Ageing Research Reviews最新文献

{"title":"From pathogenesis to precision medicine: Targeting immune imbalance in multiple sclerosis","authors":"Anjana Pithakumar ,&nbsp;Shaik Basha ,&nbsp;Aparna Ramakrishna Pai ,&nbsp;Krishna Kishore Mahato","doi":"10.1016/j.arr.2025.102921","DOIUrl":"10.1016/j.arr.2025.102921","url":null,"abstract":"<div><div>Multiple sclerosis (MS) is a chronic neuroinflammatory and neurodegenerative disease that remains a leading cause of non-traumatic disability in young adults. The urgency to advance MS research has never been greater, as global incidence and prevalence are rising, and patients continue to face delays in diagnosis, incomplete response to therapies, and limited options for progressive disease. Recent progress in defining disease stages, understanding sex- and gender-related influences, and identifying modifiable risk factors emphasizes the critical need for timely translation of scientific insights into precision medicine approaches. While FDA-approved therapies have substantially altered the course of relapsing forms of MS, therapeutic gaps in progressive disease highlight a pressing unmet clinical challenge. Advances in neuroimaging, digital biomarkers, and patient-centered monitoring now converge with the rapid growth of artificial intelligence (AI)–based tools, creating an unprecedented opportunity to refine diagnostic precision, predict progression, and personalize interventions. The integration of these technologies offers transformative potential to move beyond conventional monitoring toward predictive and adaptive care. This review synthesizes current knowledge of MS pathophysiology, immunity, and therapy, while underscoring the immediate relevance of harnessing AI and digital innovations to address current challenges and shape the future of precision medicine.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"113 ","pages":"Article 102921"},"PeriodicalIF":12.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145318939","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 muscle-brain axis in type 2 diabetes: Molecular pathways linking sarcopenia and cognitive decline","authors":"Dionysios Xenos ,&nbsp;Francesca Mancinetti ,&nbsp;Patrizia Mecocci ,&nbsp;Virginia Boccardi","doi":"10.1016/j.arr.2025.102955","DOIUrl":"10.1016/j.arr.2025.102955","url":null,"abstract":"<div><div>Type 2 diabetes mellitus (T2DM) is increasingly recognized as a shared pathological substrate for both sarcopenia and cognitive decline, particularly Alzheimer’s disease (AD). This review synthesizes current evidence on the converging molecular pathways linking insulin resistance, hyperglycaemia, mitochondrial dysfunction, oxidative stress, and chronic inflammation to muscle wasting and neurodegeneration. Central to this interplay is the muscle–brain axis, a bidirectional communication network mediated by myokines, exercise-induced cytokines that influence metabolic and neural homeostasis. Key myokines such as IGF-1, irisin, BDNF, FGF21, and SPARC promote myogenesis, synaptic plasticity, and neuroprotection, while others including myostatin, IL-8, and GDF-15 exert detrimental effects. Context-dependent molecules such as IL-6, IL-15, lactate, and cathepsin-B show dual roles modulated by aging, inflammation, and metabolic state. Emerging data support that improved glycaemic control, enhanced insulin sensitivity, and sustained physical activity can attenuate both sarcopenia and cognitive decline. This review aims to summarize current evidence describing how insulin resistance, chronic hyperglycaemia, mitochondrial dysfunction, oxidative stress, and inflammation interact to promote both muscle wasting and neurodegeneration.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"113 ","pages":"Article 102955"},"PeriodicalIF":12.