Ageing Research Reviews最新文献

{"title":"Regulated cell death in acute myocardial infarction: Molecular mechanisms and therapeutic implications","authors":"Lili Zhu ,&nbsp;Yiyang Liu ,&nbsp;Kangkai Wang ,&nbsp;Nian Wang","doi":"10.1016/j.arr.2024.102629","DOIUrl":"10.1016/j.arr.2024.102629","url":null,"abstract":"<div><div>Acute myocardial infarction (AMI), primarily caused by coronary atherosclerosis, initiates a series of events that culminate in the obstruction of coronary arteries, resulting in severe myocardial ischemia and hypoxia. The subsequent myocardial ischemia/reperfusion (I/R) injury further aggravates cardiac damage, leading to a decline in heart function and the risk of life-threatening complications. The complex interplay of multiple regulated cell death (RCD) pathways plays a pivotal role in the pathogenesis of AMI. Each RCD pathway is orchestrated by a symphony of molecular regulatory mechanisms, highlighting the dynamic changes and critical roles of key effector molecules. Strategic disruption or inhibition of these molecular targets offers a tantalizing prospect for mitigating or even averting the onset of RCD, thereby limiting the extensive loss of cardiomyocytes and the progression of detrimental myocardial fibrosis. This review systematically summarizes the mechanisms underlying various forms of RCD, provides an in-depth exploration of the pathogenesis of AMI through the lens of RCD, and highlights a range of promising therapeutic targets that hold the potential to revolutionize the management of AMI.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"104 ","pages":"Article 102629"},"PeriodicalIF":12.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142792552","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 activation of microglia by the complement system in neurodegenerative diseases","authors":"He Zhao ,&nbsp;Yayun Lv ,&nbsp;Jiasen Xu ,&nbsp;Xiaoyu Song ,&nbsp;Qi Wang ,&nbsp;Xiaoyu Zhai ,&nbsp;Xiaohui Ma ,&nbsp;Jingjing Qiu ,&nbsp;Limei Cui ,&nbsp;Yan Sun","doi":"10.1016/j.arr.2024.102636","DOIUrl":"10.1016/j.arr.2024.102636","url":null,"abstract":"<div><div>Neurodegenerative diseases (NDDs) are a group of neurological disorders characterized by the progressive loss of neuronal structure and function, leading to cognitive and behavioral impairments. Despite significant research advancements, there is currently no definitive cure for NDDs. With global aging on the rise, the burden of these diseases is becoming increasingly severe, highlighting the urgency of understanding their pathogenesis and developing effective therapeutic strategies. Microglia, specialized macrophages in the central nervous system, play a dual role in maintaining neural homeostasis. They are involved in clearing cellular debris and apoptotic cells, but in their activated state, they release inflammatory factors that contribute significantly to neuroinflammation. The complement system (CS), a critical component of the innate immune system, assists in clearing damaged cells and proteins. However, excessive or uncontrolled activation of the CS can lead to chronic neuroinflammation, exacerbating neuronal damage. This review aims to explore the roles of microglia and the CS in the progression of NDDs, with a specific focus on the mechanisms through which the CS activates microglia by modulating mitochondrial function. Understanding these interactions may provide insights into potential therapeutic targets for mitigating neuroinflammation and slowing neurodegeneration.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"104 ","pages":"Article 102636"},"PeriodicalIF":12.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142796709","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":"Targeting tau in Alzheimer’s and beyond: Insights into pathology and therapeutic strategies","authors":"Sunidhi Singh ,&nbsp;Sumaiya Khan ,&nbsp;Mohammad Shahid ,&nbsp;Meryam Sardar ,&nbsp;Md.Imtaiyaz Hassan ,&nbsp;Asimul Islam","doi":"10.1016/j.arr.2024.102639","DOIUrl":"10.1016/j.arr.2024.102639","url":null,"abstract":"<div><div>Tauopathies encompass a group of approximately 20 neurodegenerative diseases characterized by the accumulation of the microtubule-associated protein tau in brain neurons. The pathogenesis of intracellular neurofibrillary tangles, a hallmark of tauopathies, is