GeroScience最新文献

{"title":"Plasma proteomics-based brain aging signature and incident dementia risk","authors":"Minghao Kou, Hao Ma, Xuan Wang, Yoriko Heianza, Lu Qi","doi":"10.1007/s11357-024-01407-6","DOIUrl":"https://doi.org/10.1007/s11357-024-01407-6","url":null,"abstract":"<p>Investigating brain-enriched proteins with machine learning methods may enable a brain-specific understanding of brain aging and provide insights into the molecular mechanisms and pathological pathways of dementia. The study aims to analyze associations of brain-specific plasma proteomic aging signature with risks of incident dementia. In 45,429 dementia-free UK Biobank participants at baseline, we generated a brain-specific biological age using 63 brain-enriched plasma proteins with machine learning methods. The brain age gap was estimated, and Cox proportional hazards models were used to study the association with incident all-cause dementia, Alzheimer’s disease (AD), and vascular dementia. Per-unit increment in the brain age gap <i>z</i>-score was associated with significantly higher risks of all-cause dementia (hazard ratio [95% confidence interval], 1.67 [1.56–1.79], <i>P</i> &lt; 0.001), AD (1.85 [1.66–2.08], <i>P</i> &lt; 0.001), and vascular dementia (1.86 [1.55–2.24], <i>P</i> &lt; 0.001), respectively. Notably, 2.1% of the study population exhibited extreme old brain aging defined as brain age gap <i>z</i>-score &gt; 2, correlating with over threefold increased risks of all-cause dementia and vascular dementia (3.42 [2.25–5.20], <i>P</i> &lt; 0.001, and 3.41 [1.05–11.13], <i>P</i> = 0.042, respectively), and fourfold increased risk of AD (4.45 [2.32–8.54], <i>P</i> &lt; 0.001). The associations were stronger among participants with healthier lifestyle factors (all <i>P</i>-interaction &lt; 0.05). These findings were corroborated by magnetic resonance imaging assessments showing that a higher brain age gap aligns global pathophysiology of dementia, including global and regional atrophy in gray matter, and white matter lesions (<i>P</i> &lt; 0.001). The brain-specific proteomic age gap is a powerful biomarker of brain aging, indicative of dementia risk and neurodegeneration.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"199 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142601256","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Functional and vascular neuroimaging in maritime pilots with long-term sleep disruption","authors":"Lara J. Mentink, Matthias J. P. van Osch, Leanne J. Bakker, Marcel G. M. Olde Rikkert, Christian F. Beckmann, Jurgen A. H. R. Claassen, Koen V. Haak","doi":"10.1007/s11357-024-01417-4","DOIUrl":"https://doi.org/10.1007/s11357-024-01417-4","url":null,"abstract":"<p>The mechanism underlying the possible causal association between long-term sleep disruption and Alzheimer’s disease remains unclear Musiek et al. 2015. A hypothesised pathway through increased brain amyloid load was not confirmed in previous work in our cohort of maritime pilots with long-term work-related sleep disruption Thomas et al. Alzheimer’s Res Ther 2020;12:101. Here, using functional MRI, T2-FLAIR, and arterial spin labeling MRI scans, we explored alternative neuroimaging biomarkers related to both sleep disruption and AD: resting-state network co-activation and between-network connectivity of the default mode network (DMN), salience network (SAL) and frontoparietal network (FPN), vascular damage and cerebral blood flow (CBF). We acquired data of 16 maritime pilots (56 ± 2.3 years old) with work-related long-term sleep disruption (23 ± 4.8 working years) and 16 healthy controls (59 ± 3.3 years old), with normal sleep patterns (Pittsburgh Sleep Quality Index ≤ 5). Maritime pilots did not show altered co-activation in either the DMN, FPN, or SAL and no differences in between-network connectivity. We did not detect increased markers of vascular damage in maritime pilots, and additionally, maritime pilots did not show altered CBF-patterns compared to healthy controls. In summary, maritime pilots with long-term sleep disruption did not show neuroimaging markers indicative of preclinical AD compared to healthy controls. These findings do not resemble those of short-term sleep deprivation studies. This could be due to resiliency to sleep disruption or selection bias, as participants have already been exposed to and were able to deal with sleep disruption for multiple years, or to compensatory mechanisms Mentink et al. PLoS ONE. 2021;15(12):e0237622. This suggests the relationship between sleep disruption and AD is not as strong as previously implied in studies on short-term sleep deprivation, which would be beneficial for all shift workers suffering from work-related sleep disruptions.