Ageing research reviews最新文献

{"title":"Inflamm-aging as a diverse and context-dependent process: from species and population differences to individual trajectories.","authors":"Maximilien Franck, Camille Daunizeau, Jacob E Aronoff, Kamaryn Tanner, Benjamin C Trumble, Claudio Franceschi, Johannes Hertel, Tamás Fülöp, Maël Lemoine, Michael Gurven, Alan A Cohen","doi":"10.1016/j.arr.2025.102880","DOIUrl":"https://doi.org/10.1016/j.arr.2025.102880","url":null,"abstract":"<p><p>Inflamm-aging is widely considered a hallmark of aging, yet emerging evidence challenges its universality. Here, we re-examine inflamm-aging through an eco-evolutionary lens, underlining its context dependence across biological scales. Combining mechanistic, evolutionary, comparative, anthropological, genetic, and environmental evidence, we show how fundamental inflammatory mechanisms are integrated and regulated in diverse biological contexts, representing a suite of flexible stress responses. Drawing on studies from non-industrialized populations, which suggest that inflamm-aging reflects mismatches between evolved human biology and industrialized exposomes, we explore how population-specific evolutionary histories and environmental exposures shape differential predispositions and trajectories of inflamm-aging. We propose that, to the extent that inflammation represents this broad suite of stress responses, increases in at least some dimensions of inflammation with age should be nearly universal, as other physiological processes break down and internal stresses mount. However, the particular set of internal stressors that is triggered in a given species, environmental context, or individual is likely more specific, implying that there is unlikely to be any universal signature of inflamm-aging. The question of whether inflamm-aging is universal thus hinges on whether it is defined broadly as any increase in activation of any inflammatory systems, or more narrowly as a particular suite, such as those activated in industrialized populations with high levels of sedentary behavior and cardiometabolic diseases. Inflamm-aging is ultimately a norm of reaction - an aging-related inflammatory profile whose phenotypic expression varies with genotype and environment - and research should therefore focus on understanding how ecological, evolutionary, and environmental factors modulate inflammation and its age-related trajectory.</p>","PeriodicalId":93862,"journal":{"name":"Ageing research reviews","volume":" ","pages":"102880"},"PeriodicalIF":12.4,"publicationDate":"2025-08-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144982132","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Biomolecular phase separation of microtubule-associated protein Tau and its role in the genesis of Brain Disorders.","authors":"Aurgha Kamal Bhandari, Aman Singh Dhami, Rishi Thanavanthan Hemanthlumar, Nishant Mishra, Beula Joslyn, Sindhujit Roy, Jaisri Srinivasan, Kailash Prasad Prajapathi, Karunakar Kar, Bibin Gnanadhason Anand","doi":"10.1016/j.arr.2025.102879","DOIUrl":"https://doi.org/10.1016/j.arr.2025.102879","url":null,"abstract":"<p><p>Microtubule-associated tau (MAP) is a crucial component for cellular cytoskeleton stability. However, upon hyperphosphorylation, these tau proteins detach from microtubules, leading to the genesis of clumpy fibrillar-rich β or paired helical filamental structures known as amyloids. Such deposits predispose a multitude of fatal disorders, including Alzheimer's Disease. The initial event behind such genesis is still a mystery. Today, numerous research studies try to untangle the initial events that lead to the formation of homogeneous and heterogeneous multicomponent plaques in the case of AD, remain elusive. Since tauopathies are linked to neurodegeneration and the tau tangles damage the neurons and glia, the question of what events trigger the phosphorylation of tau, leading to the molecular crowding of tau repeats, remains largely unknown. Such molecular crowding or initial events before primary nucleation are driven by liquid-liquid phase separation (LLPS), where tau or tau, along with various biomolecules forming dynamic interaction networks leading to the formation of homotypic and heterotypic condensates, ultimately result in co-existing phases before transitioning to nucleation. This review has explored the fundamental principles of LLPS in tau, aiming to establish a link between tau condensates and their pathogenic forms followed by the factors that modulate its phase transition. Our review hopes to provide the scientific community with a strong foundation to build upon, to understand the importance and gravity of studying tau phase separation and the new opportunities it hides within itself.