Ageing Research Reviews最新文献

{"title":"Conserved biological processes in partial cellular reprogramming: Relevance to aging and rejuvenation","authors":"Roberto A. Avelar ,&nbsp;Daniel Palmer ,&nbsp;Anton Y. Kulaga ,&nbsp;Georg Fuellen","doi":"10.1016/j.arr.2025.102737","DOIUrl":"10.1016/j.arr.2025.102737","url":null,"abstract":"<div><div>Partial or transient cellular reprogramming is defined by the limited induction of pluripotency factors without full dedifferentiation of cells to a pluripotent state. Comparing in vitro and in vivo mouse studies, and in vitro studies in humans, supported by visualizations of data interconnections, we show consistent patterns in how such reprogramming modulates key biological processes. Generally, partial reprogramming drives dynamic chromatin remodelling, involving histone modifications that regulate accessibility and facilitate pluripotency gene activation while silencing somatic identity. These changes are accompanied by modifications in stress response programs, such as inflammation, autophagy, and cellular senescence, as well as improved mitochondrial activity and dysregulation of extracellular matrix pathways. We also underscore the challenges in evaluating complex processes like aging and cellular senescence, given the variability in biomarkers used across studies. Overall, we highlight biological processes consistently influenced by reprogramming while noting that some effects are context-dependent, varying according to cell type, species, sex, recovery time, and the reprogramming method employed. These insights inform future research and potential therapeutic applications in aging and regenerative medicine.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"108 ","pages":"Article 102737"},"PeriodicalIF":12.5,"publicationDate":"2025-03-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143694699","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cognitive frailty: A comprehensive clinical paradigm beyond cognitive decline","authors":"Mariagiovanna Cozza ,&nbsp;Virginia Boccardi","doi":"10.1016/j.arr.2025.102738","DOIUrl":"10.1016/j.arr.2025.102738","url":null,"abstract":"<div><div>Cognitive frailty is an emerging concept in research and clinical practice that incorporates both physical frailty and mild cognitive impairment (MCI) or subjective cognitive decline (SCD). Unlike traditional approaches that separate physical frailty and dementia, cognitive frailty treats these domains as interrelated and coexisting, with significant implications for clinical outcomes and predicting cognitive decline. Despite growing recognition of this interrelationship, a dualistic view of physical and cognitive processes persists. The paradigm of cognitive frailty holds promise as a biomarker- like amyloid plaques or neurofibrillary tangles- but with the advantage of identifying risk at a prefrail stage, before clinical signs of MCI or dementia emerge. This review examines the pathophysiological and clinical dimensions of cognitive frailty and promotes for its integration into routine assessments in memory clinics.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"108 ","pages":"Article 102738"},"PeriodicalIF":12.5,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143685788","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Fluid-based biomarkers for neurodegenerative diseases","authors":"Yongliang Cao ,&nbsp;Yifei Xu ,&nbsp;Meiqun Cao ,&nbsp;Nan Chen ,&nbsp;Qingling Zeng ,&nbsp;Mitchell K.P. Lai ,&nbsp;Dahua Fan ,&nbsp;Gautam Sethi ,&nbsp;Yongkai Cao","doi":"10.1016/j.arr.2025.102739","DOIUrl":"10.1016/j.arr.2025.102739","url":null,"abstract":"<div><div>Neurodegenerative diseases, such as Alzheimer’s Disease (AD), Multiple Sclerosis (MS), Parkinson’s Disease (PD), and Amyotrophic Lateral Sclerosis (ALS) are increasingly prevalent as global populations age. Fluid biomarkers, derived from cerebrospinal fluid (CSF), blood, saliva, urine, and exosomes, offer a promising solution for early diagnosis, prognosis, and disease monitoring. These biomarkers can reflect critical pathological processes like amyloid-beta (Aβ) deposition, tau protein hyperphosphorylation, α-syn misfolding, TDP-43 mislocalization and aggregation, and neuronal damage, enabling detection long before clinical symptoms emerge. Recent advances in blood-based biomarkers, particularly plasma Aβ, phosphorylated tau, and TDP-43, have shown diagnostic accuracy equivalent to CSF biomarkers, offering more accessible testing options. This review discusses the current challenges in fluid biomarker research, including variability, standardization, and sensitivity issues, and explores how combining multiple biomarkers with clinical symptoms improves diagnostic reliability. Ethical considerations, future directions involving extracellular vehicles (EVs), and the integration of artificial intelligence (AI) are also highlighted. Continued research efforts will be key to overcoming these obstacles, enabling fluid biomarkers to become crucial tools in personalized medicine for neurodegenerative diseases.