Ageing Research Reviews最新文献

{"title":"L-deprenyl extends lifespan across mammalian species: A meta-analysis of 22 longevity experiments","authors":"Michael R. Bene","doi":"10.1016/j.arr.2025.102873","DOIUrl":"10.1016/j.arr.2025.102873","url":null,"abstract":"<div><div>Identifying interventions that reproducibly extend lifespan is a central aim in geroscience, with hopes of translating these findings to enhance the health and longevity of older adults. L-deprenyl, an FDA approved medication, has been investigated for its role in aging for over three decades. To evaluate the effect of L-deprenyl on lifespan in mammals we performed a random-effects meta-analysis on 22 rodent lifespan experiments. The results indicate L-deprenyl significantly increases average lifespan with moderate effect size (SMD = 0.6773, p = 0.0002). We identified no significant evidence of publication bias in the examined studies, but did observe substantial heterogeneity. Accounting for experimental factors revealed significant effects of dose (p = 0.0233) and age at initiation (p &lt; 0.0001), with higher doses and older age associated with larger effects. Assessment of treatment effects by mean lifespan of controls suggests short-lived controls are not responsible for the observed effects. In addition to the meta-analysis, we reanalyzed a dog survival study by Ruehl et al. When accounting for age at enrollment and sex, the study no longer displayed a significant effect on survival, though power was limited by small sample size. Together, this analysis of 23 L-deprenyl lifespan experiments spans 27 years of research in 6 countries, 8 strains of rodents, 4 species, 6 doses, and 2 delivery methods, providing some of the most comprehensive data supporting the effect of a compound on lifespan in mammals. Future clinical studies examining L-deprenyls effects on health outcomes in older adults will be critical to determine the translatability of these findings.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"112 ","pages":"Article 102873"},"PeriodicalIF":12.4,"publicationDate":"2025-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144852972","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":"Understanding the influence of TLR-mediated immune system on necroptosis-induced neurodegeneration in Parkinson’s disease","authors":"Vaishnavi Suresh Jadhav,&nbsp;Dharmendra Kumar Khatri","doi":"10.1016/j.arr.2025.102872","DOIUrl":"10.1016/j.arr.2025.102872","url":null,"abstract":"<div><div>Neurodegeneration is a hallmark of various neurological disorders, including Parkinson’s disease (PD), Alzheimer’s disease (AD), stroke, and neurotropic viral infections. Although the precise etiology remains unclear, multiple pathological mechanisms contribute to disease progression, including mitochondrial dysfunction, protein aggregation, calcium excitotoxicity, endoplasmic reticulum (ER) stress, oxidative stress, immune system activation, and neuroinflammation. Among these, the immune response plays a crucial role in disease pathogenesis, acting as a defense mechanism against damage-associated molecular patterns (DAMPs), pathogen-associated molecular patterns (PAMPs), and toxic molecular species. Chronic immune activation, particularly of microglia, is a defining feature of neuroinflammation, which involves both innate and adaptive immune responses. In the central nervous system (CNS), microglia-mediated neuroinflammation leads to the release of proinflammatory cytokines, exacerbating neuronal damage. Necroptosis, a regulated form of programmed cell death, has been implicated in neuroinflammatory disorders, including PD. Persistent microglial activation in response to aggregated proteins stimulates various microglial receptors, which includes Toll-like receptor 4 (TLR4), that play a pivotal role in necroptosis activation via the myeloid differentiating primary response gene 88 (MYD88)-independent pathway. This review explores how immune system-mediated receptor activation triggers cell death pathways, with a focus on TLR-induced necroptosis in PD. In addition, we also discuss various downstream molecular mechanisms linking TLR signaling to necroptosis and discuss the potential of TLRs as therapeutic targets, offering insights for developing neuroprotective strategies in neurodegenerative diseases (NDDS).