Aging Cell最新文献

{"title":"Oocytes maintain low ROS levels to support the dormancy of primordial follicles","authors":"Shaogang Qin,&nbsp;Xinyue Chi,&nbsp;Zijian Zhu,&nbsp;Chuanhe Chen,&nbsp;Tuo Zhang,&nbsp;Meina He,&nbsp;Meng Gao,&nbsp;Ting Zhao,&nbsp;Jingwen Zhang,&nbsp;Lifan Zhang,&nbsp;Wenying Zheng,&nbsp;Ziqi Chen,&nbsp;Wenji Wang,&nbsp;Bo Zhou,&nbsp;Guoliang Xia,&nbsp;Chao Wang","doi":"10.1111/acel.14338","DOIUrl":"10.1111/acel.14338","url":null,"abstract":"<p>Primordial follicles (PFs) function as the long-term reserve for female reproduction, remaining dormant in the ovaries and becoming progressively depleted with age. Oxidative stress plays an important role in promoting female reproductive senescence during aging, but the underlying mechanisms remain unclear. Here, we find that low levels of reactive oxygen species (ROS) are essential for sustaining PF dormancy. Compared to growing follicles, oocytes within PFs were shown to be more susceptible to ROS, which accumulates and damages PFs to promote reproductive senescence. Mechanistically, oocytes within PFs were shown to express high levels of the intracellular antioxidant enzyme superoxide dismutase 1 (SOD1), counteracting ROS accumulation. Decreased SOD1 expression, as a result of aging or through the experimental deletion of the <i>Sod1</i> gene in oocytes, resulted in increased oxidative stress and triggered ferroptosis within PFs. In conclusion, this study identified antioxidant defense mechanisms protecting PFs in mouse ovaries and characterized cell death mechanisms of oxidative stress-induced PF death.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 1","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.14338","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142250031","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":"Molecular and physiological mechanisms of aging are distinct in the cardiac right and left ventricles","authors":"Benjamin D. McNair,&nbsp;Aykhan Yusifov,&nbsp;Joshua P. Thornburg,&nbsp;Caleb R. Hoopes,&nbsp;Sushumna B. Satyanarayana,&nbsp;Tathagato Roy,&nbsp;Jason P. Gigley,&nbsp;Danielle R. Bruns","doi":"10.1111/acel.14339","DOIUrl":"10.1111/acel.14339","url":null,"abstract":"<p>Aging is the primary risk factor for heart disease, the leading global cause of death. Right ventricular (RV) function predicts survival in several age-related clinical contexts, yet no therapies directly improve RV function, in large part due to a poor mechanistic understanding of RV aging and how it is distinct from the widely studied left ventricle (LV). To address this gap, we comprehensively quantified RV functional and morphological remodeling with age. We further aimed to identify molecular mechanisms of RV aging thus we performed RNAseq on RV and LV from male and female young (4 months) and aged (19–21 months) C57BL6 mice. Contrary to the concentric hypertrophic remodeling and diastolic dysfunction that occurs in the LV, the aging RV underwent eccentric remodeling with significant dilation and impaired systolic function. Transcriptomic data were also consistent with ventricle-specific aging, with few genes (13%) similarly shared between ventricles with aging. KEGG analysis identified shared aging genes in inflammatory and immune cell pathways that were confirmed by flow cytometry that demonstrated higher percent of GR1+ myeloid cells in both ventricles. Unique RV aging genes enriched in the biosynthesis of saturated fatty acids, PPAR signaling, and butanoate metabolism, and we identified putative novel RV-specific aging genes. Together, we suggest that the RV and LV are unique cardiac chambers that undergo distinct remodeling with age. These robust differences may explain why therapies designed from LV-based studies fail to improve RV function and suggest that future efforts emphasizing ventricular differences may elucidate new therapies for healthy cardiac aging.