</p>","PeriodicalId":93862,"journal":{"name":"Ageing research reviews","volume":" ","pages":"102879"},"PeriodicalIF":12.4,"publicationDate":"2025-08-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144982072","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Strategies to rescue mitochondria in Parkinson's disease: The significance of mitochondrial transfer.","authors":"Junhan Liang, Zhaoqin Su, Gongmeiyue Su, Madiha Rasheed, Shiyi Tang, Hafsa Sunniya, Mohamed Maazouzi, Yaoyuan Cui, Junxiao Wang, Xuezhe Wang, Jing Yang, Mingchao Ding, Zhao Li, Yulin Deng","doi":"10.1016/j.arr.2025.102856","DOIUrl":"10.1016/j.arr.2025.102856","url":null,"abstract":"<p><p>Parkinson's disease (PD) is a common neurodegenerative disorder characterized by dopaminergic neuronal degeneration and pathological α-synuclein accumulation. Mitochondrial dysfunction is a central feature in PD pathogenesis, contributing to impaired bioenergetics, oxidative stress, neuroinflammation, and defective organelle communication. This review synthesizes the current understanding of mitochondrial quality control mechanisms, including fission, fusion, mitophagy, and biogenesis, and their disruption in PD. Particular emphasis is placed on the role of intercellular mitochondrial transfer as a compensatory mechanism. Emerging evidence suggests that mitochondria can be transferred between neurons and glial cells through tunneling nanotubes, extracellular vesicles, and gap junctions, offering protective effects by restoring metabolic function and attenuating cellular stress. We examine the molecular mediators of these transfer pathways, the influence of PD-associated mutations, and the bidirectional dynamics between donor and recipient cells. Additionally, we explore translational strategies, including mitochondrial transplantation, bioengineered mitochondria, and stem cell-based delivery systems. While preclinical models demonstrate promising therapeutic outcomes, clinical translation faces challenges, including targeting specificity, mitochondrial viability, and immune compatibility. By integrating mechanistic insights with therapeutic developments, this review highlights mitochondrial transfer as a novel and promising approach in the future treatment of PD, potentially addressing longstanding limitations in conventional neuroprotective strategies.</p>","PeriodicalId":93862,"journal":{"name":"Ageing research reviews","volume":" ","pages":"102856"},"PeriodicalIF":12.4,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144801212","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Telomerase dynamics in stem cells: Unraveling the molecular nexus of cellular aging and regeneration.","authors":"Yanhua Jiang, Yongjian Zhou, Yutao Wang, Zhe Li, Ghulam Md Ashraf, Liang Guo","doi":"10.1016/j.arr.2025.102853","DOIUrl":"10.1016/j.arr.2025.102853","url":null,"abstract":"<p><p>The expression levels of telomerase exhibit regulatory heterogeneity across different cell types and various biological stages of cell development. The expression of telomerase is dynamically regulated across cell types and developmental stages, with its activity predominantly determined by the abundance of its catalytic subunit, telomerase reverse transcriptase (TERT). Telomerase levels are typically high in the pluripotent embryonic stem cells, germline cells, and cancer cells, and silenced in the terminally differentiated cells. Minimal telomerase activity is present in the stem and progenitor cells of highly proliferative tissues, although preventing telomere shortening is beyond common sense in the field of biology and cannot be achieved, eventually leading to replicative senescence. While telomerase silencing in somatic cells and adult stem cells acts as a barrier to tumorigenesis by limiting their lifespan, the eventual exhaustion of stem cell pools leads to tissue dysfunction and aging. Telomerase reactivation via telomerase overexpression represents a potential strategy to reverse stem cell aging and rejuvenate aged or dysfunctional tissues. In this review, we discuss the dynamics of telomere (length, activity, and expression level) in pluripotent and adult stem cells as well as their impact on aging. Notably, we have summarized the recent evidence in the application of mesenchymal stem cells immortalized through exogenous telomerase expression in regenerative medicine.