BiogerontologyPub Date : 2025-03-14DOI: 10.1007/s10522-025-10210-5
A Golubev
{"title":"Distinguishing the intrinsic and extrinsic causes of changes in human mortality by examining life-table aging rate (LAR) trajectories through the lens of generalized Gompertz-Makeham law.","authors":"A Golubev","doi":"10.1007/s10522-025-10210-5","DOIUrl":"10.1007/s10522-025-10210-5","url":null,"abstract":"<p><p>To check whether the reported waves of age-dependent changes in multiomics patterns in humans influence age-specific mortality, life-table aging rate (LAR) trajectories derived from Human Morality Database (HMD) data were modeled based on assumptions inherent in a generalized Gompertz-Makeham Law (gGML). The gGML implies that any changes in resistance to causes of death (CoD) and in exposure to CoD are translated into changes in mortality in an exponential and a linear way, respectively. Modeling suggests that undulations of LAR trajectories derived from HMD data on countries where life expectancy (LE) is above 83 years do not align with the reported waves of multiomics changes and are rather associated with changes in the exposure to CoD. As far as the exposure may be modifiable, it may be inferred from modeling that the contribution of the modifiable CoD to the total mortality is almost 100% at 25 years and reaches zero after ca. 90 years, which is no surprise. Unexpectedly, the contribution may increase by 20% at 55-65 years after the initial decrease, which reaches 30 to 70% at about 40 years. Reasons to revise approaches to attributing mortality to different CoD are discussed. Gains in LE possible upon eliminating all modifiable CoD are estimated. In the countries where LE currently exceeds 83 years, the estimates are 2.9-5.7 years for men and 1.2-2.5 for women. Thus, human LE may approach but hardly can ever exceed 90 years.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 2","pages":"71"},"PeriodicalIF":4.4,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143630145","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiogerontologyPub Date : 2025-03-14DOI: 10.1007/s10522-025-10214-1
Maria Raggio, Ivan Conte, Paolo de Girolamo, Livia D'Angelo
{"title":"Modelling orexinergic system in ageing in the African turquoise killifish.","authors":"Maria Raggio, Ivan Conte, Paolo de Girolamo, Livia D'Angelo","doi":"10.1007/s10522-025-10214-1","DOIUrl":"10.1007/s10522-025-10214-1","url":null,"abstract":"<p><p>The orexinergic system is anatomically and functionally conserved in almost all vertebrates, and the role in healthy ageing and age-associated diseases has been studied in mammals. Here, we review the main findings on the age-related regulation of orexinergic system in mammals, including human patients and highlights how the fish Nothobranchius furzeri serves as an exceptional model to spearhead research and unravel the intricate mechanisms underlying orexinergic regulation during ageing. The ageing brain of this teleost is characterized by the presence of neurodegenerative processes similar to those associated with human pathologies rather than those of healthy ageing. We present an in-depth summary and discussion on the groundbreaking advances in understanding the neuroanatomical organization of the orexinergic system, its pivotal role in mammalian and fish models, and its profound involvement in healthy ageing and age-associated diseases.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 2","pages":"72"},"PeriodicalIF":4.4,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11909093/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143630150","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Chrysin alleviates the impeded neurogenesis in accelerated brain aging by D-galactose in rats.","authors":"Ram Prajit, Nataya Sritawan, Anusara Aranarochana, Apiwat Sirichoat, Wanassanun Pannangrong, Peter Wigmore, Jariya Umka Welbat","doi":"10.1007/s10522-025-10215-0","DOIUrl":"10.1007/s10522-025-10215-0","url":null,"abstract":"<p><p>Aged-related cognitive impairments are associated with molecular neurodegenerations and impeded neurogenesis in the dentate gyrus (DG) of the damaged hippocampus. Neurogenesis requires activated cyclic AMP-responsive element-binding protein (CREB) pathway to enhance neuronal development, synaptic plasticity, cognition, learning and memory. Current research has reported that consecutive administration of D-galactose can accelerate brain aging by inducing oxidation and inflammation. The flavonoid chrysin has been demonstrated in medical dietary supplements and shown neuroprotective effect on impeded neurogenesis. This study aimed to clarify that chrysin preserves neurogenesis by modulating molecular pathway in accelerated brain aging induced by D-galactose. Signs of aging, processes of neurogenesis, and protein regulating neurogenesis were evaluated in male Sprague Dawley (SD) rats, which were allocated into four groups: vehicle rats, accelerated aging rats treated with D-galactose, normal rats receiving chrysin, and cotreated rats receiving both D-galactose and chrysin. Aging signs showed only a subsidence in volume of the granular cell layer (GCL) after consecutive administration of D-galactose. Cell proliferation, neurogenic niches, and protein regulating proliferation were downregulated in the accelerated aging rats. Likewise, cell survivals and proteins related to CREB pathway were depleted in rats receiving D-galactose. Nevertheless, rats cotreated with chrysin maintained in all parameters that were adversely affected by D-galactose. In conclusion, chrysin could alleviate the disruption of molecular regulation of neurogenesis in accelerated brain aging induced by D-galactose.