Aging and Disease最新文献

{"title":"Enhanced Chondrogenic Potential and Osteoarthritis Treatment Using Cyaonoside A-Induced MSC Delivered via a Hyaluronic Acid-Based Hydrogel System.","authors":"Xingyan An, Qirong Zhou, Shihao Sheng, Anfu Deng, Han Liu, Xiuhui Wang, Qin Zhang, Yingying Jing, Ke Xu, Chongru He, Robert Chunhua Zhao, Jiacan Su","doi":"10.14336/AD.2024.10016","DOIUrl":"https://doi.org/10.14336/AD.2024.10016","url":null,"abstract":"<p><p>Osteoarthritis (OA) is a prevalent degenerative joint disease that significantly impacts the quality of life in the elderly. Traditional Chinese medicine, particularly Medicinal Cyathula Root and its active component Cyaonoside A (CyA), has been utilized to treat OA by promoting chondrocyte proliferation, inhibiting inflammatory factors, and maintaining joint homeostasis. Concurrently, mesenchymal stem cells (MSC) derived from placental umbilical cord, bone marrow, and adipose tissue have gained attention for their potential in OA treatment due to their chondrogenic differentiation capabilities. This study explored the therapeutic synergy of CyA and MSC for enhanced cartilage regeneration. Optimal chondrogenic differentiation was achieved by treating MSC with 0.5 mg/mL CyA for 3 days, significantly increasing the expression of key cartilage-specific genes ACAN, COL2A, and SOX9. Comparative gene expression and pathway analyses revealed that CyA-induced MSC (C-MSC) modulate critical signaling pathways, including TGF-β, PI3K-Akt, and Wnt, demonstrating their potential in cartilage repair. Furthermore, C-MSC-derived exosomes exhibited superior anti-inflammatory and anti-apoptotic effects compared to MSC-derived exosomes in IL-1β-treated human chondrocytes, enhancing chondrogenic gene expression and reducing cartilage degradation. To enable targeted delivery, a novel injectable hydrogel system (HAMA@C-MSC) was developed using methylacrylated hyaluronic acid (HAMA). This hydrogel facilitated uniform cell distribution, maintained structural integrity, and demonstrated excellent biocompatibility and biosafety, with no cytotoxic or hemolytic effects. In vivo studies using a rat destabilization of the medial meniscus OA model confirmed that HAMA@C-MSC significantly improved cartilage structure, enhanced chondrocyte regeneration, and restored collagen integrity, outperforming other treatment groups as validated through imaging, histology, and molecular analyses. These findings highlight HAMA@C-MSC as a promising therapeutic strategy for OA, leveraging the synergistic effects of C-MSC and advanced hydrogel technology to achieve enhanced cartilage regeneration and joint protection.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-01-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143254526","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Unveiling Lipid Droplet Transport Dynamics as Biomarkers of Senescence Using Label-Free, Time-Lapse Holotomography.","authors":"Amarnath Singam, Nikita Gopakumar, Apoorva Chauhan, Kimberly Ramirez, Jeong Hee Kim, Chandrabali Bhattacharya, Jingchun Chen, Deok-Ho Kim, Seungman Park","doi":"10.14336/AD.2024.1408","DOIUrl":"https://doi.org/10.14336/AD.2024.1408","url":null,"abstract":"<p><p>Accumulation and density of lipid droplets (LDs) in cells have been identified as a potential biomarker to detect senescent cells. However, their intracellular dynamic transport and alterations during senescence remain largely unclear. To address this knowledge gap, senescence was induced in human microglia cells using hydrogen peroxide (H₂O₂) to investigate both short-term and long-term effects of H₂O₂ treatment on LD dynamics. We captured time-lapse holotomograms of LDs using label-free refractive index (RI)-based holotomography and quantified 11 dynamic parameters of LDs through single-particle tracking. These quantified parameters were then compared across healthy cells, short-term H₂O₂-treated pre-senescent cells (H₂O₂-treated cells), and long-term H₂O₂-induced senescent cells (senescent cells). The results revealed that LD dynamics are significantly altered in both H₂O₂-treated pre-senescent cells and H₂O₂-induced senescent cells, though with differing trends. Healthy cells exhibited higher values in all LD dynamic parameters compared to senescent cells, with the exception of the mean directional change rate, which is lower. In addition, H₂O₂-treated cells showed higher values in dynamic parameters such as total displacement, mean straight-line velocity, and confinement ratio compared to healthy and senescent cells, due to the observed linear migration of LDs during H₂O₂ treatment. We found that the altered movement of LDs is closely related to H₂O₂-induced damage to microtubule networks. These findings suggest that altered LD dynamics, along with associated molecules and pathways, may serve as potential biomarkers for identifying senescent cells, thereby aiding in the development of novel therapeutic targets and senolytics.