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 1","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.14339","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142250115","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":"Causal associations and shared genetic etiology of neurodegenerative diseases with epigenetic aging and human longevity","authors":"Yu Guo,&nbsp;Guojuan Ma,&nbsp;Yukai Wang,&nbsp;Tingyan Lin,&nbsp;Yang Hu,&nbsp;Tianyi Zang","doi":"10.1111/acel.14271","DOIUrl":"10.1111/acel.14271","url":null,"abstract":"<p>The causative mechanisms underlying the genetic relationships of neurodegenerative diseases with epigenetic aging and human longevity remain obscure. We aimed to detect causal associations and shared genetic etiology of neurodegenerative diseases with epigenetic aging and human longevity. We obtained large-scale genome-wide association study summary statistics data for four measures of epigenetic age (GrimAge, PhenoAge, IEAA, and HannumAge) (<i>N</i> = 34,710), multivariate longevity (healthspan, lifespan, and exceptional longevity) (<i>N</i> = 1,349,462), and for multiple neurodegenerative diseases (<i>N</i> = 6618–482,730), including Lewy body dementia, Alzheimer's disease (AD), Parkinson's disease, amyotrophic lateral sclerosis, and multiple sclerosis. Main analyses were conducted using multiplicative random effects inverse-variance weighted Mendelian randomization (MR), and conditional/conjunctional false discovery rate (cond/conjFDR) approach. Shared genomic loci were functionally characterized to gain biological understanding. Evidence showed that AD patients had 0.309 year less in exceptional longevity (IVW beta = −0.309, 95% CI: −0.38 to −0.24, <i>p</i> = 1.51E-19). We also observed suggestively significant causal evidence between AD and GrimAge age acceleration (IVW beta = −0.10, 95% CI: −0.188 to −0.013, <i>p</i> = 0.02). Following the discovery of polygenic overlap, we identified rs78143120 as shared genomic locus between AD and GrimAge age acceleration, and rs12691088 between AD and exceptional longevity. Among these loci, rs78143120 was novel for AD. In conclusion, we observed that only AD had causal effects on epigenetic aging and human longevity, while other neurodegenerative diseases did not. The genetic overlap between them, with mixed effect directions, suggested complex shared genetic etiology and molecular mechanisms.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"23 11","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11561668/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142277479","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":"E5 treatment showing improved health-span and lifespan in old Sprague Dawley rats","authors":"Kavita Singh,&nbsp;Shraddha I. Khairnar,&nbsp;Akshay Sanghavi,&nbsp;Tanuja T. Yadav,&nbsp;Neha Gupta,&nbsp;Jay Arora,&nbsp;Harold L. Katcher","doi":"10.1111/acel.14335","DOIUrl":"10.1111/acel.14335","url":null,"abstract":"<p>Aging and, in particular, the emergence of age-related disorders is associated with tissue dysfunction and macromolecular damage, some of which can be attributable to accumulated oxidative damage. In the current study, we determine the potential of ‘plasma-derived fraction (E5)’ for cellular rejuvenation and extending the lifespan of Sprague Dawley (SD) rats. This is a unique study wherein we have used 24-month-old rats and monitored them until the end of their lifespan with and without E5 treatment. In the present investigation, the SD rats were separated into two groups old control group and the treatment group (<i>n</i> = 8). The treatment group received four injections of E5 every alternate day for 8 days, and eight injections every alternate day for 16 days. Body weight, grip strength, cytokines, and biochemical markers were measured for more than 400 days of the study. Clinical observation, necropsy, and histology were performed. The E5 treatment exhibited great potential by showing significantly improved grip strength, remarkably decreased pro-inflammatory markers of chronic inflammation and oxidative stress, as well as biomarkers for vital organs (BUN, SGPT, SGOT, and triglycerides), and increased anti-oxidant levels. Clinical examinations, necropsies, and histopathology revealed that the animals treated with the E5 had normal cellular structure and architecture. In conclusion, this unique ‘plasma-derived exosome’ treatment (E5) alone is adequate to improve the health-span and extend the lifespan of the old SD rats significantly.