Aging Cell最新文献

{"title":"Age-Associated Transcriptomic and Epigenetic Alterations in Mouse Hippocampus.","authors":"Merve Bilgic, Rinka Obata, Vlada-Iuliana Panfil, Ziying Zhu, Mai Saeki, Yukiko Gotoh, Yusuke Kishi","doi":"10.1111/acel.70233","DOIUrl":"https://doi.org/10.1111/acel.70233","url":null,"abstract":"<p><p>Aging represents a major risk for human neurodegenerative disorders, such as dementia and Alzheimer's disease, and is associated with a functional decline in neurons and impaired synaptic plasticity, leading to a gradual decline in memory. Previous research has identified molecular and functional changes associated with aging through transcriptomic studies and neuronal excitability measurements, while the role of chromatin-level regulation in vulnerability to aging-related diseases is not well understood. Moreover, the causal relationship between molecular alterations and aging-associated decline in functions of different cell types remains poorly understood. Here, we systematically characterized gene regulatory networks in a cell type-specific manner in the aging mouse hippocampus, a central brain region involved in learning and memory formation, by simultaneously profiling gene expression and chromatin accessibility at a single-nucleus level. The analysis of multiome (RNA and ATAC) sequencing recapitulated the diversity of glial and neuronal cell types in the hippocampus and revealed transcriptomic and chromatin accessibility level changes in different cell types, among which oligodendrocytes and dentate gyrus (DG) neurons exhibited the most drastic changes. We found pronounced aging-dependent chromatin-level changes among neurons, especially for genes related to synaptic plasticity. Our data suggest that BACH2, a candidate transcription factor implicated in aging-mediated functional decline of DG neurons, potentially regulates genes associated with synaptic plasticity, cell death, and inflammation during aging. Taken together, our single-nucleus multiome analysis reveals potential cell type-specific regulators involved in the aging of neurons and glial cells.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":" ","pages":"e70233"},"PeriodicalIF":7.1,"publicationDate":"2025-09-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145184268","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":"Enhancing Late-Life Survival and Mobility via Mitohormesis by Reducing Mitochondrial Calcium Levels.","authors":"Doruntina Bresilla, Ines Tawfik, Martin Hirtl, Sonja Gabrijelčič, Julian Ostaku, Fabienne Mossegger, Lia Wurzer, Susanne Lederer, Katarina Kalinova, Ernst Malle, Markus Schosserer, Kim Zarse, Michael Ristow, Corina T Madreiter-Sokolowski","doi":"10.1111/acel.70247","DOIUrl":"https://doi.org/10.1111/acel.70247","url":null,"abstract":"<p><p>Mitochondrial calcium (Ca²⁺) homeostasis plays a critical role in aging and cellular fitness. In the search for novel antiaging approaches, we explored how genetic and pharmacological inhibition of mitochondrial Ca²⁺ uptake influences the lifespan and health of Caenorhabditis elegans. Using live-cell imaging, we demonstrate that RNA interference-mediated knockdown of mcu-1, the nematode ortholog of the mitochondrial Ca²⁺ uniporter (MCU), reduces mitochondrial Ca²⁺ levels, thereby extending lifespan and preserving motility during aging, while compromising early-life survival. This longevity benefit requires intervention before day 14 and coincides with a transient increase in reactive oxygen species (ROS), which activates pathways involving pmk-1, daf-16, and skn-1, orthologs of human p38 mitogen-activated protein kinase (p38 MAPK), forkhead box O (FOXO), and nuclear factor erythroid 2-related factor 2 (NRF2), respectively. This pathway promotes antioxidant defense mechanisms and preserves mitochondrial structure and function during aging, maintaining larger, more interconnected mitochondria and restoring the oxidized/reduced nicotinamide adenine dinucleotide (NAD⁺/NADH) ratio and oxygen consumption rates to youthful levels. Pharmacological inhibition of mitochondrial Ca²⁺ uptake using the MCU inhibitor mitoxantrone mirrors the effects of mcu-1 knockdown, extending lifespan and improving fitness in aged nematodes. In human foreskin fibroblasts, short-term mitoxantrone treatment also transiently elevates ROS production and induces enhanced expression and activity of antioxidant defense enzymes, underscoring the translational relevance of findings from nematodes to human cells. Our findings suggest that modulation of mitochondrial Ca²⁺ uptake induces mitohormesis through ROS-mediated signaling, promoting improved longevity and healthspan in nematodes, with possible implications for healthy aging in humans.