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-01-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143253999","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Connection Between the Gut Microbiome and Epigenetic Modification in Age-Related Cancer: A Narrative Review.","authors":"Florida Owens, Joseph Souchak, Valeria Nazaire, Juliet Akkaoui, Rajib Shil, Candy Carbajal, Kingshuk Panda, David Caraballo Delgado, Inge Claassen, Santiago Moreno, Samantha Yi, Yishu Dong, Nirbachita Adrita, Lee-Seng Lau, Nazira El-Hage","doi":"10.14336/AD.2024.1618","DOIUrl":"https://doi.org/10.14336/AD.2024.1618","url":null,"abstract":"<p><p>As individuals age, physiological changes influence the composition and function of the gut microbiome, significantly impacting the onset and progression of various illnesses, including cancer. Notably, the gut microbiome affects epigenetic modifications such as DNA methylation and histone alterations. Furthermore, it contributes to the age-related decline in immune system efficiency, increasing susceptibility to infections and cancers. This dual role of the gut microbiome-both a protective factor and a risk factor-is a key aspect of its importance in maintaining long-term health, making it a significant topic of discussion in this review. Moreover, a challenge faced by the elderly is the concurrent use of multiple medications. Polypharmacy can interact with the gut microbiome, potentially altering its efficacy, leading to adverse drug reactions, and affecting vital microbiome diversity. The effects of these interactions on cancer therapies and the overall health of elderly patients are becoming increasingly important. Understanding the complex relationship between aging, the gut microbiome, cancer, and polypharmacy is crucial for developing more effective therapeutic strategies and improving patient outcomes. Here, we discuss recent advances in understanding age-related physiological changes in the microbiome and their significance in cancer development and therapy. Specifically, we will explor how epigenetic changes acquired during aging, along with ongoing prescriptions of multiple medications and the decline of immune function, contribute to the intricate relationship between aging and cancer.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-01-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143254522","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Age-Associated Activation of the cGAS-STING Pathway and Impairment of DNA Damage Repair in Human Primary Alveolar Type II Cells.","authors":"Chih-Ru Lin, Hassan Hayek, Hannah Simborio, Loukmane Karim, Karim Bahmed, Sudhir Bolla, Nathaniel Marchetti, Gerard J Criner, Ying Tian, Beata Kosmider","doi":"10.14336/AD.2024.1175","DOIUrl":"https://doi.org/10.14336/AD.2024.1175","url":null,"abstract":"<p><p>Homeostatic imbalance and lung function decline are central physiological characteristics of aging and susceptibility to respiratory diseases. Senescence contributes to tissue damage and alveolar epithelial cell injury and decreases reparative capacity. Alveolar type II (ATII) cells have stem cell potential and self-renew to regenerate the alveoli after damage. They were isolated from younger and older non-smoker and smoker organ donors to define their function in the lung. Smoking and older age increased ATII cell senescence as detected by high β-galactosidase activity and P21 levels by Western blotting and RT-PCR. Also, the number of ATII cells was the lowest in lung tissue in older smokers. This was associated with increased stress signaling, as shown by elevated 4-HNE and G3BP1 expression in ATII cells, and inflammation indicated by high IL-8 levels in BAL fluid. In addition, DNA damage and decreased repair were observed using the comet assay, especially in ATII cells isolated from older smokers. This was accompanied by the highest levels of cytosolic double-strand DNA in this group and correlated with the activated cGAS-STING pathway and increased IRF3 expression. Moreover, telomere shortening, accumulation of TERRA molecules, and increased ZBP1 protein expression in ATII cells were associated with smoking and older age. Reduced NRF2 and DJ-1 expression in ATII cells was detected by Western blotting, especially in older smokers, which suggests an antioxidant defense system dysfunction. Our study provides insights into the impaired interconnected signaling network, which can contribute to ATII cell senescence.