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"23 12","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.14335","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142250114","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":"In vitro immuno-prevention of nitration/dysfunction of myogenic stem cell activator HGF, towards developing a strategy for age-related muscle atrophy","authors":"Sakiho Tanaka,&nbsp;Alaa Elgaabari,&nbsp;Miyumi Seki,&nbsp;So Kuwakado,&nbsp;Kahona Zushi,&nbsp;Junri Miyamoto,&nbsp;Shoko Sawano,&nbsp;Wataru Mizunoya,&nbsp;Kenshiro Ehara,&nbsp;Naruha Watanabe,&nbsp;Yohei Ogawa,&nbsp;Hikaru Imakyure,&nbsp;Reina Fujimaru,&nbsp;Rika Osaki,&nbsp;Kazuki Shitamitsu,&nbsp;Kaoru Mizoguchi,&nbsp;Tomoki Ushijima,&nbsp;Takahiro Maeno,&nbsp;Takashi Nakashima,&nbsp;Takahiro Suzuki,&nbsp;Mako Nakamura,&nbsp;Judy E. Anderson,&nbsp;Ryuichi Tatsumi","doi":"10.1111/acel.14337","DOIUrl":"10.1111/acel.14337","url":null,"abstract":"<p>In response to peroxynitrite (ONOO⁻) generation, myogenic stem satellite cell activator HGF (hepatocyte growth factor) undergoes nitration of tyrosine residues (Y198 and Y250) predominantly on fast IIa and IIx myofibers to lose its binding to the signaling receptor c-met, thereby disturbing muscle homeostasis during aging. Here we show that rat anti-HGF monoclonal antibody (mAb) 1H41C10, which was raised in-house against a synthetic peptide FTSNPEVR_nitroY₁₉₈EV, a site well-conserved in mammals, functions to confer resistance to nitration dysfunction on HGF. 1H41C10 was characterized by recognizing both nitrated and non-nitrated HGF with different affinities as revealed by Western blotting, indicating that the paratope of 1H41C10 may bind to the immediate vicinity of Y198. Subsequent experiments showed that 1H41C10-bound HGF resists peroxynitrite-induced nitration of Y198. A companion mAb-1H42F4 presented similar immuno-reactivity, but did not protect Y198 nitration, and thus served as the control. Importantly, 1H41C10-HGF also withstood Y250 nitration to retain c-met binding and satellite cell activation functions in culture. The Fab region of 1H41C10 exerts resistivity to Y250 nitration possibly due to its localization in the immediate vicinity to Y250, as supported by an additional set of experiments showing that the 1H41C10-Fab confers Y250-nitration resistance which the Fc segment does not. Findings highlight the in vitro preventive impact of 1H41C10 on HGF nitration-dysfunction that strongly impairs myogenic stem cell dynamics, potentially pioneering cogent strategies for counteracting or treating age-related muscle atrophy with fibrosis (including sarcopenia and frailty) and the therapeutic application of investigational HGF drugs.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"23 10","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-09-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.14337","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142250032","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":"CASIN exerts anti-aging effects through RPL4 on the skin of naturally aging mice","authors":"Yijia Zhang,&nbsp;Xueer Wang,&nbsp;Jianyuan Huang,&nbsp;Xinyue Zhang,&nbsp;Lingwei Bu,&nbsp;Yarui Zhang,&nbsp;Fengting Liang,&nbsp;Shenhua Wu,&nbsp;Min Zhang,&nbsp;Lu Zhang,&nbsp;Lin Zhang","doi":"10.1111/acel.14333","DOIUrl":"10.1111/acel.14333","url":null,"abstract":"<p>Skin aging has been associated with the onset of various skin issues, and recent studies have identified an increase in Cdc42 activity