initiated by hyperphosphorylated tau protein isoforms that cause neuronal death and lead to diseases like Alzheimer’s, Parkinson’s disease, frontotemporal dementia, and other complex neurodegenerative diseases. Current applications of tau biomarkers, including imaging, cerebrospinal fluid, and blood-based assays, assist in the evaluation and diagnosis of tauopathies. Emerging research is providing various potential strategies to prevent cellular toxicity caused by tau aggregation such as: 1) suppressing toxic tau aggregation, 2) preventing post-translational modifications of tau, 3) stabilizing microtubules and 4) designing tau-directed immunogens. This review aims to discuss the role of tau in tauopathies along with neuropathological features of the different tauopathies and the new developments in treating tau aggregation with the therapeutics for treating and possibly preventing tauopathies.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"104 ","pages":"Article 102639"},"PeriodicalIF":12.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142824817","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":"Metabolic dysfunction contributes to mood disorders after traumatic brain injury","authors":"Lang Liu ,&nbsp;Peijun Jia ,&nbsp;Tongzhou Liu ,&nbsp;Jiaxin Liang ,&nbsp;Yijia Dang ,&nbsp;Yousef Rastegar-Kashkooli ,&nbsp;Qiang Li ,&nbsp;Jingqi Liu ,&nbsp;Jiang Man ,&nbsp;Ting Zhao ,&nbsp;Na Xing ,&nbsp;Fushun Wang ,&nbsp;Xuemei Chen ,&nbsp;Jiewen Zhang ,&nbsp;Chao Jiang ,&nbsp;Marietta Zille ,&nbsp;Zhenhua Zhang ,&nbsp;Xiaochong Fan ,&nbsp;Junmin Wang ,&nbsp;Jian Wang","doi":"10.1016/j.arr.2024.102652","DOIUrl":"10.1016/j.arr.2024.102652","url":null,"abstract":"<div><div>Traumatic brain injury (TBI) presents significant risks concerning mortality and morbidity. Individuals who suffer from TBI may exhibit mood disorders, including anxiety and depression. Both preclinical and clinical research have established correlations between TBI and disturbances in the metabolism of amino acids, lipids, iron, zinc, and copper, which are implicated in the emergence of mood disorders post-TBI. The purpose of this review is to elucidate the impact of metabolic dysfunction on mood disorders following TBI and to explore potential strategies for mitigating anxiety and depression symptoms. We researched the PubMed and Web of Science databases to delineate the mechanisms by which metabolic dysfunction contributes to mood disorders in the context of TBI. Particular emphasis was placed on the roles of glutamate, kynurenine, lipids, iron, zinc, and copper metabolism. Metabolic dysfunction is linked to mood disorders post-TBI through multiple pathways, encompassing the glutamatergic system, the kynurenine pathway, endocannabinoids, iron deposition, iron-related ferroptosis, zinc deficiency, and copper dysregulation. Furthermore, this review addresses the influence of metabolic dysfunction on mood disorders in the elderly demographic following TBI. Targeting metabolic dysfunction for therapeutic intervention appears promising in alleviating symptoms of anxiety and depression that arise after TBI. While further investigation is warranted to delineate the underlying pathophysiologic mechanisms of mood disorders post-TBI, current evidence underscores the potential contribution of metabolic dysfunction to these conditions. Therefore, rectifying metabolic dysfunction represents a viable and strategic approach to addressing mood disorders following TBI.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"104 ","pages":"Article 102652"},"PeriodicalIF":12.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142923684","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":"Association between adult-onset hearing loss and dementia biomarkers: A systematic review","authors":"Aleksandra B. Lasica ,&nbsp;Jack Sheppard ,&nbsp;Ruan-Ching Yu ,&nbsp;Gill Livingston ,&nbsp;Nicola Ridgway ,&nbsp;Rohani Omar ,&nbsp;Anne G.M. Schilder ,&nbsp;Sergi G. Costafreda","doi":"10.1016/j.arr.2024.102647","DOIUrl":"10.1016/j.arr.2024.102647","url":null,"abstract":"<div><h3>Background and objective</h3><div>People with adult-onset hearing loss (AoHL) are at increased dementia risk. In this study, we explore potential aetiological mechanisms by synthesising the evidence on the association between AoHL and neuropathological, cerebrospinal fluid (CSF), blood and imaging biomarkers of dementia.