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-01-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143254524","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oxidative Stress Promotes Axonal Atrophy through Alterations in Microtubules and EB1 Function.","authors":"Samuel Shields, Emilia Gregory, Oliver Wilkes, IIlana Gozes, Natalia Sanchez-Soriano","doi":"10.14336/AD.2024.0839","DOIUrl":"https://doi.org/10.14336/AD.2024.0839","url":null,"abstract":"<p><p>Axons are crucial for transmitting neurochemical signals. As organisms age, the ability of neurons to maintain their axons declines; hence, aged axons are more susceptible to damage or dysfunction. Understanding how aging causes axonal vulnerability is crucial for developing strategies to enhance overall resilience of neurons and prevent neuronal deterioration during aging and in age-related neurodegenerative diseases. Increasing levels of reactive oxygen species (ROS) causes oxidative stress - a hallmark of aging and age-related diseases. Despite this association, a causal relationship between oxidative stress and neuronal aging remains unclear, particularly in how subcellular physiology may be affected by ROS. By using Drosophila-derived primary neuronal cultures and a recently developed in vivo neuronal model of aging, which involves the visualisation of Drosophila medulla neurons, we investigated the interplay between oxidative stress, neuronal aging and the microtubule cytoskeleton. Our results showed that oxidative stress is a key driver of axonal and synaptic decay, as shown by an enhanced appearance of axonal swellings, microtubule alterations (in both axons and synapses) and morphological transformation of axonal terminals during aging. We demonstrated that increasing the levels of ROS sensitises microtubule plus end-binding protein 1 (EB1), leading to microtubule defects that effect neuronal integrity. Furthermore, manipulating EB1 proved to be a valuable therapeutic strategy to prevent aging hallmarks enhanced in conditions of elevated ROS. In summary, we demonstrate a mechanistic pathway linking cellular oxidative stress with changes in the microtubule cytoskeleton leading to axonal deterioration during aging and provide evidence of the therapeutic potential of enhancing microtubule plus-end physiology to improve the resilience of axons.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143253978","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Advancing Hydrocephalus Management: Pathogenesis Insights, Therapeutic Innovations, and Emerging Challenges.","authors":"Xiuyun Liu, Hui Zhi, Marek Czosnyka, Chiara Robba, Zofia Czosnyka, Jennifer Lee Summers, Huijie Yu, Xiaoguang Tong, Guoyi Gao, Gelei Xiao, Kai Yu, Yan Xing, Renling Mao, Shaoya Yin, Yangong Chao, Hongliang Li, Ke Pu, Keke Feng, Meijun Pang, Dong Ming","doi":"10.14336/AD.2024.1434","DOIUrl":"https://doi.org/10.14336/AD.2024.1434","url":null,"abstract":"<p><p>Hydrocephalus is a prevalent neurological disorder, particularly impactful in older adults, characterized by high incidence and numerous complications that impose a significant burden on healthcare systems. This review aims to provide a comprehensive description of hydrocephalus pathogenesis, focusing on cellular and molecular insights derived from animal models. We also present the latest advances in hydrocephalus research and highlight potential therapeutic targets. Lastly, the review advocates the integration of findings from both animal and human studies to achieve better outcomes and examines the potential of emerging technologies. We wish to raise public attention about this disease in an aging society. Current animal models for hydrocephalus involve acquired hydrocephalus models and genetic/congenital hydrocephalus models. Studies from animals have shown that the main mechanisms of models can be broadly classified into nine