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145579113","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":"Utilizing accelerated and delayed murine models of aging to address the “healthspan issue” – A review of skeletal muscle health","authors":"Matthew J. Johnston ,&nbsp;Holly M. Brown-Borg","doi":"10.1016/j.arr.2025.102946","DOIUrl":"10.1016/j.arr.2025.102946","url":null,"abstract":"<div><div>The gap between lifespan and healthspan is increasing globally, resulting in millions of individuals spending additional years burdened by frailty or disease. This disparity, paired with the increasingly aged populations of Western nations, poses a palpable predicament to public health and the economy. Deterioration of the skeletal muscle system is a key contributor to illness, loss of independence, and diminishing healthspan. Muscle quality correlates to longevity due to its significant role in metabolic homeostasis and autonomous mobility, reducing instances of adverse events such as falls and fractures. The age-related loss of muscle mass and function is termed sarcopenia, affecting older adults ubiquitously without intervention through regular resistance training. Although clinical manifestations of sarcopenia are well characterized, the molecular mechanisms underlying its pathogenesis remain incompletely understood, limiting the development of targeted, mechanism-based interventions. To identify interventions beyond exercise that delay sarcopenia, it is necessary to identify early onset physiological alterations defining this process. Genetically modified mouse models of accelerated or delayed aging offer valuable insight into the cellular mechanisms that drive or mitigate sarcopenia. The latter is often achieved by disrupting the somatotropic axis, as multiple models exist that either lack growth hormone (GH) production or a functional GH receptor (GHR) paired with a secondary deficiency in insulin like growth factor-1 (IGF-1), which reliably extends lifespan across various species. This review evaluates GH’s paradoxical role in muscular maintenance and contrasts the skeletal muscle health of various murine models of aging in effort to better outline the molecular underpinnings of sarcopenia.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"113 ","pages":"Article 102946"},"PeriodicalIF":12.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145558626","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":"Irisin-mediated hepatic autophagy remodels nutritional metabolism to prevent cognitive dysfunction","authors":"Xinjie Zhang,&nbsp;Yizhuo Yang,&nbsp;Hanan Song,&nbsp;Xuan Hu,&nbsp;Xiaobing Wang,&nbsp;Yanli Yu","doi":"10.1016/j.arr.2025.102936","DOIUrl":"10.1016/j.arr.2025.102936","url":null,"abstract":"<div><div>Cognitive impairment has emerged as a serious global health challenge and is closely associated with metabolic disorders. Autophagy dysfunction leading to metabolic disorders has become a key factor in neurodegenerative diseases. The liver, as the central organ of systemic metabolism, regulates metabolic homeostasis through hepatic autophagy, thereby affecting the clearance of toxic proteins in the brain and energy supply. Hepatic autophagy dysfunction can increase free fatty acids, which attack the blood-brain barrier and lead to neurodegenerative diseases. Irisin enters the liver via the bloodstream, activates AMPK to promote hepatic autophagy, reduces the production of lipotoxic substances, alleviates neuroinflammation, and ensures effective synaptic signaling. Previous studies have demonstrated that irisin can improve neurodegenerative diseases, but no connection has yet been established between irisin, hepatic autophagy, and cognition. Therefore, this review discusses the positive role of irisin in preventing cognitive impairment through hepatic autophagy. Future studies should employ multi-omics approaches to deeply analyze the metabolic network regulated by irisin and explore its potential in the treatment of neurological diseases. Irisin is expected to serve as a key bridge connecting exercise, metabolic health, and neuroprotection, thus paving the way for the prevention and treatment of cognitive decline and neurodegenerative diseases.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"113 ","pages":"Article 102936"},"PeriodicalIF":12.