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"14 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142599404","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cardioprotection and neurobehavioral impact of swimming training in ovariectomized rats","authors":"Alejandro Martín Ibañez, Joshua Godoy Coto, Valeria Romina Martínez, Alejandra del Milagro Yeves, Franco Juan Cruz Dolcetti, Sofía Cervellini, Lucía Echavarría, Jorge Omar Velez-Rueda, Juan Manuel Lofeudo, Enrique Leo Portiansky, María José Bellini, Ernesto Alejandro Aiello, Irene Lucía Ennis, Verónica Celeste De Giusti","doi":"10.1007/s11357-024-01422-7","DOIUrl":"https://doi.org/10.1007/s11357-024-01422-7","url":null,"abstract":"<p>Cardiovascular (CV) disease is the major cause of mortality. Estrogens (E) exert multiple CV and neuroprotective effects. During menopause, CV and cognitive pathologies increase dramatically. At present, it is known that E exert many of their beneficial effects through the G protein-coupled estrogen receptor (GPER). Exercise reduces the risk of developing CV diseases. Sodium/proton exchanger (NHE-1) is overexpressed in ovariectomized (OVX) rats, probably due to the increase in reactive oxidative species (ROS). Insulin-like growth factor 1 (IGF-1), the main humoral mediator of exercise, inhibits the NHE-1. We aim to explore the subcellular mechanisms involved in the heart and brain impact of physiological exercise in OVX rats. We speculate that physical training, via IGF-1, prevents the increase in ROS, improving heart and brain physiological functions during menopause. Exercise diminished cardiac ROS production and increased catalase (CAT) activity in OVX rats. In concordance, IGF-1 treatment reduces brain ROS, surely contributing to the improvement in brain behavior. Moreover, the aerobic routine was able to prevent, and IGF-1 therapy to revert, NHE-1 hyperactivity in OVX rats. Finally, our results confirm the proposed signaling pathway as IGF-1/PI3K-AKT/NO. Surprisingly, GPER inhibitor (G36) was able to abolish the IGF-1 effect, suggesting that directly or indirectly GPER is part of the IGF-1 pathway. We propose that IGF-1 is the main responsible for the protective effect of aerobic training both in the heart and brain in OVX rats. Moreover, we showed that not only it is possible to prevent but also to revert the menopause-induced NHE-1 hyperactivity by exercise/IGF-1 cascade.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"95 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142598317","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Stay social, stay young: a bioanthropological outlook on the processes linking sociality and ageing","authors":"Vincenzo Iannuzzi, Nicolas Narboux-Nême, Andrea Lehoczki, Giovanni Levi, Cristina Giuliani","doi":"10.1007/s11357-024-01416-5","DOIUrl":"https://doi.org/10.1007/s11357-024-01416-5","url":null,"abstract":"<p>In modern human societies, social interactions and pro-social behaviours are associated with better individual and collective health, reduced mortality, and increased longevity. Conversely, social isolation is a predictor of shorter lifespan. The biological processes through which sociality affects the ageing process, as well as healthspan and lifespan, are still poorly understood. Unveiling the physiological, neurological, genomic, epigenomic, and evolutionary mechanisms underlying the association between sociality and longevity may open new perspectives to understand how lifespan is determined in a broader socio/evolutionary outlook. Here we summarize evidence showing how social dynamics can shape the evolution of life history traits through physiological and genetic processes directly or indirectly related to ageing and lifespan. We start by reviewing theories of ageing that incorporate social interactions into their model. Then, we address the link between sociality and lifespan from two separate points of view: (i) considering evidences from comparative evolutionary biology and bioanthropology that demonstrates how sociality contributes to natural variation in lifespan over the course of human evolution and among different human groups in both pre-industrial and post-industrial society, and (ii) discussing the main physiological, neurological, genetic, and epigenetic molecular processes at the interface between sociality and ageing. We highlight that the exposure to chronic social stressors deregulates neurophysiological and immunological pathways and promotes accelerated ageing and thereby reducing lifespan. In conclusion, we describe how sociality and social dynamics are intimately embedded in human biology, influencing healthy ageing and lifespan, and we highlight the need to foster interdisciplinary approaches including social sciences, biological anthropology, human ecology, physiology, and genetics.