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"108 ","pages":"Article 102739"},"PeriodicalIF":12.5,"publicationDate":"2025-03-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143694701","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Dietary polyphenols as geroprotective compounds: From Blue Zones to hallmarks of ageing","authors":"Sergio Davinelli ,&nbsp;Alessandro Medoro ,&nbsp;Frank B. Hu ,&nbsp;Giovanni Scapagnini","doi":"10.1016/j.arr.2025.102733","DOIUrl":"10.1016/j.arr.2025.102733","url":null,"abstract":"<div><div>Following the demographic shift towards an ageing population over the past century, particularly in developed countries, the concept of healthspan has gained increasing acceptance as a key framework for understanding the drivers of healthy ageing. Accordingly, long-lived individuals, such as nonagenarians and centenarians, who remain free from chronic diseases, provide a valuable model to investigate the complex interplay of biological, genetic, and environmental factors that contribute to exceptional longevity. Although there are other longevity hotspots worldwide, five regions, known as Blue Zones, are widely recognized for their exceptionally long-lived populations. Among the various determinants of healthy ageing, the eating patterns of long-lived individuals in Blue Zones include a variety of polyphenol-rich foods, which may contribute to their healthy phenotype. A significant body of evidence suggests that polyphenols, a large family of compounds ubiquitously found in plant-based foods, may exhibit geroprotective activity by influencing underlying biological mechanisms of ageing and promoting optimal longevity. While identifying several knowledge gaps that future investigations should address, the goal of this review is to provide an overview of how specific polyphenols found in foods commonly consumed by long-lived individuals residing in the Blue Zones may mitigate the risk of age-related diseases. Additionally, we discuss how these compounds, by acting on evolutionarily conserved mechanisms associated with ageing, have the potential to modulate the intricate network of the hallmarks of ageing.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"108 ","pages":"Article 102733"},"PeriodicalIF":12.5,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143685891","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impact of diet and exercise on mitochondrial quality and mitophagy in Alzheimer's disease","authors":"Jangampalli Adi Pradeepkiran ,&nbsp;Md. Ariful Islam ,&nbsp;Ujala Sehar ,&nbsp;Arubala P. Reddy ,&nbsp;Murali Vijayan ,&nbsp;P. Hemachandra Reddy","doi":"10.1016/j.arr.2025.102734","DOIUrl":"10.1016/j.arr.2025.102734","url":null,"abstract":"<div><div>Alzheimer's disease (AD) is a devastating neurodegenerative disorder that affects millions of people worldwide. It is characterized by the accumulation of beta-amyloid and phosphorylated tau, synaptic damage, and mitochondrial abnormalities in the brain, leading to the progressive loss of cognitive function and memory. In AD, emerging research suggests that lifestyle factors such as a healthy diet and regular exercise may play a significant role in delaying the onset and progression of the disease. Mitochondria are often referred to as the powerhouse of the cell, as they are responsible for producing the energy to cells, including neurons to maintain cognitive function. Our article elaborates on how mitochondrial quality and function decline with age and AD, leading to an increase in oxidative stress and a decrease in ATP production. Decline in mitochondrial quality can impair cellular functions contributing to the development and progression of disease with the loss of neuronal functions in AD. This article also covered mitophagy, the process by which damaged or dysfunctional mitochondria are selectively removed from the cell to maintain cellular homeostasis. Impaired mitophagy has been implicated in the progression and pathogenesis of AD. We also discussed the impact of impaired mitophagy implicated in AD, as the accumulation of damaged mitochondria can lead to increased oxidative stress. We expounded how dietary interventions and exercise can help to improve mitochondrial quality, and mitochondrial function and enhance mitophagy in AD. A diet rich in antioxidants, polyphenols, and mitochondria-targeted small molecules has been shown to enhance mitochondrial function and protect against oxidative stress, particularly in neurons with aged and mild cognitively impaired subjects and AD patients. Promoting a healthy lifestyle, mainly balanced diet and regular exercise that support mitochondrial health, in an individual can potentially delay the onset and progression of AD. In conclusion, a healthy diet and regular exercise play a crucial role in maintaining mitochondrial quality and mitochondrial function, in turn, enhancing mitophagy and synaptic activities that delay AD in the elderly populations.