</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"112 ","pages":"Article 102872"},"PeriodicalIF":12.4,"publicationDate":"2025-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144852976","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":"Biomarkers of multimorbidity: A systematic review","authors":"Maria Beatrice Zazzara ,&nbsp;Federico Triolo ,&nbsp;Leonardo Biscetti ,&nbsp;Ersilia Paparazzo ,&nbsp;Marco Fiorillo ,&nbsp;Davide Liborio Vetrano ,&nbsp;Graziano Onder ,&nbsp;on behalf of the BIO-SIGN Study Investigators","doi":"10.1016/j.arr.2025.102870","DOIUrl":"10.1016/j.arr.2025.102870","url":null,"abstract":"<div><div>The development of multiple chronic diseases in the same individual (i.e., multimorbidity) results from the loss of homeostasis across several biological systems. Identifying pathophysiological pathways common to multiple diseases, using accessible biomarkers, could increase our understanding of multimorbidity and improve its prognostication and management. We conducted a systematic review of peer-reviewed articles published till September 2024 that investigated biomarkers of multimorbidity. Due to study heterogeneity, a synthesis without meta-analysis was performed on 43 studies employing harvest plots based on direction of effect, sample size and study quality. Findings highlight how inflammatory and metabolic biomarkers, such as interleukin-6 (IL-6) and glycated haemoglobin (HbA1c) especially, but also triglycerides, low-density lipoprotein (LDL) cholesterol and kidney and liver markers, along with markers of neurodegeneration including Neurofilament Light Chain (NfL) and Phospho-Tau 217 (p-tau 217), were directly associated with multimorbidity. Nonetheless, evidence for hormonal and vascular activation markers, as well as more novel geroscience biomarkers, remains limited. These markers could have a key role in identifying individuals at high risk of developing or worsening multimorbidity. The review also highlights how methodological challenges, including heterogeneity in study design, populations, and multimorbidity definitions, impact on comparability and generalizability of findings. Addressing these gaps through standardized, longitudinal studies and multi-omics approaches is crucial to improve our understanding of the pathophysiological mechanisms of multimorbidity. In summary, this review outlines the independent association of diverse biomarkers with multimorbidity, opening to the possibility of identifying specific pathophysiological pathways for risk stratification and possible target of future personalized interventions.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"112 ","pages":"Article 102870"},"PeriodicalIF":12.4,"publicationDate":"2025-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144859978","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":"From clock to clock: Therapeutic target discovery for aging and age-related diseases","authors":"Jianjiu Chen ,&nbsp;Geoffrey Ho Duen Leung ,&nbsp;Howell Leung ,&nbsp;Alina Ustiugova ,&nbsp;Anastasia Shneyderman ,&nbsp;Mike Korzinkin ,&nbsp;David Gennert ,&nbsp;Frank W. Pun ,&nbsp;Alex Aliper ,&nbsp;Feng Ren ,&nbsp;Alex Zhavoronkov","doi":"10.1016/j.arr.2025.102871","DOIUrl":"10.1016/j.arr.2025.102871","url":null,"abstract":"<div><div>The aging population worldwide necessitates the development of novel therapeutics that enhance the quality of life by preventing and treating age-related diseases. In this review, we first discuss the advantages of a dual-purpose target identification strategy for aging and age-related diseases, with assessment of the hallmarks of aging as an approach to identify such dual-purpose targets. Resulting from a convergence of aging research with machine learning (ML) and other artificial intelligence (AI) models, aging clocks were initially developed as aging biomarkers, but its value in identifying therapeutic targets is also increasingly recognized. Building on recently published aging clocks, we reestablish a significant proportion of known drug targets by identifying clock-associated genes, highlighting the potential of these clocks for target identification. Lastly, we discuss other applications of aging clocks in drug development such as population stratification and disease and treatment monitoring. With the growing availability of multi-omics data and rapid advancements in ML and AI, we anticipate accelerated progress in aging clock research, paving the way for innovative treatments to meet the healthcare needs of a global aging population.