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145477381","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 senescent drivers in Alzheimer's disease: From bench to bedside","authors":"Runjin Zhou ,&nbsp;Xiaoling Lin ,&nbsp;Zhenge Liao ,&nbsp;Jian Lin ,&nbsp;Ruixue Zheng ,&nbsp;Haojie Ni ,&nbsp;Wei Liu ,&nbsp;Zhanpeng Feng ,&nbsp;Qiuxing He ,&nbsp;Xingdong Lin ,&nbsp;Chunzhi Tang ,&nbsp;Juxian Song ,&nbsp;Weimin Ning","doi":"10.1016/j.arr.2025.102978","DOIUrl":"10.1016/j.arr.2025.102978","url":null,"abstract":"<div><div>Alzheimer's disease (AD) is the most common neurodegenerative disorder associated with dementia. Cellular senescence, widely acknowledged as a key hallmark of aging, has increasingly been recognized as a significant factor in the pathogenesis of AD, although the precise mechanisms underlying this relationship have yet to be fully understood. In the brains of individuals with AD, neurons, glial cells, and cerebrovascular endothelial cells exhibit premature senescence, characterized by irreversible cell cycle arrest, resistance to apoptosis, and the secretion of a diverse range of bioactive molecules collectively referred to as the senescence-associated secretory phenotype (SASP). These senescent cells profoundly influence the neural microenvironment through the release of SASP factors, thus exacerbating Aβ- and tau-induced neurotoxicity, promoting neuroinflammatory responses, and impairing the integrity of the blood-brain barrier (BBB), ultimately giving rise to a self-sustaining \"senescence-neurodegeneration\" cycle. Despite progress in therapies targeting Aβ and tau pathology, their clinical effectiveness remains limited, highlighting the urgent need for alternative therapeutic strategies. This review presents a comprehensive analysis of the molecular mechanisms connecting AD with cellular senescence, examines how the senescent microenvironment contributes to neurodegeneration, and evaluates the therapeutic potential of senotherapeutic interventions—including senolytics and senomorphics—as novel approaches for the clinical management of AD.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"114 ","pages":"Article 102978"},"PeriodicalIF":12.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145679579","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":"Serotonin-mediated regulation of mitophagy in Alzheimer's disease: Mechanistic insights and therapeutic potential","authors":"Omme Fatema Sultana ,&nbsp;Madhuri Bandaru ,&nbsp;MST Anika Bushra ,&nbsp;P. Hemachandra Reddy ,&nbsp;Arubala P. Reddy","doi":"10.1016/j.arr.2025.102957","DOIUrl":"10.1016/j.arr.2025.102957","url":null,"abstract":"<div><div>This review delves into the intricate relationship between serotonin signaling, mitophagy and mitochondrial dysfunction in Alzheimer's disease (AD), with a focus on the mechanistic pathways that link these processes and their potential therapeutic implications. A neurodegenerative condition called Alzheimer's disease is marked by cognitive deterioration. It is increasingly recognized as being influenced by impaired mitochondrial function and mitophagy, the selective degradation of damaged mitochondria. Serotonin, a neurotransmitter traditionally known for its role in mood regulation, has emerged as a critical modulator of mitochondrial dynamics and quality control through its interaction with key pathways such as the PINK1-Parkin and cAMP/PKA signaling pathways. In AD, alterations in serotonin levels and receptor function are associated with disruptions in mitophagy, leading to the accumulation of dysfunctional mitochondria, increased oxidative stress, and subsequent neuronal damage. This review synthesizes current evidence that links serotonin dysregulation to mitochondrial pathology in AD, exploring how impaired serotonin signaling exacerbates mitochondrial dysfunction and contributes to amyloid-beta (Aβ), phosphorylation of Tau (p-Tau) accumulations, and increased neuroinflammation. Additionally, we assessed the therapeutic potential of serotonin-targeting agents, particularly selective serotonin reuptake inhibitors (SSRIs), in restoring mitophagy, enhancing mitochondrial integrity, and attenuating neurodegeneration. By highlighting existing knowledge gaps and key controversies, this review underscores the promise of serotonin-mitochondria pathways as novel therapeutic targets and advocates for focused investigation into receptor-specific, mitophagy-centered interventions for AD.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"114 ","pages":"Article 102957"},"PeriodicalIF":12.