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"108 ","pages":"Article 102734"},"PeriodicalIF":12.5,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143694702","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Prevention of cardiovascular disease for healthy aging and longevity: A new scoring system and related “mechanisms-hallmarks-biomarkers”","authors":"Chunsong Hu","doi":"10.1016/j.arr.2025.102727","DOIUrl":"10.1016/j.arr.2025.102727","url":null,"abstract":"<div><div>Healthy “environment-sleep-emotion-exercise-diet” intervention [E(e)SEEDi] lifestyle can improve the quality of life, prolong aging and promote longevity due to improvement of human immunity and prevention of cardiovascular diseases (CVD). Here, the author reviewed the associations between these core elements with CVD and cardiovascular aging, and developed a new scoring system based on the healthy E(e)SEEDi lifestyle for prediction and evaluation of life expectancy. These core factors are assigned 20 points each (120 points in total), and a higher score predicts healthier aging and longevity. The E(e)SEEDi represents “a tree of life” bearing the fruits of longevity as well as “a rocket of anti-ageing” carrying people around the world on a journey of longevity. In conclusion, the E(e)SEEDi can delay aging and increase the life expectancy due to the role of a series of cellular and molecular “mechanisms-hallmarks-biomarkers”. It’s believed that the novel scoring system has a huge potential and beautiful prospects.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"107 ","pages":"Article 102727"},"PeriodicalIF":12.5,"publicationDate":"2025-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143652637","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Targeted partial reprogramming as a novel therapeutic strategy for age-related decline","authors":"Max Rose ,&nbsp;Eli Y. Adashi","doi":"10.1016/j.arr.2025.102731","DOIUrl":"10.1016/j.arr.2025.102731","url":null,"abstract":"<div><div>Cellular reprogramming has emerged as a promising strategy for the amelioration of age-associated cellular phenotypes. <em>In-vivo</em> reprogramming approaches, however, have been limited by a lack of specificity and oncogenic risk. Recent breakthroughs have addressed these limitations, constituting a significant progression toward the development of safe and effective therapeutics for age-related pathologies.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"108 ","pages":"Article 102731"},"PeriodicalIF":12.5,"publicationDate":"2025-03-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143652638","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unraveling the mystery of citrate transporters in Alzheimer’s disease: An updated review","authors":"Anirban Goutam Mukherjee ,&nbsp;Shatakshi Mishra ,&nbsp;Abilash Valsala Gopalakrishnan ,&nbsp;Sandra Kannampuzha ,&nbsp;Reshma Murali ,&nbsp;Uddesh Ramesh Wanjari ,&nbsp;Stany B ,&nbsp;Balachandar Vellingiri ,&nbsp;Harishkumar Madhyastha ,&nbsp;Deepankumar Kanagavel ,&nbsp;Murali Vijayan","doi":"10.1016/j.arr.2025.102726","DOIUrl":"10.1016/j.arr.2025.102726","url":null,"abstract":"<div><div>A key molecule in cellular metabolism, citrate is essential for lipid biosynthesis, energy production, and epigenetic control. The etiology of Alzheimer's disease (AD), a progressive neurodegenerative illness marked by memory loss and cognitive decline, may be linked to dysregulated citrate transport, according to recent research. Citrate transporters, which help citrate flow both inside and outside of cells, are becoming more and more recognized as possible participants in the molecular processes underlying AD. Citrate synthase (CS), a key enzyme in the tricarboxylic acid (TCA) cycle, supports mitochondrial function and neurotransmitter synthesis, particularly acetylcholine (ACh), essential for cognition. Changes in CS activity affect citrate availability, influencing energy metabolism and neurotransmitter production. Choline, a precursor for ACh, is crucial for neuronal function. Lipid metabolism, oxidative stress reactions, and mitochondrial function can all be affected by aberrant