Ageing Research Reviews最新文献

{"title":"Sarcopenia and the biological determinants of aging: A narrative review from a geroscience perspective","authors":"Mariá Nunes-Pinto ,&nbsp;Renato Gorga Bandeira de Mello ,&nbsp;Milena Nunes Pinto ,&nbsp;Cédric Moro ,&nbsp;Bruno Vellas ,&nbsp;Laurent O. Martinez ,&nbsp;Yves Rolland ,&nbsp;Philipe de Souto Barreto","doi":"10.1016/j.arr.2024.102587","DOIUrl":"10.1016/j.arr.2024.102587","url":null,"abstract":"<div><h3>Background</h3><div>The physiopathology of sarcopenia shares common biological cascades with the aging process, as does any other age-related condition. However, our understanding of the interconnected pathways between diagnosed sarcopenia and aging remains limited, lacking sufficient scientific evidence.</div></div><div><h3>Methods</h3><div>This narrative review aims to gather and describe the current evidence on the relationship between biological aging determinants, commonly referred to as the hallmarks of aging, and diagnosed sarcopenia in humans.</div></div><div><h3>Results</h3><div>Among the twelve hallmarks of aging studied, there appears to be a substantial association between sarcopenia and mitochondrial dysfunction, epigenetic alterations, deregulated nutrient sensing, and altered intercellular communication. Although limited, preliminary evidence suggests a promising association between sarcopenia and genomic instability or stem cell exhaustion.</div></div><div><h3>Discussion</h3><div>Overall, an imbalance in energy regulation, characterized by impaired mitochondrial energy production and alterations in circulatory markers, is commonly associated with sarcopenia and may reflect the interplay between aging physiology and sarcopenia biology.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"103 ","pages":"Article 102587"},"PeriodicalIF":12.5,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142689922","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":"Mechanisms of muscle cells alterations and regeneration decline during aging","authors":"Guntarat Chinvattanachot ,&nbsp;Daniel Rivas ,&nbsp;Gustavo Duque","doi":"10.1016/j.arr.2024.102589","DOIUrl":"10.1016/j.arr.2024.102589","url":null,"abstract":"<div><div>Skeletal muscles are essential for locomotion and body metabolism regulation. As muscles age, they lose strength, elasticity, and metabolic capability, leading to ineffective motion and metabolic derangement. Both cellular and extracellular alterations significantly influence muscle aging. Satellite cells (SCs), the primary muscle stem cells responsible for muscle regeneration, become exhausted, resulting in diminished population and functionality during aging. This decline in SC function impairs intercellular interactions as well as extracellular matrix production, further hindering muscle regeneration. Other muscle-resident cells, such as fibro-adipogenic progenitors (FAPs), pericytes, and immune cells, also deteriorate with age, reducing local growth factor activities and responsiveness to stress or injury. Systemic signaling, including hormonal changes, contributes to muscle cellular catabolism and disrupts muscle homeostasis. Collectively<u>,</u> these cellular and environmental components interact, disrupting muscle homeostasis and regeneration in advancing age. Understanding these complex interactions offers insights into potential regenerative strategies to mitigate age-related muscle degeneration.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"102 ","pages":"Article 102589"},"PeriodicalIF":12.5,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142683749","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 ageing and disuse on neuromuscular junction and mitochondrial function and morphology: Current evidence and controversies","authors":"Evgeniia Motanova ,&nbsp;Marco Pirazzini ,&nbsp;Samuele Negro ,&nbsp;Ornella Rossetto ,&nbsp;Marco Narici","doi":"10.1016/j.arr.2024.102586","DOIUrl":"10.1016/j.arr.2024.102586","url":null,"abstract":"<div><div>Inactivity and ageing can have a detrimental impact on skeletal muscle and the neuromuscular junction (NMJ). Decreased physical activity results in muscle atrophy, impaired mitochondrial function, and NMJ instability. Ageing is associated with a progressive decrease in muscle mass, deterioration of mitochondrial function in the motor axon terminals and in myofibres, NMJ instability and loss of motor units. Focusing on the impact of inactivity and ageing, this review examines the consequences on NMJ stability and the role of mitochondrial dysfunction, delving into their complex relationship with ageing and disuse. Evidence suggests that mitochondrial dysfunction can be a pathogenic driver for NMJ alterations, with studies revealing the role of