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"112 ","pages":"Article 102871"},"PeriodicalIF":12.4,"publicationDate":"2025-08-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144841639","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":"Decoding JMJD proteins in cardiovascular and cerebrovascular diseases: From structure to function","authors":"Guangzhi Hao ,&nbsp;Yiyang Chen ,&nbsp;Yong Liang ,&nbsp;Jiayan Li ,&nbsp;Yushu Dong ,&nbsp;Yang Yang","doi":"10.1016/j.arr.2025.102869","DOIUrl":"10.1016/j.arr.2025.102869","url":null,"abstract":"<div><div>Cardiovascular and cerebrovascular diseases remain major causes of death and disability worldwide. Their susceptibility is closely linked to epigenetic modifications triggered by environmental factors. The Jumonji C domain-containing (JMJD) protein family consists of Fe²⁺- and 2-oxoglutarate (2OG)-dependent oxidases that primarily mediate histone demethylation or hydroxylation of specific amino acid residues, functioning as critical histone demethylases in epigenetic regulation. Recent studies have identified JMJD proteins as pivotal epigenetic regulators in various cardiovascular and cerebrovascular diseases, including cardiac hypertrophy (CH), atherosclerosis (AS), myocardial ischemia-reperfusion injury (MIRI), and ischemic stroke (IS). These proteins are deeply involved in pathological processes such as oxidative stress, macrophage polarization, mitochondrial autophagy, and apoptosis. Accordingly, elucidating the functions of JMJD proteins has gained increasing attention. This review summarizes the structural characteristics of JMJD family members and highlights their roles in cardiovascular and cerebrovascular disorders. These insights may help guide future pharmacological strategies targeting JMJD proteins.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"112 ","pages":"Article 102869"},"PeriodicalIF":12.4,"publicationDate":"2025-08-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144839336","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":"Application of Traditional Chinese Medicine in the different pathological stages of ischemic stroke: Target immune cells","authors":"Yulu Wang ,&nbsp;Yuanyi Wang ,&nbsp;Lele Liu ,&nbsp;Zhen Hui ,&nbsp;Sulei Wang ,&nbsp;Guoxue Zhu ,&nbsp;Lining Wang ,&nbsp;Zhennian Zhang ,&nbsp;Yue Hu","doi":"10.1016/j.arr.2025.102866","DOIUrl":"10.1016/j.arr.2025.102866","url":null,"abstract":"<div><div>Immune cells play a pivotal role in the complex pathophysiology of ischemic stroke (IS), with their functions dynamically shifting throughout the disease's progression. Throughout the different pathological stages of IS, various immune cells, such as microglia, T cells, neutrophils, NK cells, and mononuclear/macrophages, contribute uniquely to the disease's trajectory. Although thrombolytic therapy remains the standard treatment for IS, its efficacy is limited by a narrow therapeutic window, underscoring the need for alternative or adjunctive therapeutic strategies. Increasingly, the therapeutic potential of Traditional Chinese Medicine (TCM) has gained recognition for its beneficial effects across multiple phases of IS. Notably, TCM interventions have been shown to attenuate early inflammatory responses and neural injury by targeting immune cells, particularly microglia. Furthermore, during the recovery phase, TCM may promote white matter repair and functional recovery through the regulation of neuroimmune interactions. This review offers a comprehensive analysis of the dynamic roles and signaling pathways of immune cells in IS, and further investigates the mechanistic basis of TCM's immunomodulatory effects. While considerable progress has been made, significant challenges remain in fully elucidating the underlying mechanisms of TCM and in optimizing its integration into current IS treatment frameworks.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"112 ","pages":"Article 102866"},"PeriodicalIF":12.4,"publicationDate":"2025-08-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144818623","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":"Pathogens accelerate features of human aging: A review of molecular mechanisms","authors":"Amy D. Proal ,&nbsp;Michael B. VanElzakker","doi":"10.1016/j.arr.2025.102865","DOIUrl":"10.1016/j.arr.2025.102865","url":null,"abstract":"<div><div>Many models of aging assume that processes such as cellular senescence or epigenetic alteration occur under sterile conditions. However, humans sustain infection with viral, bacterial, fungal, and parasite pathogens across the course of a lifetime, many of which are capable of long-term persistence in host tissue and nerves. These pathogens—especially members of the human virome like herpesviruses, as well as intracellular bacteria and parasites—express proteins and metabolites capable of interfering with host