types. A variety of drug-targeted therapy methods and non-surgical treatment methods have been used in clinical practice. But current treatment approaches primarily focus on symptomatic relief and intracranial pressure control rather than addressing the underlying pathological mechanisms. We call for the development of more accurate and representative animal models to achieve better outcomes and examine the potential of emerging technologies, such as artificial intelligence and neuroimaging. In summary, this review synthesizes recent findings in hydrocephalus research, identifies promising therapeutic targets and interventions, and critically evaluates the limitations of current research paradigms, aiming to align preclinical studies with clinical endpoints. Continued studies and multidisciplinary collaboration are essential to develop effective interventions and facilitate new treatments into bedside.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-01-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143254523","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"NR1D1 Inhibition Enhances Autophagy and Mitophagy in Alzheimer's Disease Models.","authors":"Shi-Qi Zhang, Zhangming Niu, Alexander Anisimov, Fang Shi, Shenglong Deng, Xianglu Xiao, Shu-Qin Cao, Jun-Ping Pan, He-Ling Wang, Maria J Lagartos-Donate, Nihal Gullu Bozbas, Ping-Jie Wang, Ruixue Ai, Yan Li, Guang Yang, Sofie Lautrup, Evandro F Fang","doi":"10.14336/AD.2024.1654","DOIUrl":"10.14336/AD.2024.1654","url":null,"abstract":"<p><p>Alzheimer's disease (AD) is marked by extracellular beta-amyloid (Aβ) plaques and intracellular Tau tangles, leading to progressive cognitive decline and neuronal dysfunction. Impaired autophagy, a process by which a cell breaks down and destroys damaged or abnormal proteins and other substances, contributes to AD progression. This study investigated Nuclear Receptor Subfamily 1 Group D Member 1 (NR1D1) as a potential therapeutic target for modulating autophagy. We show that NR1D1 depletion significantly enhances autophagic flux and mitophagy in human cell lines as well as wildtype and AD Caenorhabditis elegans (C. elegans) models. Our findings revealed that NR1D1 knockdown increased autophagy markers and activated the proteins Sirtuin 1 (SIRT1) and CTSB cathepsin B (Cathepsin B), both linked to autophagy function. In 5 familial AD mutations (5xFAD) mice, Nr1d1 knockdown restored the expression level of autophagy markers. C. elegans experiments revealed that depletion of the worm ortholog of NR1D1, nhr-85, improved neuronal mitophagy, enhanced associative memory in amyloid-β models, and extended lifespan. These findings suggest NR1D1 as a promising therapeutic target for improving cellular autophagy mechanisms in AD.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-01-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142982455","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Chronic Cerebral Deterioration - A Comprehensive View of Old-Age Cerebral Deterioration.","authors":"Jan Willem van Dalen","doi":"10.14336/AD.2024.1073","DOIUrl":"https://doi.org/10.14336/AD.2024.1073","url":null,"abstract":"<p><p>The current one-dimensional view of pathological brain changes in older persons leading to cognitive complaints, mild cognitive impairment, and ultimately dementia is incomplete. It neglects the earliest, non-cognitive, and multifaceted symptoms of gradually accumulating cerebral damage. Subtle personality changes, balance problems, muscle wasting, weight loss, changing sleep patterns and declining blood pressure and cholesterol, precede memory problems and cognitive impairment. Chronic cerebral deterioration offers a new comprehensive concept, capturing symptoms across late-life cerebral dysfunction domains, and revising alleged dementia 'risk factors' more realistically into prodromal signs of cerebral deterioration. This may reduce research waste on dementia prevention unsuccessfully targeting prodromes and help identify people at the highest risk of developing care needs. It will improve counselling of older people with signs and symptoms when memory or other cognitive impairments are not yet present. Emphasizing total cerebral function over cognition alone focuses on what is clinically most relevant: the patient's need of care.