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":" ","pages":"e70247"},"PeriodicalIF":7.1,"publicationDate":"2025-09-26","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145147142","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":"Muscle Regeneration Can Be Rescued in a Telomerase Deficient Zebrafish Model of Ageing by MMP Inhibition.","authors":"Yue Yuan, Carlene Dyer, Robert D Knight","doi":"10.1111/acel.70238","DOIUrl":"https://doi.org/10.1111/acel.70238","url":null,"abstract":"<p><p>Ageing progressively impairs skeletal muscle regeneration, contributing to reduced mobility and quality of life. While the molecular changes underlying muscle ageing have been well characterised, their impact on muscle stem cell (muSC) behaviour during regeneration remains poorly understood. Here, we leverage telomerase-deficient tert mutant zebrafish larvae as an in vivo model of accelerated ageing to perform real-time analysis of muSC dynamics following muscle injury. We demonstrate that the ageing-like inflammatory environment in tert mutant disrupts muSC migration, impairs activation and proliferation, and compromises regenerative capacity. We further show that sustained inflammation, mediated by persistent macrophage presence and elevated matrix metalloproteinase (MMP) activity, limits muSC recruitment and migration efficiency. Pharmacological inhibition of MMP9/13 activity and genetic depletion of macrophages partially restore muSC migratory behaviour and regenerative outcomes. Notably, we demonstrate that muSC migration dynamics correlate with regenerative success, providing a functional readout for therapeutic screening. Our findings reveal zebrafish tert mutants offer a tractable system for dissecting age-associated changes to cell behaviour and for identifying rejuvenation interventions.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":" ","pages":"e70238"},"PeriodicalIF":7.1,"publicationDate":"2025-09-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145135984","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":"Tau Axonal Sorting and Interaction With Synaptic Plasticity Modulators Is Domain- and Isoform-Dependent in Human iPSC-Derived Neurons.","authors":"Michael Bell-Simons, Helen Breuer, Laura Wunderlich, Hanin Chmes, Daniel Adam, Jennifer Klimek, Sarah Buchholz, Hans Zempel","doi":"10.1111/acel.70215","DOIUrl":"https://doi.org/10.1111/acel.70215","url":null,"abstract":"<p><p>Somatodendritic missorting of the axonal microtubule-associated protein Tau is an early hallmark of Alzheimer's disease (AD) and other tauopathies. Tau missorting causes synaptic loss and neuronal dysfunction, but the mechanisms underlying both normal axonal sorting and pathological missorting remain unclear. The six human brain Tau isoforms show different axodendritic distribution, but the Tau domains governing intracellular sorting and essential interactors are unknown. Here, we aimed to identify domains or motifs of human Tau and cellular binding partners required for efficient axonal Tau sorting and to unravel isoform-specific Tau interactors. Using human MAPT-KO induced pluripotent stem cell (iPSC)-derived glutamatergic neurons, we analyzed the sorting behavior of more than 20 truncation- or phosphorylation-mutant Tau constructs and used TurboID-based proximity labeling and proteomics to identify sorting- and isoform-specific Tau interactors. We found that efficient axonal Tau sorting was independent of the N-terminal tail, the C-terminal repeat domains, AD-associated phosphorylation, and the general microtubule affinity of Tau, but it requires the presence of the proline-rich region 2 (PRR2). Our interactome data revealed peroxisomal accumulation of the Tau N-terminal half, while axonal Tau interacted with the PP2A activator HSP110. Further, we found 0N4R-specific interactions of Tau with regulators of presynaptic exocytosis and postsynaptic plasticity, which are partially associated with AD pathogenesis, including members of the CDC42 pathway and the RAB11 proteins, while 0N3R-Tau bound to various cytoskeletal elements. In sum, our study i) postulates that axonal Tau sorting relies on the PRR2 domain but not on microtubule affinity and ii) unravels a potential isoform-specific role in synaptic function and AD-related dysfunction.