in naturally aging mice. While previous literature has suggested that CASIN, a specific inhibitor of Cdc42 activity, may possess anti-aging properties, its specific effects on the epidermis and dermis, as well as the underlying mechanisms in naturally aging mice, remain unclear. Our study revealed that CASIN demonstrated the ability to increase epidermal and dermal thickness, enhance dermal-epidermal junction, and stimulate collagen and elastic fiber synthesis in 9-, 15-, and 24-month-old C57BL/6 mice in vivo. Moreover, CASIN was found to enhance the proliferation, differentiation, and colony formation and restore the cytoskeletal morphology of primary keratinocytes in naturally aging skin in vitro. Furthermore, the anti-aging properties of CASIN on primary fibroblasts in aging mice were mediated by the ribosomal protein RPL4 using proteomic sequencing, influencing collagen synthesis and cytoskeletal morphology both in vitro and in vivo. Meanwhile, both subcutaneous injection and topical application exhibited anti-aging effects for a duration of 21 days. Additionally, CASIN exhibited anti-inflammatory properties, while reduced expression of RPL4 was associated with increased inflammation in the skin of naturally aging mice. Taken together, our results unveil a novel function of RPL4 in skin aging, providing a foundational basis for future investigations into ribosomal proteins. And CASIN shows promise as a potential anti-aging agent for naturally aging mouse skin, suggesting potential applications in the field.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"23 12","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.14333","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142250116","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":"Identification of AS1842856 as a novel small-molecule GSK3α/β inhibitor against Tauopathy by accelerating GSK3α/β exocytosis","authors":"Da-Long He,&nbsp;Xiao-Yu Zhang,&nbsp;Jing-Yang Su,&nbsp;Qi Zhang,&nbsp;Ling-Xiao Zhao,&nbsp;Ting-Yao Wu,&nbsp;Hang Ren,&nbsp;Rong-Jun Jia,&nbsp;Xian-Fang Lei,&nbsp;Wen-Jia Hou,&nbsp;Wen-Ge Sun,&nbsp;Yong-Gang Fan,&nbsp;Zhan-You Wang","doi":"10.1111/acel.14336","DOIUrl":"10.1111/acel.14336","url":null,"abstract":"<p>Glycogen synthase kinase-3α/β (GSK3α/β) is a critical kinase for Tau hyperphosphorylation which contributes to neurodegeneration. Despite the termination of clinical trials for GSK3α/β inhibitors in Alzheimer's disease (AD) treatment, there is a pressing need for novel therapeutic strategies targeting GSK3α/β. Here, we identified the compound AS1842856 (AS), a specific forkhead box protein O1 (FOXO1) inhibitor, reduced intracellular GSK3α/β content in a FOXO1-independent manner. Specifically, AS directly bound to GSK3α/β, promoting its translocation to the multivesicular bodies (MVBs) and accelerating exocytosis, ultimately decreasing intracellular GSK3α/β content. Expectedly, AS treatment effectively suppressed Tau hyperphosphorylation in cells exposed to okadaic acid or expressing the Tau^P301S mutant. Furthermore, AS was visualized to penetrate the blood–brain barrier (BBB) using an imaging mass microscope. Long-term treatment of AS enhanced cognitive function in P301S transgenic mice by mitigating Tau hyperphosphorylation through downregulation of GSK3α/β expression in the brain. Altogether, AS represents a novel small-molecule GSK3α/β inhibitor that facilitates GSK3α/β exocytosis, holding promise as a therapeutic agent for GSK3α/β hyperactivation-associated disorders.