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"245 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142598472","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Centenarians of the Basque Country are resilient to cancer","authors":"Sara Cruces-Salguero, Igor Larrañaga, Javier Mar, Ander Matheu","doi":"10.1007/s11357-024-01425-4","DOIUrl":"https://doi.org/10.1007/s11357-024-01425-4","url":null,"abstract":"<p>Cancer is one of the leading causes of death and its prevalence increases with age. While centenarians exhibit extreme longevity and potential to avoid or delay aging-related diseases, their response to cancer is still barely explored. Our study took advantage of the Electronic Health Records to retrospectively compare the severity of cancer in centenarians (<i>n</i> = 649) and non-centenarians (<i>n</i> = 62,753) in the Basque Country (province of Gipuzkoa), Spain, through analyzing all the recorded diagnoses throughout their lifetime. Descriptive statistics were applied to discern differences between the two population groups in terms of prevalence of tumor types, number of diagnoses, and treatments. Survival analysis was performed through Kaplan–Meier estimator. We found that centenarians had fewer cancer diagnoses (17.1%, <i>n</i> = 111) than non-centenarians (40.5%, <i>n</i> = 25,405), and notably avoided the most aggressive cancer types and did not develop metastasis. Furthermore, they barely had records of treatments or drugs and had extended survival both since the first and last diagnosis of cancer. These results suggest resilience of the centenarians against malignant cancers explaining, in part, their extended longevity.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"148 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-11-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142597086","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The influence of a human macronutrient-matched diet on phenotypes in old mice","authors":"Mary A. Darrah, Abigail G. Longtine, Nathan T. Greenberg, Sophia A. Mahoney, Ravinandan Venkatasubramanian, Nicholas S. VanDongen, Julie A. Reisz, Angelo D’Alessandro, Douglas R. Seals, Yara Bernaldo de Quiros Miranda, Zachary S. Clayton","doi":"10.1007/s11357-024-01423-6","DOIUrl":"https://doi.org/10.1007/s11357-024-01423-6","url":null,"abstract":"<p>Preclinical rodent models are essential research tools for improving understanding of physiological aging processes in humans. However, the translatability of findings obtained leveraging rodent models to humans is limited, likely due in part to differences in macronutrient composition of the diets. Here, we investigated the impact of a 3-month diet intervention in old male C57BL/6JN mice in which the macronutrient composition was aligned with that of a midlife/older adult in the United States, compared to a traditional rodent diet, and assessed various phenotypes that are typically altered with aging. Following the diet period, mice fed the human macronutrient-matched diet had greater quadricep and subcutaneous adipose and visceral adipose tissue masses compared to animals fed a traditional mouse diet. Frailty, assessed using a clinical frailty index, was lower, while grip strength was higher in mice fed the human-matched diet. Circulating metabolite and inflammatory cytokine profiles were altered in mice fed the human-matched diet. Notably, mortality rate (assessed in animals who died or were euthanized per veterinary recommendation before the pre-determined end of study euthanasia), tended to be lower in mice fed the human-matched diet. The present study underscores the importance of diet in rodent studies of aging, as differences in macronutrient composition can affect various physiological processes in old mice that are relevant to aging research.