks of biological cardiovascular aging and their capture using imaging and other noninvasive techniques and examine how this information may be used to understand aging trajectories, with the aim of guiding individual- and population-level interventions to promote healthy aging.