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"24 1","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-09-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.14336","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142250117","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":"Extracellular vesicle-encapsulated miR-30c-5p reduces aging-related liver fibrosis","authors":"Alice C. Rodrigues,&nbsp;Yujing J. Heng,&nbsp;Frank J. Slack","doi":"10.1111/acel.14310","DOIUrl":"10.1111/acel.14310","url":null,"abstract":"<p>Aging is associated with decreased health span, and despite the recent advances made in understanding the mechanisms of aging, no antiaging drug has been approved for therapy. Therefore, strategies to promote a healthy life in aging are desirable. Previous work has shown that chronic treatment with extracellular vesicles (EVs) from young mice prolongs lifespan in old mice, but the mechanism of action of this effect on liver metabolism is not known. Here we investigated the role of treatment with EVs derived from young sedentary (EV-C) or exercised (EV-EX) mice in the metabolism of old mice and aimed to identify key youthful-associated microRNA (miRNA) cargos that could promote healthy liver function. We found that aged mice treated with either EV-C or EV-EX had higher insulin sensitivity, higher locomotor activity resulting in longer distance traveled in the cage, and a lower respiratory exchange ratio compared to mice treated with EVs from aged mice (EV-A). In the liver, treatment with young-derived EVs reduced aging-induced liver fibrosis. We identified miR-30c in the EVs as a possible youth-associated miRNA as its level was higher in circulating EVs of young mice. Treatment of aged mice with EVs transfected with miR-30c mimic reduced stellate cell activation in the liver and reduced fibrosis compared to EV-negative control by targeting Foxo3. Our results suggest that by delivering juvenile EVs to old mice, we can improve their liver health. Moreover, we identified miR-30c as a candidate for antiaging liver therapy.</p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"23 12","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-09-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.14310","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142250119","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":"Featured Cover","authors":"Xiao Lu,&nbsp;Dachuan Li,&nbsp;Zhidi Lin,&nbsp;Tian Gao,&nbsp;Zhaoyang Gong,&nbsp;Yuxuan Zhang,&nbsp;Hongli Wang,&nbsp;Xinlei Xia,&nbsp;Feizhou Lu,&nbsp;Jian Song,&nbsp;Guangyu Xu,&nbsp;Jianyuan Jiang,&nbsp;Xiaosheng Ma,&nbsp;Fei Zou","doi":"10.1111/acel.14346","DOIUrl":"https://doi.org/10.1111/acel.14346","url":null,"abstract":"<p>Cover legend: The cover image is based on the Article <i>HIF-1α-induced expression of the m6A reader YTHDF1 inhibits the ferroptosis of nucleus pulposus cells by promoting SLC7A11 translation</i> by Xiao Lu et al., https://doi.org/10.1111/acel.14210<figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"23 9","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.14346","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142231033","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":"Additional Cover","authors":"Kerriann K. Badal,&nbsp;Abhishek Sadhu,&nbsp;Bindu L. Raveendra,&nbsp;Carrie McCracken,&nbsp;Sebastian Lozano-Villada,&nbsp;Amol C. Shetty,&nbsp;Phillip Gillette,&nbsp;Yibo Zhao,&nbsp;Dustin Stommes,&nbsp;Lynne A. Fieber,&nbsp;Michael C. Schmale,&nbsp;Anup Mahurkar,&nbsp;Robert D. Hawkins,&nbsp;Sathyanarayanan V. Puthanveettil","doi":"10.1111/acel.14347","DOIUrl":"https://doi.org/10.1111/acel.14347","url":null,"abstract":"<p>Cover legend: The cover image is based on the Article <i>Single-neuron analysis of aging-associated changes in learning reveals impairments in transcriptional plasticity</i> by Kerriann K. Badal et al., https://doi.org/10.1111/acel.14228 Image Credit: Phillip Gillette and Lynne Fieber\u0000\u0000 <figure>\u0000 <div><picture>\u0000 <source></source></picture><p></p>\u0000 </div>\u0000 </figure>\u0000 </p>","PeriodicalId":55543,"journal":{"name":"Aging Cell","volume":"23 9","pages":""},"PeriodicalIF":7.8,"publicationDate":"2024-09-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://onlinelibrary.wiley.com/doi/epdf/10.1111/acel.14347","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142231035","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}