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 2","pages":"70"},"PeriodicalIF":4.4,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143630144","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiogerontologyPub Date : 2025-03-14DOI: 10.1007/s10522-025-10212-3
Leonardo Biscetti, Salvatore Vaiasicca, Belinda Giorgetti, Paola Sarchielli, Fiorenza Orlando, Alessandro Di Rienzo, Erika Carrassi, Mirko Di Rosa, Serena Marcozzi, Tiziana Casoli, Giuseppe Pelliccioni
{"title":"Neuroinflammation increases in old and oldest-old rats except for dura mater meningeal tissue with significant gender differences: a translational perspective.","authors":"Leonardo Biscetti, Salvatore Vaiasicca, Belinda Giorgetti, Paola Sarchielli, Fiorenza Orlando, Alessandro Di Rienzo, Erika Carrassi, Mirko Di Rosa, Serena Marcozzi, Tiziana Casoli, Giuseppe Pelliccioni","doi":"10.1007/s10522-025-10212-3","DOIUrl":"10.1007/s10522-025-10212-3","url":null,"abstract":"<p><p>Neuroinflammaging is the nervous system version of inflammaging, the low-grade inflammation that develops with advanced age, aside from active disease or infection. Despite neuroinflammaging has been widely investigated, some important issues still need to be resolved such as the analysis of the extremely old subjects and the evaluation of specific brain areas. On this background, we conducted a study to analyze expression of inflammatory and anti-inflammatory genes in Wistar rats of different ages, including the oldest-old, in different brain regions. We found that pro-inflammatory mediators were generally up-regulated with age in cortex, hippocampus, and striatum, especially in the oldest-old group. Specifically, TNF-α showed an increment in expression with age in striatum, IL-1β and IFN-γ in hippocampus, and MCP-1 in cortex, hippocampus and striatum. Conversely, CX3CL1 and NOS2 showed a significant reduction of expression in the cortex of the oldest-old group. A different situation was observed in dura mater where TNF-α, IL-6, IL-1β, CX3CL1, and MCP-1 expression decreased in the older groups in comparison with the younger groups. With age the anti-inflammatory cytokines IL-4 and IL-10 were down-regulated in cortex, and TGF-β1 in dura mater, while IL-4 was up-regulated in the oldest-old group in hippocampus. Finally, we observed that female brains underwent an age-related increase of pro-inflammatory cytokines expression compared to males, except for striatum, and a general down-regulation of anti-inflammatory cytokines within each age group. Protein validation of selected factors by ELISA tests supported the observed changes. These data may represent a basis for future research about the neurobiology of aging, in particular in the neurodegenerative disorder framework.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 2","pages":"73"},"PeriodicalIF":4.4,"publicationDate":"2025-03-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143630154","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiogerontologyPub Date : 2025-03-12DOI: 10.1007/s10522-025-10217-y
Vadim E Fraifeld, Suresh I S Rattan
{"title":"Stem cells in ageing and longevity: a new section in Biogerontology.","authors":"Vadim E Fraifeld, Suresh I S Rattan","doi":"10.1007/s10522-025-10217-y","DOIUrl":"10.1007/s10522-025-10217-y","url":null,"abstract":"","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 2","pages":"69"},"PeriodicalIF":4.4,"publicationDate":"2025-03-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143613237","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Novel immunoinformatics-guided activation of CISD1 with compound 4'-methoxy-3',5,7-trihydroxyflavanone for the prevention of age-related cardiomyopathy.","authors":"Abdur-Rehman Munir, Javed Iqbal Wattoo, Kaniz Fatima, Kubra Ilyas","doi":"10.1007/s10522-025-10211-4","DOIUrl":"10.1007/s10522-025-10211-4","url":null,"abstract":"<p><p>Aging is a principal driver of cardiomyopathy, characterized by mitochondrial dysfunction, oxidative stress, and progressive telomere shortening in cardiomyocytes. These pathological changes impair cellular bioenergetics and regenerative capacity, accelerating cardiac deterioration. However, targeted interventions to mitigate these effects remain limited. This research investigates the therapeutic potential of CISD1 activation as a novel strategy to counteract aging-associated cardiac decline. Using advanced Immunoinformatic approaches, including molecular docking, protein structure modelling, and molecular dynamics simulations, we assess the role of CISD1 upregulation