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-01-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142982367","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Pros and Cons of Human Brain Organoids to Study Alzheimer's Disease.","authors":"Andrea Sainz, Fernando Pérez, Alberto Pérez-Samartín, Mitradas Panicker, Asier Ruiz, Carlos Matute","doi":"10.14336/AD.2024.1409","DOIUrl":"https://doi.org/10.14336/AD.2024.1409","url":null,"abstract":"<p><p>There is increasing pressure for researchers to reduce their reliance on animals, particularly in early-stage research. The main reason for that change arises from the different biological behavior of humans that leads to frequent failure of translating data from bench to bed. The advent of organoid technology ten years ago, along with the feasibility of obtaining brain organoids in most laboratories, has created considerable expectations not exempting frustration. In this review, we make a critical appraisal of the advantages and limitations of studying Alzheimer's disease in brain cortical organoids derived from inducible pluripotent stem cells (iPSCs). While dealing with human neurons and glia in 3D poses a tremendous advantage versus murine brain cells, organoids typically lack microglia, blood vessels, immune interactions as well as proper CNS neuropil. In turn, they have relatively few oligodendrocytes and low myelination. In addition, lengthy procedures to get proper mature organoids constitute an additional limitation that may also affect the native biological properties of neurons and glia. We conclude that human brain organoids, while popular and useful, remain a model that needs further refinement before bringing substantial value to study Alzheimer's disease.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142982457","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Physical Prehabilitation for Older Patients with Cancer before Complex Medical-Surgical Interventions: An Umbrella Review.","authors":"Dana Loudovici-Krug, Louise André, Heiner Paul Blumensaat, Marion Granger, Laetitia Stefani, Josephine Kühnemund, Christina Lemhöfer, Claire Falandry","doi":"10.14336/AD.2024.0957","DOIUrl":"https://doi.org/10.14336/AD.2024.0957","url":null,"abstract":"<p><p>Prehabilitation has become a field of increasing interest over recent decades. However, few studies specifically investigated prehabilitation for older patients with cancer. The objective of this umbrella review was to summarize evidence on prehabilitation programs to identify the physical interventions that may be applied with benefit to older cancer patients who will undergo complex medical-surgical procedures. The protocol was registered in Prospero. Major databases, namely PubMed, Embase, CINAHL, Cochrane, Web of Science and Prospero, were searched until summer 2020 and a second search was performed until November 2023. All systematic reviews and meta-analyses were included, dealing with the major topic of prehabilitation for older patients with cancer diagnosis. Among 1425 records (633 until 2020, 792 until November 2023), 14 reviews were selected for inclusion. According to the AMSTAR-2 checklist, the median quality score was 11 (range: 5-12). Total duration of prehabilitation ranged from 1 to 5 weeks, session duration from 20 to 50 minutes, session frequency from 3 to 6 per week. Reported program modes were aerobic and resistance exercises. Concerning the outcome measures, the functional as well as the respiratory status was significantly affected. Quality of life did not benefit significantly, but showed a positive trend. The length of hospital stay was not significantly improved in the majority of the studies. In contrast, most systematic reviews reported significantly lower numbers of total postoperative complications. Functional recovery was enhanced in half of the found reviews. Prehabilitation is a growing field, notably also in reviews focussing on oncological care for elderly patients included in this umbrella review. Aerobic and resistance exercises are the core of the majority of the programs evaluated but their characteristics (total duration, frequency) are partly heterogeneous. Prehabilitation for older patients may also include other modalities of geriatric interventions like nutritional or psychological optimization.</p>","PeriodicalId":7434,"journal":{"name":"Aging and Disease","volume":" ","pages":""},"PeriodicalIF":7.0,"publicationDate":"2025-01-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142982456","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}