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":" ","pages":"e70215"},"PeriodicalIF":7.1,"publicationDate":"2025-09-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145129600","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":"A Rare Hematopoietic Stem Cell-Derived Megakaryocyte Progenitor Accumulates via Enhanced Survival and Contributes to Exacerbated Thrombopoiesis Upon Aging.","authors":"Bryce A Manso, Paloma Medina, Stephanie Smith-Berdan, Alessandra Rodriguez Y Baena, Elmira Bachinsky, Lydia Mok, Angela Deguzman, Sarah Beth Avila, Connor Van Voorhis, Saran Chattopadhyaya, Marcel G E Rommel, Jenna Myers, Vanessa D Jönsson, E Camilla Forsberg","doi":"10.1111/acel.70221","DOIUrl":"10.1111/acel.70221","url":null,"abstract":"<p><p>Distinct routes of cellular production from hematopoietic stem cells (HSCs) have defined our current view of hematopoiesis. Recently, we and others have challenged classical views of platelet generation, demonstrating that megakaryocyte progenitors (MkPs) and ultimately platelets can be specified via an alternate and additive route of HSC-direct specification specifically during aging. This \"shortcut\" pathway generates hyperactive platelets likely to contribute to age-related platelet-mediated morbidities. Here, we used single-cell RNA/CITEseq to demonstrate that these age-unique, noncanonical (nc)MkPs can be prospectively defined and experimentally isolated from wild-type mice. Surprisingly, this revealed that a rare population of ncMkPs also exists in young mice. Young and aged ncMkPs are functionally distinct from each other and from their canonical (c)MkP counterparts, with aged ncMkPs paradoxically and uniquely exhibiting enhanced survival and platelet generation capacity. We further demonstrate that aged HSCs generate significantly more ncMkPs than their younger counterparts, yet this is accomplished without strict clonal restriction. Together, these findings reveal significant phenotypic, functional, and aging-dependent heterogeneity among the MkP pool and uncover unique features of megakaryopoiesis throughout life, potentially offering cellular and molecular targets for the mitigation of age-related adverse thrombotic events.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":" ","pages":"e70221"},"PeriodicalIF":7.1,"publicationDate":"2025-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145129568","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 Reduces Intestinal Stem Cell Activity in Killifish and Intermittent Fasting Reverses Intestinal Gene Expression Patterns.","authors":"Michael Kothmayer, Sylvia Laffer, Philipp Widmayer, Elmar E Ebner, Fehima Ugarak, David Martin, Stefan H Geyer, Kareem Elsayad, Wolfgang J Weninger, Sabine Lagger, Klara Weipoltshammer, Oliver Pusch, Christian Schöfer","doi":"10.1111/acel.70229","DOIUrl":"https://doi.org/10.1111/acel.70229","url":null,"abstract":"<p><p>The process of aging is associated with a decline in cell, tissue, and organ function, leading to a range of health problems. Increasing evidence indicates that dietary restriction can counteract age-dependent effects and improve health and longevity in whole organisms, but less is known about the influence of aging and the impact of nutrition on individual organs of an organism. In this study, we examined the intestine of the very short-lived aging model system, the African turquoise killifish (Nothobranchius furzeri), throughout its lifetime. We investigated the effects of age and nutrition on the preservation of gut tissue at stages corresponding to human neonatal, adolescent, adult, and old age, and integrated morphological measurements, histology, and transcriptomics. The intestinal mucosa is characterized by folds and intervening interfold regions, where intestinal stem cells localize. The stem cells occur in clusters, and the cycle time of stem cells increases with age. We also observed a reduction in intestinal length and volume with age. Age-dependent transcriptomic profiling revealed significant changes in the expression of peripheral circadian clock genes and stem cell niche markers. Notably, the majority of these genes maintained their adult gene expression levels in old age following intermittent fasting during adulthood. Therefore, our results demonstrate that the decline in structural intestinal tissue homeostasis is associated with a decline in stem cell activity that can be counteracted by intermittent fasting. Since the intestinal mucosa of killifish is similar to that of mammals, the results of this study can be translated to general gut biology.