citrate transport, and these changes are linked to dementia. Furthermore, the two main pathogenic characteristics of AD, tau hyperphosphorylation and amyloid-beta (Aβ) aggregation, may be impacted by disturbances in citrate homeostasis. The goal of this review is to clarify the complex function of citrate transporters in AD and provide insight into how they contribute to the development and course of the illness. We aim to provide an in-depth idea of which particular transporters are dysregulated in AD and clarify the functional implications of these dysregulated transporters in brain cells. To reduce neurodegenerative processes and restore metabolic equilibrium, we have also discussed the therapeutic potential of regulating citrate transport. Gaining insight into the relationship between citrate transporters and the pathogenesis of AD may help identify new indicators for early detection and creative targets for treatment. This study offers hope for more potent ways to fight this debilitating illness and is a crucial step in understanding the metabolic foundations of AD.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"107 ","pages":"Article 102726"},"PeriodicalIF":12.5,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143618019","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Impacts of ageing on the efficacy of CAR-T cell therapy","authors":"Shimao Qi,&nbsp;Jiaqian Li,&nbsp;Xinyu Gu,&nbsp;Yalan Zhang,&nbsp;Weilin Zhou,&nbsp;Fengling Wang,&nbsp;Wei Wang","doi":"10.1016/j.arr.2025.102715","DOIUrl":"10.1016/j.arr.2025.102715","url":null,"abstract":"<div><div>Chimeric antigen receptor T cells recognizing CD19 (19CAR-T) cell therapy has achieved robust clinical efficacy when treating some hematological malignancies, but which patient subgroups benefit mostly remains elusive. Here we summarized the data of 541 patients from 30 clinical trials who underwent 19 CAR-T therapy and analyzed the different clinical responses between young (&lt;44 years), middle-aged (45–59 years) and elderly (&gt;60 years) patients and found that the young patients showed a higher level of complete response (CR) rate. Therefore, we then summarize the advances of studies focusing on the effects of age on anti-tumor efficacy of CAR-T therapy and analyze the reasons for the low CR rate after CAR-T cell therapy in elderly patients with tumors, aiming to provide hints for oncologists to select the most suitable candidate for this cancer immunotherapy.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"107 ","pages":"Article 102715"},"PeriodicalIF":12.5,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143588728","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Cognition on the move: Examining the role of physical exercise and neurogenesis in counteracting cognitive aging","authors":"Sahand Farmand ,&nbsp;Andrea Du Preez ,&nbsp;Curie Kim ,&nbsp;Chiara de Lucia ,&nbsp;Marc-David Ruepp ,&nbsp;Brendon Stubbs ,&nbsp;Sandrine Thuret","doi":"10.1016/j.arr.2025.102725","DOIUrl":"10.1016/j.arr.2025.102725","url":null,"abstract":"<div><div>Structural and functional aspects of the hippocampus have been shown to be sensitive to the aging process, resulting in deficits in hippocampal-dependent cognition. Similarly, adult hippocampal neurogenesis (AHN), described as the generation of new neurons from neural stem cells in the hippocampus, has shown to be negatively affected by aging throughout life. Extensive research has highlighted the role of physical exercise (PE) in positively regulating hippocampal-dependent cognition and AHN. Here, by critically reviewing preclinical and clinical studies, we discuss the significance of PE in reversing age-associated changes of the hippocampus via modulation of AHN. We indicate that PE-induced changes operate on two main levels. On the first level, PE can potentially cause structural modifications of the hippocampus, and on the second level, it regulates the molecular and cellular pathways involved. These changes result in the vascular remodelling of the neurogenic niche, as well as the secretion of neurotrophic and antioxidant factors, which can in turn activate quiescent neural stem cells, while restoring their proliferation capacity and boosting their survival - features which are negatively impacted during aging. Understanding these mechanisms will allow us to identify new targets to tackle cognitive aging and improve quality of life.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"107 ","pages":"Article 102725"},"PeriodicalIF":12.5,"publicationDate":"2025-03-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143598427","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":1,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}