immune signaling, mitochondrial function, gene expression, and the epigenetic environment. This paper reviews these and other key mechanisms by which infectious agents can accelerate features of human aging. This includes hijacking of host mitochondria to gain replication substrates, or the expression of proteins that distort the signaling of host longevity-regulating pathways. We further delineate mechanisms by which pathogen activity contributes to age-related disease development: for example, Alzheimer’s amyloid-β plaque can act as an antimicrobial peptide that forms in response to infection. Overall, because many pathogens dysregulate mTOR, AMPK, or related immunometabolic signaling, healthspan interventions such as low-dose rapamycin, metformin, glutathione, and NAD+ may exert part of their effect by controlling persistent infection. The lack of diagnostics capable of detecting tissue-resident pathogen activity remains a critical bottleneck. Emerging tools—such as ultrasensitive protein assays, cfRNA metagenomics, and immune repertoire profiling—may enable integration of pathogen detection into biological age tracking. Incorporating infection into aging models is essential to more accurately characterize drivers of senescence and to optimize therapeutic strategies that target both host and microbial contributors to aging.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"112 ","pages":"Article 102865"},"PeriodicalIF":12.4,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144812769","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":"Group-based trajectory modelling for cognitive changes in middle-aged and older adults: A systematic review","authors":"Huan Zhang ,&nbsp;Hongli Chen ,&nbsp;Xiaotong Ding ,&nbsp;Qing Wang ,&nbsp;Jingjing Gu ,&nbsp;Shuaifang Wei ,&nbsp;Jiajun Xue ,&nbsp;Yulin Liang ,&nbsp;Zheng Li","doi":"10.1016/j.arr.2025.102855","DOIUrl":"10.1016/j.arr.2025.102855","url":null,"abstract":"<div><h3>Background</h3><div>Cognitive health constitutes a critical component of healthy aging. This study aims to review studies that employed group-based trajectory modeling approaches systematically to examine cognitive trajectories, identify associated determinants, and investigate the relationship with health outcomes.</div></div><div><h3>Methods</h3><div>A systematic search was performed in five databases for articles that identified two or more cognitive trajectories. The study was conducted following the PRISMA statement.</div></div><div><h3>Results</h3><div>Thirty-five studies, published from 2007 to 2024 across multiple countries, with sample sizes ranging from 318 to 19422 participants, were ultimately included in this study. The “High Stable” and “Moderate Decline” trajectories were the most frequently observed patterns. Key protective factors associated with the stable group included higher education, active lifestyle (e.g., cognitive/physical activities, high quality and appropriate duration of sleep, no smoking), and strong social networks. Older people with cardiovascular diseases, diabetes, and depression tend to experience rapid cognitive decline. Although relatively few studies have focused on biomarkers and brain structural changes, available evidence suggests that factors such as APOE ε4 carriage higher Aβ/global amyloid load, elevated t-tau+ , and entorhinal cortical thinning are associated with cognitive decline trajectories. In addition, several studies highlighted significant consequences linked to rapid cognitive deterioration, such as high incidence of dementia, mortality, and disability.</div></div><div><h3>Conclusion</h3><div>A substantial proportion of aging individuals maintain cognitive function over time, which may be supported by protective strategies like cognitive/physical engagement, healthy sleep, social connection, and disease management. The adverse outcomes linked to decline trajectories underscore the need for future research on modifiable factors. Comparing predictors across subgroups provides insights into cognitive resilience and proactive protection. Further exploration of biological measures is crucial for understanding cognitive aging and enabling earlier dementia prevention.