mitochondrial defects in motor neuron degeneration and NMJ instability. Two perspectives behind NMJ instability are discussed: one is that mitochondrial dysfunction in skeletal muscle triggers NMJ deterioration, the other envisages dysfunction of motor terminal mitochondria as a primary contributor to NMJ instability. While evidence from these studies supports both perspectives on the relationship between NMJ dysfunction and mitochondrial impairment, gaps persist in the understanding of how mitochondrial dysfunction can cause NMJ deterioration. Further research, both in humans and in animal models, is essential for unravelling the mechanisms and potential interventions for age- and inactivity-related neuromuscular and mitochondrial alterations.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"102 ","pages":"Article 102586"},"PeriodicalIF":12.5,"publicationDate":"2024-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142670073","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":"Targeted protein degradation: expanding the technology to facilitate the clearance of neurotoxic proteins in neurodegenerative diseases","authors":"Xin Wang ,&nbsp;Wen Shuai ,&nbsp;Panpan Yang ,&nbsp;Yinyang Liu,&nbsp;Yiwen Zhang,&nbsp;Guan Wang","doi":"10.1016/j.arr.2024.102584","DOIUrl":"10.1016/j.arr.2024.102584","url":null,"abstract":"<div><div>In neurodegenerative diseases (NDDs), disruptions in protein homeostasis hinder the clearance of misfolded proteins, causing the formation of misfolded protein oligomers and multimers. The accumulation of these abnormal proteins results in the onset and progression of NDDs. Removal of non-native protein is essential for cell to maintain proteostasis. In recent years, targeted protein degradation (TPD) technologies have become a novel means of treating NDDs by removing misfolded proteins through the intracellular protein quality control system. The TPD strategy includes the participation of two primary pathways, namely the ubiquitin-proteasome pathway (for instance, PROTAC, molecular glue and hydrophobic tag), and the autophagy-lysosome pathway (such as LYTAC, AUTAC and ATTEC). In this review, we systematically present the mechanisms of various TPD strategies employed for neurotoxic protein degradation in NDDs. The article provides an overview of the design, <em>in vitro</em> and <em>in vivo</em> anti-NDD activities and pharmacokinetic properties of these small-molecular degraders. Finally, the advantages, challenges and perspectives of these TPD technologies in NDDs therapy are discussed, providing ideas for further development of small molecule degraders in the realm of NDDs.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"102 ","pages":"Article 102584"},"PeriodicalIF":12.5,"publicationDate":"2024-11-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142650025","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":"Impact of coffee intake on human aging: Epidemiology and cellular mechanisms","authors":"Cátia R. Lopes ,&nbsp;Rodrigo A. Cunha","doi":"10.1016/j.arr.2024.102581","DOIUrl":"10.1016/j.arr.2024.102581","url":null,"abstract":"<div><div>The conception of coffee consumption has undergone a profound modification, evolving from a noxious habit into a safe lifestyle actually preserving human health. The last 20 years also provided strikingly consistent epidemiological evidence showing that the regular consumption of moderate doses of coffee attenuates all-cause mortality, an effect observed in over 50 studies in different geographic regions and different ethnicities. Coffee intake attenuates the major causes of mortality, dampening cardiovascular-, cerebrovascular-, cancer- and respiratory diseases-associated mortality, as well as some of the major causes of functional deterioration in the elderly such as loss of memory, depression and frailty. The amplitude of the benefit seems discrete (17 % reduction) but nonetheless corresponds to an average increase in healthspan of 1.8 years of lifetime. This review explores evidence from studies in humans and human tissues supporting an ability of coffee and of its main components (caffeine and chlorogenic acids) to preserve the main biological mechanisms responsible for the aging process, namely genomic instability, macromolecular damage, metabolic and proteostatic impairments with particularly robust effects on the control of stress adaptation and inflammation and unclear effects on stem cells and regeneration. Further studies are required to detail these mechanistic benefits in aged individuals, which may offer new insights into understanding of the biology of aging and the development of new senostatic strategies. Additionally, the safety of this lifestyle factor in the elderly prompts a renewed attention to recommending the maintenance of coffee consumption throughout life as a healthy lifestyle and to further exploring who gets the greater benefit with what schedules of which particular types and doses of coffee.