in enhancing mitochondrial bioenergetics, reducing oxidative stress, and preserving telomere integrity. Our Immunoinformatic findings reveal that CISD1 activation stabilizes mitochondrial function, mitigates oxidative damage, and slows telomere attrition, thereby sustaining cardiomyocyte function and delaying cellular senescence. Our research identifies 4'-Methoxy-3', 5,7-trihydroxy flavanone as a potential small-molecule activator of CISD1, offering a promising pharmacological approach to modulate mitochondrial dynamics in aging cardiomyocytes. By directly addressing the mechanistic link between CISD1, mitochondrial stability, and telomere preservation, this research bridges a critical gap in understanding age-related cardiomyopathy and provides a foundation for targeted therapeutic interventions. Our findings suggest that CISD1 activation could restore cellular homeostasis in aged cardiac tissues, reducing the risk of heart failure and other aging-related cardiovascular diseases. These insights advance age-related disease intervention strategies by targeting fundamental molecular pathways involved in cardiomyocyte aging.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 2","pages":"68"},"PeriodicalIF":4.4,"publicationDate":"2025-03-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143603843","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiogerontologyPub Date : 2025-03-06DOI: 10.1007/s10522-025-10209-y
Saleh I Alaqel, Mohd Imran, Abida Khan, Naira Nayeem
{"title":"Aging, vascular dysfunction, and the blood-brain barrier: unveiling the pathophysiology of stroke in older adults.","authors":"Saleh I Alaqel, Mohd Imran, Abida Khan, Naira Nayeem","doi":"10.1007/s10522-025-10209-y","DOIUrl":"10.1007/s10522-025-10209-y","url":null,"abstract":"<p><p>The progressive decline of vascular integrity and blood-brain barrier (BBB) function is associated with aging, a major risk factor for stroke. This review describes the cellular and molecular changes in the brain microvasculature of the neurovascular unit (NVU) that contribute to the development of BBB dysfunction in aging, such as endothelial cell senescence, oxidative stress, and degradation of tight junction proteins. Stroke severity and recovery are exacerbated by BBB breakdown, leading to neuroinflammation, neurotoxicity, and cerebral oedema while identifying molecular mechanisms such as the NLRP3 inflammasome, matrix metalloproteinases (MMPs), and non-coding RNAs (e.g., miRNAs and circRNAs) that drive BBB disruption in aging and stroke. Real-time assessment of BBB permeability in stroke pathophysiology is made possible using advanced imaging techniques, such as dynamic contrast-enhanced MRI and positron emission tomography. Furthermore, biomarkers, including claudin-5, PDGFRβ, or albumin concentration, serve as markers of BBB integrity and vascular health. Restoration of BBB function and stroke recovery with emerging therapeutic strategies, including sirtuin modulators (SIRT1 and SIRT3 activators to enhance endothelial function and mitochondrial health), stem cell-derived extracellular vesicles (iPSC-sEVs for BBB repair and neuroprotection), NLRP3 inflammasome inhibitors (MCC950 to attenuate endothelial pyroptosis and inflammation), hydrogen-rich water therapy (to counteract oxidative stress-induced BBB damage), and neuropeptides such as cortistatin (to regulate neuroinflammation and BBB stability), is promising. This review explores the pathophysiological mechanisms of BBB dysfunction in aging and stroke, their relation to potential therapeutic targets, and novel approaches to improve vascular health and neuroprotection.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 2","pages":"67"},"PeriodicalIF":4.4,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143565920","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiogerontologyPub Date : 2025-03-06DOI: 10.1007/s10522-025-10206-1
Ching Wah Donna Li, Catrin Herpich, Ulrike Haß, Bastian Kochlik, Daniela Weber, Tilman Grune, Kristina Norman
{"title":"Essential amino acids and branched-chain amino acids are associated with skeletal muscle and inflammatory parameters in older age.","authors":"Ching Wah Donna Li, Catrin Herpich, Ulrike Haß, Bastian Kochlik, Daniela Weber, Tilman Grune, Kristina Norman","doi":"10.1007/s10522-025-10206-1","DOIUrl":"10.1007/s10522-025-10206-1","url":null,"abstract":"<p><p>Aging is associated with a decline in muscle mass and function, increasing the risk of adverse health outcomes. Amino acid profiling has emerged as a potential tool for assessing skeletal muscle health. This study examines the associations between fasting plasma amino acids, muscle function, and inflammation in healthy older and young adults. Data from 131 participants (101 older adults, 71.5±4.9 years; 30 young adults, 25.5±3.9 years) were analyzed. Skeletal muscle mass was assessed using bioimpedance analysis, and hand grip strength was measured with a dynamometer. Plasma amino acids, kynurenine, and inflammatory markers (CRP, IL-6) were quantified using ultraperformance liquid chromatography with tandem mass spectrometry and commercial