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"244 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142597084","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The role of inflammation induced by necroptosis in the development of fibrosis and liver cancer in novel knockin mouse models fed a western diet","authors":"Ramasamy Selvarani, HoangVan Michelle Nguyen, Natesan Pazhanivel, Muthusamy Raman, Sunho Lee, Roman F. Wolf, Sathyaseelan S. Deepa, Arlan Richardson","doi":"10.1007/s11357-024-01418-3","DOIUrl":"https://doi.org/10.1007/s11357-024-01418-3","url":null,"abstract":"<p>Non-resolving, chronic inflammation (inflammaging) is believed to play an important role in aging and age-related diseases. The goal of this study was to determine if inflammation induced by necroptosis arising from the liver plays a role in chronic liver disease (CLD) and liver cancer in mice fed a western diet (WD). Necroptosis was induced in liver using two knockin (KI) mouse models that overexpress genes involved in necroptosis (Ripk3 or Mlkl) specifically in liver (i.e., <i>hRipk3-KI</i> and <i>hMlkl-KI</i> mice). These mice and control mice (not overexpressing Ripk3 or Mlkl) were fed a WD (high in fat, sucrose, and cholesterol) starting at 2 months of age for 3, 6, and 12 months. Feeding the WD induced necroptosis in the control mice, which was further elevated in the <i>hRipk3-KI</i> and <i>hMlkl-KI</i> mice and was associated with a significant increase in inflammation in the livers of the <i>hRipk3-KI</i> and <i>hMlkl-KI</i> mice compared to control mice fed the WD. Overexpressing Ripk3 or Mlkl significantly increased steatosis and fibrosis compared to control mice fed the WD. Mice fed the WD for 12 months developed liver tumors (hepatocellular adenomas): 28% of the control mice developing tumors compared to 62% of the <i>hRipk3-KI</i> and <i>hMlkl-KI</i> mice. The <i>hRipk3-KI</i> and <i>hMlkl-KI</i> mice showed significantly more and larger tumor nodules. Our study provides the first direct evidence that inflammation induced by necroptosis arising from hepatocytes can lead to the progression of hepatic steatosis to fibrosis in obese mice that eventually results in an increased incidence in hepatocellular adenomas.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"1 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-11-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142597141","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Physical activity and DNA methylation–based markers of ageing in 6208 middle-aged and older Australians: cross-sectional and longitudinal analyses","authors":"Haoxin Tina Zheng, Danmeng Lily Li, Makayla W. C. Lou, Allison M. Hodge, Melissa C. Southey, Graham G. Giles, Roger L. Milne, Brigid M. Lynch, Pierre-Antoine Dugué","doi":"10.1007/s11357-024-01408-5","DOIUrl":"https://doi.org/10.1007/s11357-024-01408-5","url":null,"abstract":"<p>Epigenetic age quantifies biological age using DNA methylation information and is a potential pathway by which physical activity benefits general health. We aimed to assess the cross-sectional and longitudinal associations between physical activity and epigenetic age in middle-aged and older Australians. Blood DNA methylation data for 6208 participants (40% female) in the Melbourne Collaborative Cohort Study (MCCS) were available at baseline (1990–1994, mean age, 59 years) and, of those, for 1009 at follow-up (2003–2007, mean age, 69 years). Physical activity measurements (weighted scores at baseline and follow-up and total MET hours per week at follow-up) were calculated from self-reported questionnaire data. Five blood methylation–based markers of ageing (<i>PCGrimAge</i>, <i>PCPhenoAge</i>, <i>bAge</i>, <i>DNAmFitAge</i>, and <i>DunedinPACE</i>) and four fitness-related markers (<i>DNAmGaitspeed</i>, <i>DNAmGripmax</i>, <i>DNAmVO2max</i>, and <i>DNAmFEV1</i>) were calculated and adjusted for age. Linear regression was used to examine the cross-sectional and longitudinal associations between physical activity and epigenetic age. Effect modification by age, sex, and BMI was assessed. At baseline, a standard deviation (SD) increment in physical activity was associated with 0.03-SD (<i>DNAmFitAge</i>, 95%CI = 0.01, 0.06, <i>P</i> = 0.02) to 0.07-SD (<i>bAge</i>, 95%CI = 0.04, 0.09, <i>P</i> = 2 × 10⁻⁸) lower epigenetic age. These associations were attenuated after adjustment for other lifestyle variables. Only weak evidence was found for the longitudinal association (<i>N</i> = 1009) of changes in physical activity and epigenetic age (e.g. <i>DNAmFitAge</i>: adjusted <i>β</i> = − 0.04, 95%CI = − 0.08, 0.01). The associations were not modified by age, sex, or BMI. In middle-aged and older Australians, higher levels of self-reported physical activity were associated with slightly lower epigenetic age.