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"102 ","pages":"Article 102581"},"PeriodicalIF":12.5,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142670076","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":"Astrocytic proteostasis in the tale of aging and neurodegeneration","authors":"Felipe Cabral-Miranda ,&nbsp;Isadora Matias ,&nbsp;Flávia Carvalho Alcantara Gomes","doi":"10.1016/j.arr.2024.102580","DOIUrl":"10.1016/j.arr.2024.102580","url":null,"abstract":"<div><div>Homeostasis of proteins (proteostasis), which governs protein processing, folding, quality control, and degradation, is a fundamental cellular process that plays a pivotal role in various neurodegenerative diseases and in the natural aging process of the mammalian brain. While the role of neuronal proteostasis in neuronal physiology is well characterized, the contribution of proteostasis of glial cells, particularly of astrocytes, has received fairly less attention in this context. Here, we summarize recent data highlighting proteostasis dysfunction in astrocytes and its putative implication to neurodegenerative diseases and aging. We discuss how distinct proteostasis nodes and pathways in astrocytes may specifically contribute to brain function and different age-associated pathologies. Finally, we argue that the understanding of astrocytic proteostasis role in neuronal physiology and functional decay may arise as a potential new avenue of intervention in neurodegenerative diseases and grant relevant data in the biology of aging.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"103 ","pages":"Article 102580"},"PeriodicalIF":12.5,"publicationDate":"2024-11-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142670072","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":"The catabolic - anabolic cycling hormesis model of health and resilience","authors":"Edward J. Calabrese ,&nbsp;Mark P. Mattson","doi":"10.1016/j.arr.2024.102588","DOIUrl":"10.1016/j.arr.2024.102588","url":null,"abstract":"<div><div>A major goal of aging research is to identify ways of extending productive and disease-free lifespans. Here we present the catabolic – anabolic cycling hormesis (CACH) model for optimizing health. The CACH model is based on the concept that cells and organ systems respond to catabolic challenges in ways that bolster their resilience and that an anabolic recovery period is required to effectuate the benefits of the catabolic challenge. As two prominent real-world examples we highlight the literature on the molecular and cellular mechanisms by which physical exercise and intermittent fasting bolster cellular and organismal performance and resilience, and suppress disease processes. Over periods of weeks and months the CACH of exercise and fasting promote optimal health. The hormesis concept is integral to the CACH model and predicts an upper limit to the beneficial effects of catabolic – anabolic cycling that reflects a limit of biological plasticity. This paper extends the hormesis model of health by proposing that 1) it is comprised of two complementary phases: catabolic (adaptive stress responses and conservation of resources) and anabolic (growth and plasticity) and, 2) that CACH is metabolically integrated, quantitatively flexible and dynamically regulated. This model has important implications for future basic and translational research in the fields of aging and related disease processes.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"102 ","pages":"Article 102588"},"PeriodicalIF":12.5,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142650026","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":"Semaglutide as a possible therapy for healthy aging: Targeting the hallmarks of aging","authors":"Gabriela Ueta Ortiz ,&nbsp;Ellen Cristini de Freitas","doi":"10.1016/j.arr.2024.102582","DOIUrl":"10.1016/j.arr.2024.102582","url":null,"abstract":"<div><div>With an aging population, the investigation of therapies that promote healthy aging becomes increasingly urgent. Here we discuss how Semaglutide can be a potential therapy to contribute to this goal by targeting key hallmarks of aging, such as inflammation, oxidative stress and stem cell exhaustion.