immunosorbent assays, respectively. Older adults exhibited lower levels of glutamic acid, isoleucine, leucine, phenylalanine, kynurenine, and kynurenine-to-tryptophan (KYN:TRP) ratio compared to younger individuals (all p<0.05). In older adults, branched-chain and essential amino acids correlated positively with skeletal muscle index (SMI) and hand grip strength, whereas in young adults, only glutamic acid, proline, and KYN:TRP showed positive associations with SMI (all p<0.05). CRP and IL-6 were associated with several amino acids in older adults but not in younger individuals. These findings suggest that age-related shifts in amino acid profiles may reflect underlying changes in muscle metabolism and function, highlighting their potential as early indicators of muscle decline.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 2","pages":"66"},"PeriodicalIF":4.4,"publicationDate":"2025-03-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11882671/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143565925","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
BiogerontologyPub Date : 2025-02-26DOI: 10.1007/s10522-025-10205-2
Jia Xu, Zhe Song
{"title":"The role of different physical exercises as an anti-aging factor in different stem cells.","authors":"Jia Xu, Zhe Song","doi":"10.1007/s10522-025-10205-2","DOIUrl":"10.1007/s10522-025-10205-2","url":null,"abstract":"<p><p>The senescence process is connected to the characteristics of cellular aging. Understanding their causal network helps develop a framework for creating new treatments to slow down the senescence process. A growing body of research indicates that aging may adversely affect stem cells (SCs). SCs change their capability to differentiate into different cell types and decrease their potential for renewal as they age. Research has indicated that consistent physical exercise offers several health advantages, including a reduced risk of age-associated ailments like tumors, heart disease, diabetes, and neurological disorders. Exercise is a potent physiological stressor linked to higher red blood cell counts and an enhanced immune system, promoting disease resistance. Sports impact mesenchymal SCs (MSCs), hematopoietic SCs (HSCs), neuronal SCs (NuSCs), and muscular SCs (MuSCs), among other aged SCs types. These changes to the niche will probably affect the amount and capability of adult SCs after exercise. In this work, we looked into how different types of SCs age. The impact of physical activity on the aging process has been studied. Additionally, there has been discussion and study on the impact of different sports and physical activities on SCs as an anti-aging component.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 2","pages":"63"},"PeriodicalIF":4.4,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143498596","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
{"title":"Harnessing the FOXO-SIRT1 axis: insights into cellular stress, metabolism, and aging.","authors":"Saurabh Gupta, Muhammad Afzal, Neetu Agrawal, Waleed Hassan Almalki, Mohit Rana, Saurabh Gangola, Suresh V Chinni, Benod Kumar K, Haider Ali, Sachin Kumar Singh, Saurabh Kumar Jha, Gaurav Gupta","doi":"10.1007/s10522-025-10207-0","DOIUrl":"10.1007/s10522-025-10207-0","url":null,"abstract":"<p><p>Aging and metabolic disorders share intricate molecular pathways, with the Forkhead box O (FOXO)- Sirtuin 1 (SIRT1) axis emerging as a pivotal regulator of cellular stress adaptation, metabolic homeostasis, and longevity. This axis integrates nutrient signaling with oxidative stress defence, modulating glucose and lipid metabolism, mitochondrial function, and autophagy to maintain cellular stability. FOXO transcription factors, regulated by SIRT1 deacetylation, enhance antioxidant defence mechanisms, activating genes such as superoxide dismutase (SOD) and catalase, thereby counteracting oxidative stress and metabolic dysregulation. Recent evidence highlights the dynamic role of reactive oxygen species (ROS) as secondary messengers in redox signaling, influencing FOXO-SIRT1 activity in metabolic adaptation. Additionally, key redox-sensitive regulators such as nuclear factor erythroid 2-related factor 2 (Nrf2) and Peroxisome proliferator-activated receptor gamma coactivator-1 alpha (PGC-1α) interact with this pathway, orchestrating mitochondrial biogenesis and adaptive stress responses. Pharmacological interventions, including alpha-lipoic acid (ALA), resveratrol, curcumin and NAD<sup>+</sup> precursors, exhibit therapeutic potential by enhancing insulin sensitivity, reducing oxidative burden, and restoring metabolic balance. This review synthesizes current advancements in FOXO-SIRT1 regulation, its emerging role in redox homeostasis, and its therapeutic relevance, offering insights into future strategies for combating metabolic dysfunction and aging-related diseases.</p>","PeriodicalId":8909,"journal":{"name":"Biogerontology","volume":"26 2","pages":"65"},"PeriodicalIF":4.4,"publicationDate":"2025-02-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143514523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}