</div></div><div><h3>Methods</h3><div>We systematically searched electronic databases from inception to 30 April 2024 for cross-sectional and longitudinal studies, including quantitative data on the association between AoHL and dementia biomarkers. Study quality was assessed with the Mixed Methods Appraisal Tool (MMAT).</div></div><div><h3>Results</h3><div>Sixty-six studies reporting 63 cross-sectional and 10 longitudinal analyses were included. Twenty-one studies met all MMAT quality criteria. We report a narrative synthesis due to the heterogeneity of the included studies. In CSF-based or blood-based assays or imaging, five out of six cross-sectional analyses found that AoHL was associated with elevated <em>in vivo</em> tau levels, whilst four out of 17 reported a link with elevated <em>in vivo</em> β-amyloid measures. One longitudinal analysis identified an association between AoHL and a steeper increase of CSF tau, but not Aβ₄₂, levels over time. Twenty-five out of 44 cross-sectional and six out of nine longitudinal analyses identified associations between AoHL and grey matter atrophy of the temporal regions, particularly the medial temporal lobe. Studies using other biomarkers had inconsistent findings.</div></div><div><h3>Conclusions</h3><div>AoHL was usually associated with more temporal regions grey matter atrophy both cross-sectionally and longitudinally, and elevated <em>in vivo</em> tau but not β-amyloid. Increasing atrophy and higher tau, leading to decreased cognitive reserve may be how hearing loss increases dementia risk.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"104 ","pages":"Article 102647"},"PeriodicalIF":12.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142923685","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":"Drug repositioning for Parkinson’s disease: An emphasis on artificial intelligence approaches","authors":"Iman Karimi-Sani ,&nbsp;Mehrdad Sharifi ,&nbsp;Nahid Abolpour ,&nbsp;Mehrzad Lotfi ,&nbsp;Amir Atapour ,&nbsp;Mohammad-Ali Takhshid ,&nbsp;Amirhossein Sahebkar","doi":"10.1016/j.arr.2024.102651","DOIUrl":"10.1016/j.arr.2024.102651","url":null,"abstract":"<div><div>Parkinson’s disease (PD) is one of the most incapacitating neurodegenerative diseases (NDDs). PD is the second most common NDD worldwide which affects approximately 1–2 percent of people over 65 years. It is an attractive pursuit for artificial intelligence (AI) to contribute to and evolve PD treatments through drug repositioning by repurposing existing drugs, shelved drugs, or even candidates that do not meet the criteria for clinical trials. A search was conducted in three databases Web of Science, Scopus, and PubMed. We reviewed the data related to the last years (1975-present) to identify those drugs currently being proposed for repositioning in PD. Moreover, we reviewed the present status of the computational approach, including AI/Machine Learning (AI/ML)-powered pharmaceutical discovery efforts and their implementation in PD treatment. It was found that the number of drug repositioning studies for PD has increased recently. Repositioning of drugs in PD is taking off, and scientific communities are increasingly interested in communicating its results and finding effective treatment alternatives for PD. A better chance of success in PD drug discovery has been made possible due to AI/ML algorithm advancements. In addition to the experimentation stage of drug discovery, it is also important to leverage AI in the planning stage of clinical trials to make them more effective. New AI-based models or solutions that increase the success rate of drug development are greatly needed.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"104 ","pages":"Article 102651"},"PeriodicalIF":12.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142928251","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":"Age differences in pedestrian navigational skills and performance: A systemic review and meta-analysis","authors":"Tong Bill Xu ,&nbsp;Viraj Nitin Govani ,&nbsp;Saleh Kalantari","doi":"10.1016/j.arr.2024.102591","DOIUrl":"10.1016/j.arr.2024.102591","url":null,"abstract":"<div><h3>Objectives</h3><div>This study summarized current findings on age differences (young vs. older adults) in pedestrian navigational performance, spatial learning, and examined moderating effects of experimental environment (e.g., real-world vs. virtual environments).