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145643601","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":"Aging in women – The microbiome perspective","authors":"Maria Laura Ferrando,&nbsp;Fabio Busonero,&nbsp;Francesca Crobu,&nbsp;Serena Sanna","doi":"10.1016/j.arr.2025.102950","DOIUrl":"10.1016/j.arr.2025.102950","url":null,"abstract":"<div><div>Menopause is a hallmark of women's aging and is frequently portrayed as a medical issue. It also encompasses social and biological aspects often neglected and not well-understood, leaving women with insufficient support and attention. With the decline in estrogen levels, starting years before menopause is fully established, women experience various physical symptoms, and the risk of many age-related diseases increases sharply soon after these hormonal changes occur. Notably, these hormonal shifts also significantly impact the vaginal and gut microbiomes, contributing to dysbiosis and influencing the onset and progression of several diseases. Here, we examined the complex and dynamic relationship among aging, menopause, and microbiome changes with a particular focus on the vaginal and gut ecosystems. Emerging research highlights diet as a potential modulator for maintaining microbiome health during menopause. A deeper understanding of microbiome changes across life stages suggests the potential for microbiome-targeted strategies to support well-aging in women.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"113 ","pages":"Article 102950"},"PeriodicalIF":12.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145575038","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":"Outcome measures for health interventions targeting multimorbid older adults: A systematic review","authors":"Massimiliano Fedecostante ,&nbsp;Paolo Balietti ,&nbsp;Alessia Beccacece ,&nbsp;Barbara Carrieri ,&nbsp;Massimiliano Orso ,&nbsp;Alessandra Coin ,&nbsp;Chiara Ceolin ,&nbsp;Giuseppe Sergi ,&nbsp;Francesca Cecchi ,&nbsp;Marco Baccini ,&nbsp;Diego Longo ,&nbsp;Licia Iacoviello ,&nbsp;Rosa Liperoti ,&nbsp;Fabrizia Lattanzio ,&nbsp;Antonio Cherubini","doi":"10.1016/j.arr.2025.102940","DOIUrl":"10.1016/j.arr.2025.102940","url":null,"abstract":"<div><h3>Background</h3><div>Older adults with multimorbidity are often excluded from clinical trials. Traditional disease-centered endpoints may be inadequate for this population, presenting unique challenges related to frailty, functional decline and disability.</div></div><div><h3>Objectives</h3><div>To systematically review the literature on outcomes considered relevant in interventions targeting older adults with multimorbidity, based on both patient and healthcare professionals’ perspectives.</div></div><div><h3>Methods</h3><div>This systematic review followed PRISMA 2020 guidelines and was registered in PROSPERO (CRD42023478249). We searched five electronic databases for primary quantitative and qualitative studies including patients aged ≥ 60 years with ≥ 2 chronic conditions. Outcomes were categorized into six domains: 1) Physical conditions/outcomes; 2) Mental conditions/outcomes; 3) Psychosocial outcomes/general health; 4) Healthcare utilization and costs; 5) Patients’ behaviors; 6) Care process outcomes. We conducted a narrative synthesis and compared outcomes across qualitative and quantitative studies.</div></div><div><h3>Results</h3><div>Seventy-one studies were included (53 quantitative, 16 qualitative, 2 mixed-methods). The most frequently reported outcomes fell under Psychosocial outcomes / General health (69.0 %), followed by Care process outcomes (52.1 %) and Healthcare utilization and costs (49.3 %). Qualitative studies more often addressed Mental health outcomes (43.8 %). Maintaining independence, physical function, and quality of life emerged as most important outcomes for older adults.</div></div><div><h3>Conclusions</h3><div>In intervention studies involving older adults with multimorbidity, outcomes should move beyond disease-specific measures to include independence, physical function and quality of life. Outcome selection should account for patient clinical heterogeneity, frailty, and life expectancy to ensure relevance and impact in this complex population.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"113 ","pages":"Article 102940"},"PeriodicalIF":12.