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":" ","pages":"e70229"},"PeriodicalIF":7.1,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145123934","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":"Dual-Lineage Chondrocyte-Like Cells in the Nucleus Pulposus of Aging Intervertebral Discs Are Accelerated by Hedgehog Signaling Inactivation.","authors":"Lei Zhang, Chunmei Xiu, Hongji You, Jianquan Chen","doi":"10.1111/acel.70248","DOIUrl":"https://doi.org/10.1111/acel.70248","url":null,"abstract":"<p><p>Intervertebral disc (IVD) degeneration, a major contributor to chronic low back pain, is characterized by the age-related replacement of notochord-derived nucleus pulposus cells (NPCs) with chondrocyte-like or fibrotic cells (CLCs). However, the cellular origins of CLCs and mechanisms driving their emergence remain contentious. Using genetic lineage tracing with Shh-Cre and Gli1-CreER^T2 to track notochordal and non-notochordal cells, respectively, we demonstrate that CLCs arise from dual lineages: notochordal NPCs and non-notochordal Gli1⁺ progenitors. We identified three CLC subtypes, including nested (N-CLCs), clustered (C-CLCs), and disordered (D-CLCs), with distinct morphological and/or molecular profiles. N-CLCs and C-CLCs originate from NPCs, whereas D-CLCs derive from Gli1⁺ cells infiltrating the NP. Furthermore, conditional ablation of Smo, an essential transducer of Hh signaling, in adult discs accelerated degeneration and promoted both NP-derived (Krt19⁺ N-CLCs) and non-NPC-derived (Krt19^- D-CLCs) populations. These results establish that Hh signaling suppresses dual-lineage CLC expansion during aging. Our findings resolve controversies surrounding CLC origins, delineate their dynamic progression during degeneration, and highlight Hh signaling as a promising therapeutic target to counteract pathological cell fate shifts in aging discs.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":" ","pages":"e70248"},"PeriodicalIF":7.1,"publicationDate":"2025-09-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145111630","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":"Telomerase modRNA Offers a Novel RNA-Based Approach to Treat Human Pulmonary Fibrosis.","authors":"Jia Li Ye, Klaudia Grieger, Dongchao Lu, Christina Brandenberger, Malte Juchem, Maria Jordan, Lea Oehlsen, Patrick Zardo, Christopher Werlein, Christina Hesse, Katherina Sewald, Sandy Tretbar, Thomas Thum, Shambhabi Chatterjee, Christian Bär","doi":"10.1111/acel.70240","DOIUrl":"https://doi.org/10.1111/acel.70240","url":null,"abstract":"<p><p>Pulmonary Fibrosis (PF) is a life-threatening illness that is characterized by progressive scarring in the lung interstitium. There is an urgent need for new PF therapies because current treatments only slow down the progression of fibrosis, and the median life expectancy post-diagnosis is only 4-6 years. Since PF patients frequently exhibit telomere attrition, overexpressing telomerase, the enzyme responsible for synthesizing telomeres, represents a compelling therapeutic option. In this study, we in vitro transcribed human telomerase reverse transcriptase (hTERT) mRNA using modified nucleosides (modRNA). ModRNA hTERT treatment led to transient activation of telomerase activity in a dose-dependent manner in MRC-5 cells and, importantly, in primary human alveolar type II pneumocytes. Consequently, the proliferative capacity was increased, concomitant with reduced DNA damage and elongated telomere length. Notably, the induction of cellular immune response was only detectable at the highest modRNA concentration and returned to normal levels within 48 h. Next, we demonstrated that circularized, exonuclease-resistant modRNA hTERT extended the transient expression profile, which may be clinically advantageous. Finally, we provided therapeutic proof of concept in organotypic 3D ex vivo human precision-cut lung slices derived from end-stage PF patients. Intriguingly, a single modRNA hTERT treatment inhibited senescence, as indicated by significantly lower levels of senescence-associated β-galactosidase. Pro-inflammatory markers (IL6 and IL8) and, concurrently, the key fibrosis mediators TGFβ and COL1A1 were markedly reduced after modRNA and circular RNA hTERT treatment. In conclusion, the data presented herein provide initial evidence for the potential of RNA-based hTERT therapy for treating human lung fibrosis.