</p>","PeriodicalId":93862,"journal":{"name":"Ageing research reviews","volume":" ","pages":"102853"},"PeriodicalIF":12.4,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144786097","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A narrative review and expert consensus on barriers, facilitators, and research gaps to healthy and positive ageing - Position of the Multidisciplinary International Positive Ageing Group (MIPAG).","authors":"Yves Henrotin, Sofia Duque, Demirhan Diraçoglu, Gianni Franco, Giovanni Briganti, Sarah Longe, Karolina Piotrowicz, Alfonso Jose Cruz Jentoft, Tommy Cederholm, Luis Agüera Ortiz","doi":"10.1016/j.arr.2025.102847","DOIUrl":"10.1016/j.arr.2025.102847","url":null,"abstract":"<p><p>Recent developments in healthcare and scientific research have shifted the perception of ageing from a period of decline to recognising its potential for sustained functional ability, well-being, and societal contributions. In light of this perspective, a multidisciplinary panel of experts from five European countries conducted a narrative review of the literature. It convened for a one-day consensus meeting to identify key barriers, facilitators, and research priorities related to healthy ageing. Thus, this paper aims to (1) define the concept of positive ageing, (2) discuss barriers and facilitators to healthy ageing, (3) examine the role of healthcare professionals in maintaining and improving intrinsic capacity, and (4) propose a research agenda to address gaps in healthy ageing. The panel identified 70 barriers and 64 facilitators, structured within the WHO's ICOPE framework, related to intrinsic capacity. Twenty-six interventions across five domains-locomotor, sensory, psychological, cognitive capacities, and vitality- were proposed, aimed at both frail and robust individuals, focusing on social integration, psychological well-being, physiological resilience, deficit management, and disorder prevention. The panel also outlined a research agenda emphasising AI-driven ageing support, improved communication strategies, early frailty detection, and the development of locally adapted guidelines and infrastructure for healthy and positive ageing. This framework emphasizes the importance of early-life interventions and advocates for a preventive, holistic, and multidisciplinary approach to aging. In conclusion, the MIPAG's fosters a proactive mindset and early interventions throughout life to prevent the decline and optimise intrinsic capacity.</p>","PeriodicalId":93862,"journal":{"name":"Ageing research reviews","volume":" ","pages":"102847"},"PeriodicalIF":12.4,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144777220","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Lactylation and methylation: Dual epigenetic codes and potential therapeutic targets in myocardial aging.","authors":"Qian-Qian Niu, Yu-Ting Xi, Ya-Qi Guo, Zheng-Ji Piao, Chun-Rui Zhang, Tian-Yao Li, Dan-Jie Li, Peng Li, Ya-Ling Yin, Vuanghao Lim, Nik Nur Syazni Nik Mohamed Kamal","doi":"10.1016/j.arr.2025.102849","DOIUrl":"10.1016/j.arr.2025.102849","url":null,"abstract":"<p><p>Combating aging has become a central challenge in the life sciences, and myocardial aging, as a fundamental pathological process underlying the development and progression of various cardiovascular diseases, has become a key area in anti-aging research. In recent years, lactylation and methylation, two metabolism-dependent epigenetic modifications, have garnered increasing attention in the context of myocardial aging. Lactylation, mediated by lactate accumulation due to metabolic dysregulation, modifies lysine residues on both histone and non-histone proteins, thereby participating in the regulation of gene transcription, metabolic homeostasis, and inflammatory responses. In parallel, methylation affects gene expression, metabolic remodeling, and mitochondrial function through DNA, RNA, and histone modifications. This review systematically summarizes the regulatory mechanisms of lactylation and methylation in myocardial aging, with a particular focus on their interplay in histone and non-histone protein modification, metabolic regulation, and signaling pathway integration. Furthermore, we evaluate the potential of these reversible modifications as early epigenetic biomarkers and discuss multilayered intervention strategies targeting both lactylation and methylation. Such strategies highlight their translational potential in delaying myocardial aging and mitigating cardiovascular disease. Precisely modulating lactylation and methylation may offer novel theoretical frameworks and therapeutic targets for the prevention and treatment of myocardial aging.