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145534268","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":"cGAS-STING-driven inflammaging cascade in aging-related retinal diseases: From pathological mechanism to therapeutic potentials","authors":"Xiaosu Wang ,&nbsp;Zhihui Feng ,&nbsp;Sa Sun ,&nbsp;Jiehao Zhang ,&nbsp;Kexin Wang ,&nbsp;Yiwen Wang ,&nbsp;Yameng Zhao ,&nbsp;Bizhu Zhao ,&nbsp;Bo Liu ,&nbsp;Mengli Sun ,&nbsp;Zongming Song ,&nbsp;Ye Tao","doi":"10.1016/j.arr.2025.102983","DOIUrl":"10.1016/j.arr.2025.102983","url":null,"abstract":"<div><div>Aging-related retinal diseases lead to irreversible structural damages and vision loss. These conditions are characterized by cellular senescence, oxidative stress, neural degeneration, and neovascularization. Among these, chronic inflammation is a hallmark of aging, establishing a self-perpetuating vicious cycle that accelerates pathological process and physiological decline. cGAS-STING signaling pathway has been identified as a critical mediator of inflammation across multiple retinal disease contexts, functioning to regulate immune response by detecting the dsDNA resulted from tissue injury. Under pathological circumstances, it exhibits a state of persistent activation, which results in chronic inflammatory reactions in the microenvironment. The disrupted homeostasis is closely linked with the onset and progression of numerous aging-related retinal diseases. Given the strong association between cGAS-STING signaling and these conditions, this pathway may represent a promising therapeutic target for refractory retinopathies. Encouragingly, several inhibitors targeting this pathway have already been developed and yielded remarkable therapeutic outcomes. This review delineates the primary functioning factors and modulatory mechanisms of the cGAS-STING cascade. Furthermore, it discusses the specific role of cGAS-STING pathway in pathological process of age-related retinopathy and summarize the key inhibitors of the cGAS-STING pathway, highlighting their therapeutic potentials for age-related retinopathy. These findings will deepen the understanding of the crosstalk between cGAS-STING signaling and retinal aging, thus offering valuable insights for the future translation of laboratory findings into clinical interventions.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"114 ","pages":"Article 102983"},"PeriodicalIF":12.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145688929","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":"Redox-sensitive high mobility group box 1 (HMGB1) is a multifunctional regulator of cellular senescence, inflammation, and immunosuppression: Impact on the aging process","authors":"Antero Salminen","doi":"10.1016/j.arr.2025.102926","DOIUrl":"10.1016/j.arr.2025.102926","url":null,"abstract":"<div><div>Aging is a multifaceted process involving cellular senescence and a significant remodeling of the immune network driven by the senescence-associated secretory phenotype (SASP). This progressive process needs adaptable drivers to push it forward. The redox-sensitive high mobility group box 1 (HMGB1) protein is a perfect example of this kind of oxidative stress- and aging-related multifunctional protein. The HMGB1 protein is an important non-histone DNA chaperone which maintains chromatin integrity and contributes to gene expression and DNA repair. Diverse intrinsic and exogenous insults induce the translocation of the nuclear HMGB1 protein into cytoplasm and subsequently into the extracellular space. Interestingly, cellular senescence is associated with a robust release of HMGB1 from chromatin and subsequently it is secreted with other SASP factors. The extracellular HMGB1 is a pleiotropic immune regulator since it can organize both proinflammatory and immunosuppressive responses in a context-dependent manner. For instance, HMGB1 stimulates proinflammatory responses via TLR and RAGE signaling as well as by activating NLRP3 inflammasomes and cooperating with the complement system. HMGB1 can also delay the resolution of acute inflammation and thus elicit chronic inflammation. An increase in chemotaxis of myeloid cells by HMGB1 stimulates the recruitment of immunosuppressive cells, such as MDSCs and Tregs. HMGB1 also promotes the polarization of M1 macrophages toward the immunosuppressive M2 phenotype and enhances the function of inhibitory immune checkpoints. Given that the redox-sensitive HMGB1 protein is a driver of cellular senescence and a multifunctional regulator of the immune network, it seems that HMGB1 has a crucial role in the inflammaging process.</div></div>","PeriodicalId":55545,"journal":{"name":"Ageing Research Reviews","volume":"113 ","pages":"Article 102926"},"PeriodicalIF":12.4,"publicationDate":"2026-01-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145364814","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}