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":" ","pages":"e70240"},"PeriodicalIF":7.1,"publicationDate":"2025-09-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145090736","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":"An Unbiased Cell-Culture Selection Yields DNA Aptamers as Novel Senescent Cell-Specific Reagents.","authors":"Keenan S Pearson, Sarah K Jachim, Caroline D Doherty, Brandon A Wilbanks, Luis I Prieto, Maria Dugan, Darren J Baker, Nathan K LeBrasseur, L James Maher","doi":"10.1111/acel.70245","DOIUrl":"10.1111/acel.70245","url":null,"abstract":"<p><p>Cellular senescence is an irreversible form of cell-cycle arrest caused by excessive stress or damage. While various biomarkers of cellular senescence have been proposed, there are currently no universal, stand-alone indicators of this condition. The field largely relies on the combined detection of multiple biomarkers to differentiate senescent cells from non-senescent cells. Here we introduce a new approach: unbiased cell culture selections to identify senescent cell-specific folded DNA aptamers from vast libraries of trillions of random 80-mer DNAs. Senescent mouse adult fibroblasts and their non-senescent counterparts were employed for selection. We demonstrate aptamer specificity for senescent mouse cells in culture, identify a form of fibronectin as the molecular target of two selected aptamers, show increased aptamer staining in naturally aged mouse tissues, and demonstrate decreased aptamer staining when p16 expressing cells are removed in a transgenic INK-ATTAC mouse model. This work demonstrates the value of unbiased cell-based selections to identify new senescence-specific DNA reagents.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":" ","pages":"e70245"},"PeriodicalIF":7.1,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145084794","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":"Prematurely Aged Human Microglia Exhibit Impaired Stress Response and Defective Nucleocytoplasmic Shuttling of ALS Associated FUS.","authors":"Christiane Hartmann, Christina Haß, Muriel Knobloch, Israel Barrantes, Laura Fumagalli, Jessie Premereur, Franz Markert, Maite Peters, Georgia Koromila, Alexander Hartmann, Kathrin Jäger, Jette Abel, Renzo Mancuso, Alexander Storch, Michael Walter, Georg Fuellen, Andreas Hermann","doi":"10.1111/acel.70232","DOIUrl":"https://doi.org/10.1111/acel.70232","url":null,"abstract":"<p><p>Microglia, the brain's resident immune cells, are crucial for maintaining healthy brain homeostasis. However, as the brain ages, microglia can shift from a neuroprotective to a neurotoxic phenotype, contributing to chronic inflammation and promoting neurodegenerative processes. Despite the importance of understanding microglial aging, there are currently few human in vitro models to study these processes. To address this gap, we have developed a model in which human microglia undergo accelerated aging through inducible progerin expression. HMC3-Progerin cells display key age-related markers such as activation of the senescence-associated secretory phenotype (SASP) as well as an increase in DNA damage. These prematurely aged HMC3 cells show a reduced response to LPS activation, exhibit impairments in essential microglial functions including decreased migration and phagocytosis as well as transcriptomic alterations including a shift observed in aging and neurodegeneration. Additionally, we observed an impaired stress response and a defect in nucleocytoplasmic transport, especially affecting the amyotrophic lateral sclerosis (ALS) associated protein FUS. This suggests that microglia play a contributory role in driving neurodegenerative processes in the aging brain. Our microglia aging model offers a valuable tool for exploring how aged microglia affect brain function, enhancing our understanding of their role in brain aging.</p>","PeriodicalId":119,"journal":{"name":"Aging Cell","volume":" ","pages":"e70232"},"PeriodicalIF":7.1,"publicationDate":"2025-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"145084820","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}