</div></div><div><h3>Methods</h3><div>Two reviewers independently screened studies from PubMed, Web of Science, PsychInfo, and AgeLine until December 2022. Inclusion criteria: (1) empirical navigational study; (2) healthy older adults (mean age above 60); (3) age as a categorical variable; (4) peer-reviewed paper in English. Exclusion criteria: (1) overly simplified environments; (2) tasks performed with transportation; (3) small sample size (n &lt; 10).</div></div><div><h3>Results</h3><div>5981 studies were screened, 18 were eligible with 406 total participants. Three-level meta-analysis estimated standardized mean age difference of 1.15 (95 % CI: [0.64, 1.65]) in navigational performance, and 0.97 (95 % CI: [0.81, 1.13]) in spatial learning. Study environments were found to marginally moderate age differences in navigational performance, but not in spatial learning.</div></div><div><h3>Discussion</h3><div>Older adults have poorer navigational performance and spatial learning outcomes compared to their younger counterparts, with marginally greater performance differences in virtual environments than in the real world. Findings were limited by low number eligible studies, especially real-world experiments. Future studies should continue to test generalizability of high-fidelity VR and identify spatial design elements that can mitigate age differences.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"104 ","pages":"Article 102591"},"PeriodicalIF":12.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142878955","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":"Precision neurology","authors":"Steven L. Small","doi":"10.1016/j.arr.2024.102632","DOIUrl":"10.1016/j.arr.2024.102632","url":null,"abstract":"<div><div>Over the past several decades, high-resolution brain imaging, blood and cerebrospinal fluid analyses, and other advanced technologies have changed diagnosis from an exercise depending primarily on the history and physical examination to a computer- and online resource-aided process that relies on larger and larger quantities of data. In addition, randomized controlled trials (RCT) at a population level have led to many new drugs and devices to treat neurological disease, including disease-modifying therapies. We are now at a crossroads. Combinatorially profound increases in data about individuals has led to an alternative to population-based RCTs. Genotyping and comprehensive “deep” phenotyping can sort individuals into smaller groups, enabling precise medical decisions at a personal level. In neurology, precision medicine that includes prediction, prevention and personalization requires that genomic and phenomic information further incorporate imaging and behavioral data. In this article, we review the genomic, phenomic, and computational aspects of precision medicine for neurology. After defining biological markers, we discuss some applications of these “-omic” and neuroimaging measures, and then outline the role of computation and ultimately brain simulation. We conclude the article with a discussion of the relation between precision medicine and value-based care.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"104 ","pages":"Article 102632"},"PeriodicalIF":12.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142808810","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":"Biomarkers of synaptic degeneration in Alzheimer’s disease","authors":"Qian Cheng ,&nbsp;Yiou Fan ,&nbsp;Pengfei Zhang ,&nbsp;Huan Liu ,&nbsp;Jialin Han ,&nbsp;Qian Yu ,&nbsp;Xueying Wang ,&nbsp;Shuang Wu ,&nbsp;Zhiming Lu","doi":"10.1016/j.arr.2024.102642","DOIUrl":"10.1016/j.arr.2024.102642","url":null,"abstract":"<div><div>Synapse has been considered a critical neuronal structure in the procession of Alzheimer’s disease (AD), attacked by two pathological molecule aggregates (amyloid-β and phosphorylated tau) in the brain, disturbing synaptic homeostasis before disease manifestation and subsequently causing synaptic degeneration. Recently, evidence has emerged indicating that soluble oligomeric amyloid-β (AβO) and tau exert direct toxicity on synapses, causing synaptic damage. Synaptic degeneration is closely linked to cognitive