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":"9 1","pages":""},"PeriodicalIF":5.6,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142594579","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Characterizing the oral and gastrointestinal microbiome associated with healthy aging: insights from long-lived populations in Northeastern China.","authors":"Yue Ji, Hao Sun, Yingda Wang, Yanhui Li, Rennv Piao, Li Bu, Hui Xu","doi":"10.1007/s11357-024-01419-2","DOIUrl":"https://doi.org/10.1007/s11357-024-01419-2","url":null,"abstract":"<p><p>The oral and gastrointestinal (GI) tract microbiota in humans is susceptible to geographical influences and represents vital factors impacting healthy aging. The northeastern region of China, characterized by distinct dietary and climatic conditions, significantly influences the human microbiome composition. However, the microbial structure of the entire long-lived population in this area has not been evaluated. This study recruited a cohort of 142 individuals aged 55-102 residing in Northeast China, and their oral and gut microbiota were evaluated using full-length 16S rRNA gene amplicon sequencing. The results indicate that the oral and GI tract microbiota of long-lived individuals showed reduced microbial taxonomic richness and evenness compared to sub-longevity individuals. With aging, the core species experience a gradual decline in abundance, while subordinate species show an increase. The long-lived population exhibited a heightened ability to enrich beneficial bacteria including Akkermansia, Alistipes, Parabacteroides, and Eubacterium coprostanoligenes in the GI tract, which are associated with host metabolism and have the potential to act as probiotics, reducing the risks of unhealthy aging in the northeast population. Bifidobacterium sp. and Lactobacillus salivarius have been found to coexist in both the oral cavity and the GI tract of long-lived individuals. We hypothesize that beneficial bacterial taxa from the oral cavity colonize the GI tract more extensively in long-lived individuals compared to those with a shorter lifespan. These findings pave the way for identifying probiotic strains that can promote healthy aging in Northeast China.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-11-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142589922","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The COVID-19 legacy: consequences for the human DNA methylome and therapeutic perspectives.","authors":"Carlo Gaetano, Sandra Atlante, Michela Gottardi Zamperla, Veronica Barbi, Davide Gentilini, Barbara Illi, Marco Malavolta, Fabio Martelli, Antonella Farsetti","doi":"10.1007/s11357-024-01406-7","DOIUrl":"https://doi.org/10.1007/s11357-024-01406-7","url":null,"abstract":"<p><p>The COVID-19 pandemic has left a lasting legacy on human health, extending beyond the acute phase of infection. This article explores the evidence suggesting that SARS-CoV-2 infection can induce persistent epigenetic modifications, particularly in DNA methylation patterns, with potential long-term consequences for individuals' health and aging trajectories. The review discusses the potential of DNA methylation-based biomarkers, such as epigenetic clocks, to identify individuals at risk for accelerated aging and tailor personalized interventions. Integrating epigenetic clock analysis into clinical management could mark a new era of personalized treatment for COVID-19, possibly helping clinicians to understand patient susceptibility to severe outcomes and establish preventive strategies. Several valuable reviews address the role of epigenetics in infectious diseases, including the Sars-CoV-2 infection. However, this article provides an original overview of the current understanding of the epigenetic dimensions of COVID-19, offering insights into the long-term health implications of the pandemic. While acknowledging the limitations of current data, we emphasize the need for future research to unravel the precise mechanisms underlying COVID-19-induced epigenetic changes and to explore potential approaches to target these modifications.</p>","PeriodicalId":12730,"journal":{"name":"GeroScience","volume":" ","pages":""},"PeriodicalIF":5.3,"publicationDate":"2024-11-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142575871","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}