</p>","PeriodicalId":93862,"journal":{"name":"Ageing research reviews","volume":" ","pages":"102849"},"PeriodicalIF":12.4,"publicationDate":"2025-07-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144765808","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Effects of antidiabetic medications on the relationship between type 2 diabetes mellitus and cognitive impairment.","authors":"Annalisa Cozza, Chiara Chinigò, Elvira Filicetti, Giada Ida Greco, Rosamaria Lappano, Cinzia Marinaro, Lucia Muglia, Luca Soraci, Andrea Corsonello, Fabrizia Lattanzio, Mara Volpentesta","doi":"10.1016/j.arr.2025.102834","DOIUrl":"10.1016/j.arr.2025.102834","url":null,"abstract":"<p><p>Type 2 diabetes mellitus (T2DM)-related cognitive impairment (CI) has garnered increasing attention in recent research and is emerging as a highly relevant area of study. T2DM is a chronic and globally prevalent condition characterized by insulin resistance, hyperglycemia, oxidative stress, neuroinflammation, and cerebrovascular dysfunction, factors that collectively contribute to cognitive decline. Notably, T2DM is strongly associated with neurodegenerative conditions, ranging from mild cognitive impairment (MCI) to dementia. This review explores the potential neuroprotective effects of various antidiabetic drugs, including insulin-sensitizing agents (metformin and pioglitazone), sodium-glucose co-transporter 2 inhibitors (SGLT2is), glucagon-like peptide-1 receptor agonists (GLP-1 RAs), and dipeptidyl peptidase-4 inhibitors (DPP-4is). These medications exert their effects through multiple mechanisms, such as reducing neuroinflammation and oxidative stress, decreasing Aβ accumulation and apoptosis, enhancing cerebral glucose metabolism, and promoting neuroplasticity, processes directly implicated in the interplay between T2DM and cognitive decline. The review highlights the therapeutic potential of these agents in mitigating CI and supporting brain health in individuals with T2DM. However, given the conflicting nature of current clinical evidence, further research is needed to clarify their cognitive benefits, elucidate underlying mechanisms of action, and assess their long-term effects on cognitive outcomes in this population.</p>","PeriodicalId":93862,"journal":{"name":"Ageing research reviews","volume":" ","pages":"102834"},"PeriodicalIF":12.4,"publicationDate":"2025-07-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144638819","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Editor's Note to \"Biological constraint, evolutionary spandrels and antagonistic pleiotropy\".","authors":"","doi":"10.1016/j.arr.2025.102798","DOIUrl":"10.1016/j.arr.2025.102798","url":null,"abstract":"","PeriodicalId":93862,"journal":{"name":"Ageing research reviews","volume":" ","pages":"102798"},"PeriodicalIF":12.4,"publicationDate":"2025-06-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144251232","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"WITHDRAWN: Biomarker Detection and Therapy of Parkinson's and Alzheimer's disease using upconversion based approach: A Comprehensive Review.","authors":"Kabirdas B Ghorpade, Shivanshu Agrawal, Ujwal Havelikar","doi":"10.1016/j.arr.2025.102656","DOIUrl":"10.1016/j.arr.2025.102656","url":null,"abstract":"<p><p>This article has been withdrawn at the request of the author(s). The Publisher apologizes for any inconvenience this may cause. The full Elsevier Policy on Article Withdrawal can be found at https://www.elsevier.com/about/policies/article-withdrawal.</p>","PeriodicalId":93862,"journal":{"name":"Ageing research reviews","volume":" ","pages":"102656"},"PeriodicalIF":12.4,"publicationDate":"2025-01-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142960162","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Research progress in Alzheimer's disease and bone-brain axis.","authors":"Fan Zhang, Wei Zhang","doi":"10.1016/j.arr.2024.102341","DOIUrl":"10.1016/j.arr.2024.102341","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is the most common type of cognitive impairment. AD is closely related to orthopedic diseases, such as osteoporosis and osteoarthritis, in terms of epidemiology and pathogenesis. Brain and bone tissues can regulate each other in different manners through bone-brain axis. This article reviews the research progress of the relationship between AD and orthopedic diseases, bone-brain axis mechanisms of AD, and AD therapy by targeting bone-brain axis, in order to deepen the understanding of bone-brain communication, promote early diagnosis and explore new therapy for AD patients.</p>","PeriodicalId":93862,"journal":{"name":"Ageing research reviews","volume":" ","pages":"102341"},"PeriodicalIF":0.0,"publicationDate":"2024-07-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140959776","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}