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"112 ","pages":"Article 102855"},"PeriodicalIF":12.4,"publicationDate":"2025-08-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144812768","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":"Is the renin-angiotensin system a friend or foe in neurological diseases? Unveiling its role and therapeutic potential","authors":"Pratyush Porel ,&nbsp;Garry Hunjan ,&nbsp;Shamsher Singh ,&nbsp;Khadga Raj Aran","doi":"10.1016/j.arr.2025.102854","DOIUrl":"10.1016/j.arr.2025.102854","url":null,"abstract":"<div><div>The renin-angiotensin system (RAS), an important regulator of body fluid and cardiovascular homeostasis, is gradually implicated in the pathogenesis of neurological diseases due to its dysregulation. In addition to their traditional functions, components of the RAS, especially angiotensin-II (Ang-II), enhance neuroinflammation, oxidative stress, and neuronal injury. Ang-II exacerbates blood-brain barrier (BBB) disruption, promotes glial activation, and contributes to neurodegeneration via the Angiotensin type 1 (AT1) receptor (AT1R) and causes neurological diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), multiple sclerosis (MS), Huntington’s disease (HD), epilepsy, depression, and anxiety. The angiotensin (1−7) axis mediated by the Mas receptor appears to be neuroprotective, however, as it reverses the negative effects of Ang-II. In experimental models and clinical trials, blocking RAS specifically by angiotensin-converting enzyme inhibitors (ACEIs) or angiotensin receptor blockers (ARBs) has demonstrated promise in reducing neuroinflammation and neuronal damage, especially in stroke and neurodegenerative diseases. In the current era of research, neuropharmacologists have new optimism due to emerging evidence of the promising potential of RAS-modulating drugs, such as ARBs and ACEIs, in the treatment of various neurological diseases. Since RAS imbalance causes neuroinflammation, neuronal damage, and cognitive decline in conditions including AD, PD, and MS, these drugs may offer a new treatment approach. In the current era of neuropharmacology, this technique is novel since it enables more targeted therapies to address the root causes of neurodegeneration. This review explores the molecular pathways of RAS dysregulation in various neurological diseases, highlighting its therapeutic potential and paving the way for future treatment strategies.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"112 ","pages":"Article 102854"},"PeriodicalIF":12.4,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144779287","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":"Next-generation CRISPR gene editing tools in the precision treatment of Alzheimer’s and Parkinson’s disease","authors":"Harsh Kumar Meshram ,&nbsp;Sanjay Kumar Gupta ,&nbsp;Akash Gupta ,&nbsp;Kushagra Nagori ,&nbsp;Ajazuddin","doi":"10.1016/j.arr.2025.102851","DOIUrl":"10.1016/j.arr.2025.102851","url":null,"abstract":"<div><div>Emerging gene-editing technologies, such as the CRISPR system, represent a potential pathway for precision medicine targeting the genetic and molecular causes of diseases. Second-generation CRISPR technologies, including base editing, prime editing, and engineered Cas variants, have improved fidelity and offer alternative strategies for precise gene correction, transcriptional repression or activation, and modulation of pathological pathways in neurodegeneration. These tools can correct single-nucleotide mutations, reduce pathological protein accumulation, and modulate neuroinflammatory responses, all integral to the pathogenesis of Alzheimer’s disease (AD) and Parkinson’s disease (PD), both chronic, progressive neurodegenerative disorders. Unfortunately, currently available treatments are limited and primarily palliative. Preclinical studies have shown promising results, with improvements in cognitive and motor deficits in animal models. However, significant challenges must be addressed to ensure safe and effective delivery to the CNS, minimize off-target effects, and address ethical concerns. Current clinical investigations aim to translate these findings into available therapeutic options. This review also identifies the biological mechanisms, therapeutic use cases, and current limitations of next-generation CRISPR systems as tools in the context of AD and PD, providing both therapeutic and research capabilities through their unique strengths. Ultimately, the future of transactional neurogenomics will determine the clinical possibilities of CRISPR-based strategies for advancing neurodegenerative disease management beyond palliative and symptomatic treatment, toward a feasible mechanistic form of disease modification.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"111 ","pages":"Article 102851"},"PeriodicalIF":12.4,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144769366","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}