decline in AD, even in the asymptomatic stages of AD. Therefore, the identification of novel, specific, and sensitive biomarkers involved in synaptic degeneration holds significant promise for early diagnosis of AD, reducing synaptic degeneration and loss, and controlling the progression of AD. Currently, a range of biomarkers in cerebrospinal fluid (CSF), such as synaptosome-associated protein 25 (SNAP-25), synaptotagmin-1, growth-associated protein-43 (GAP-43), and neurogranin (Ng), along with functional brain imaging techniques, can detect variations in synaptic density, offering high sensitivity and specificity for AD diagnosis. However, these methods face challenges, including invasiveness, high cost, and limited accessibility. In contrast, biomarkers found in blood or urine provide a minimally invasive, cost-effective, and more accessible alternative to traditional diagnostic methods. Notably, neuron-derived exosomes in blood, which contain synaptic proteins, show variations in concentration that can serve as indicators of synaptic injury, providing an additional, less invasive approach to AD diagnosis and monitoring.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"104 ","pages":"Article 102642"},"PeriodicalIF":12.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142866581","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":"Global burden, risk factors, and projections of early-onset dementia: Insights from the Global Burden of Disease Study 2021","authors":"Shixing Feng ,&nbsp;Tianyi Wang ,&nbsp;Yang Su ,&nbsp;Jinlong Yan ,&nbsp;Yiheng Wang ,&nbsp;Zhenqiang Zhang ,&nbsp;Chaohui Yin ,&nbsp;Huaqiang Zhai","doi":"10.1016/j.arr.2024.102644","DOIUrl":"10.1016/j.arr.2024.102644","url":null,"abstract":"<div><h3>Background</h3><div>Despite increasing global awareness of dementia, reliable estimates of the disease burden associated with Early-Onset Dementia (EOD) remain insufficiently quantified. This study aims to estimate the disease burden of EOD, analyze the burden attributable to risk factors from 1990 to 2021, and project these trends to 2050 at global, regional, and national levels, providing essential data to inform public health policy.</div></div><div><h3>Methods</h3><div>By utilising data from the GBD 2021 database, this study analysed metrics such as age-standardized prevalence (ASPR), mortality (ASMR), and disability-adjusted life years (AS-DALYs) for EOD. Joinpoint Regression analysis was used to calculated average annual percent changes (AAPCs) of ASPR, ASMR, and AS-DALYs. Then, the disease burden attributable to high fasting plasma glucose (FPG), high body-mass index (BMI), and tobacco were also reported. Finally, the Bayesian age-period-cohort (BAPC) model was employed to project global ASPR, ASMR and AS-DALYs, as well as ASMR and AS-DALYs attributed to the three risk factors from 2022 to 2050.</div></div><div><h3>Results</h3><div>In 2021, the global case numbers of prevalence, mortality and DALYs for EOD were 7.75 (95 %UI: 5.82, 10.08) million, 73,386 (14,059, 232,169), and 3.77 (1.69, 8.88) million. Despite large increases in case numbers, AAPCs of ASR (0.08 % [0.02, 0.14], 0.07 % [0.05, 0.1], and 0.08 % [0.05, 0.1]) kept stable. Females exhibited higher case numbers and ASR across all disease burden indicators than males. Region- and country-level geographical heterogeneities were evident. Furthermore, global ASMR and AS-DALYs associated with high BMI and high FPG showed a steady increase, while the growth in ASMR and AS-DALYs attributable to tobacco has declined. To 2050, global case numbers of prevalence, mortality and DALYs for EOD will continue to rise, but ASRs won't change considerably. Females are anticipated to remain at a higher risk. The disease burden associated with high BMI and high FPG are expected to persist in their upward trends, whereas that related to tobacco are projected to decline.</div></div><div><h3>Conclusion</h3><div>The increasing burden of EOD underscores the critical need for tailored public health strategies and policies, a unique challenge underrecognized before.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"104 ","pages":"Article 102644"},"PeriodicalIF":12.5,"publicationDate":"2025-02-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142866583","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}