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"102 ","pages":"Article 102582"},"PeriodicalIF":12.5,"publicationDate":"2024-11-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142640279","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":"Progress in the mechanisms of pain associated with neurodegenerative diseases","authors":"Zhicheng Tian ,&nbsp;Qi Zhang ,&nbsp;Ling Wang ,&nbsp;Mengxiang Li ,&nbsp;Tianjing Li ,&nbsp;Yujie Wang ,&nbsp;Zixuan Cao ,&nbsp;Xiaofan Jiang ,&nbsp;Peng Luo","doi":"10.1016/j.arr.2024.102579","DOIUrl":"10.1016/j.arr.2024.102579","url":null,"abstract":"<div><div>Neurodegenerative diseases (NDDs) represent a class of neurological disorders characterized by the progressive degeneration or loss of neurons, impacting millions of individuals globally. In addition to the typical manifestations, pain is a prevalent symptom associated with NDDs, seriously impacting the quality of life for patients. The pathogenesis of pain associated with NDDs is intricate and multifaceted. Currently, the clinical management of NDDs-related pain symptoms predominantly relies on conventional pharmacological agents or physical therapy. However, these approaches often fail to produce satisfactory outcomes. This article summarizes the underlying mechanisms of major NDDs-associated pain: Neuroinflammation, Brain and spinal cord dysfunctions, Mitochondrial dysfunction, Risk gene and pathological protein, as well as Receptor, channel, and neurotransmitter. While numerous studies have investigated the downstream pathological processes associated with these mechanisms, there remains a significant gap in identifying the key initiating factors. Specifically, there is insufficient evidence for the upstream elements that activate microglia and astrocytes in neuroinflammation leading to pain in NDDs. Likewise, there is an absence of upstream factors elucidating how dysfunctions in the brain and spinal cord, as well as mitochondrial impairments, contribute to the development of pain. Furthermore, the specific mechanisms through which hallmark pathological proteins related to NDDs contribute to these pathological processes remain inadequately understood. The objective of this article is to synthesize the existing mechanisms underlying pain associated with NDDs, including Alzheimer's disease, Parkinson's disease, Huntington's disease, Schizophrenia, Amyotrophic lateral sclerosis, and Multiple sclerosis, while also identifying gaps and deficiencies in these mechanisms. This paper offers insights for future research trajectories. Given the intricate pathogenesis of NDDs-related pain, it emphasizes that a promising short-term strategy is combination therapy—intervening concurrently in multiple pathological processes—akin to the cocktail approach utilized in treating acquired immunodeficiency syndrome (AIDS). For long-term advancements, achieving breakthroughs in the treatment of the NDDs themselves will remain essential for alleviating accompanying pain symptoms.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"102 ","pages":"Article 102579"},"PeriodicalIF":12.5,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142634249","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":"Non-canonical pathways associated to Amyloid beta and tau protein dyshomeostasis in Alzheimer’s disease: A narrative review","authors":"Anna Maggiore ,&nbsp;Valentina Latina ,&nbsp;Maria D’Erme ,&nbsp;Giuseppina Amadoro ,&nbsp;Roberto Coccurello","doi":"10.1016/j.arr.2024.102578","DOIUrl":"10.1016/j.arr.2024.102578","url":null,"abstract":"<div><div>Alzheimer’s Disease (AD) is the most common form of dementia among elderly people. This disease imposes a significant burden on the healthcare system, society, and economy due to the increasing global aging population. Current trials with drugs or bioactive compounds aimed at reducing cerebral Amyloid beta (Aβ) plaques and tau protein neurofibrillary tangles, which are the two main hallmarks of this devastating neurodegenerative disease, have not provided significant results in terms of their neuropathological outcomes nor met the expected clinical end-points. Ageing, genetic and environmental risk factors, along with different clinical symptoms suggest that AD is a complex and heterogeneous disorder with multiple interconnected pathological pathways rather than a single disease entity. In the present review, we highlight and discuss various non-canonical, Aβ-independent mechanisms, like gliosis, unhealthy dietary intake, lipid and sugar signaling, and cerebrovascular damage that contribute to the onset and development of AD. We emphasize that challenging the traditional “amyloid cascade hypothesis” may improve our understanding of this age-related complex syndrome and help fight the progressive cognitive decline in AD.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"102 ","pages":"Article 102578"},"PeriodicalIF":12.5,"publicationDate":"2024-11-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142634231","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}