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Informant characteristics influence Clinical Dementia Rating Sum of Boxes scores-based staging of Alzheimer’s disease 信息提供者的特征会影响基于临床痴呆分级的阿尔茨海默病分期。
IF 17
Nature aging Pub Date : 2024-10-25 DOI: 10.1038/s43587-024-00732-x
Juan-Camilo Vargas-Gonzalez, Antonella Santuccione Chadha, Laura Castro-Aldrete, Maria Teresa Ferretti, Maria Carmela Tartaglia
{"title":"Informant characteristics influence Clinical Dementia Rating Sum of Boxes scores-based staging of Alzheimer’s disease","authors":"Juan-Camilo Vargas-Gonzalez, Antonella Santuccione Chadha, Laura Castro-Aldrete, Maria Teresa Ferretti, Maria Carmela Tartaglia","doi":"10.1038/s43587-024-00732-x","DOIUrl":"10.1038/s43587-024-00732-x","url":null,"abstract":"The Clinical Dementia Rating Sum of Boxes (CDR-SB) is a staging scale for Alzheimer’s disease (AD)1 and is commonly used as an outcome in clinical trials2. It relies on information provided by the patient and an informant3. The CDR-SB should reflect only the patient’s disease severity. However, we explored whether informant characteristics were associated with CDR-SB scores because that association might introduce bias in Alzheimer’s disease research. We found that the CDR-SB was 0.20 higher when informants were female, 0.39 higher when the informant was a patient’s child and 0.18 lower if the relationship was other than spouse or children. Regarding the frequency of contact, CDR-SB scores were 0.38 higher when contact was at least once a week, 0.65 higher when daily and 0.57 higher when living with the patient. Our analysis results suggest that informant characteristics can modify the CDR-SB scores and might introduce bias into Alzheimer’s disease trials and research. Vargas-Gonzalez et al. report an influence of informant characteristics on the Clinical Dementia Rating Sum of Boxes (CDR-SB), a scale designed to stage patients with Alzheimer’s disease, which is commonly used as an outcome for clinical trials.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"4 11","pages":"1538-1543"},"PeriodicalIF":17.0,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142515547","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The Clinical Dementia Rating scale is useful but caution is needed 临床痴呆评定量表很有用,但需要谨慎。
IF 17
Nature aging Pub Date : 2024-10-25 DOI: 10.1038/s43587-024-00742-9
Ronald C. Petersen
{"title":"The Clinical Dementia Rating scale is useful but caution is needed","authors":"Ronald C. Petersen","doi":"10.1038/s43587-024-00742-9","DOIUrl":"10.1038/s43587-024-00742-9","url":null,"abstract":"The Clinical Dementia Rating scale has been used in clinical research for decades. The Vargas-Gonzales study raises concerns about the subjective nature of the instrument by indicating that sex, the relationship of the informant to the participant, and the ethnicity of the participant can influence ratings, which is particularly relevant in an era of increasing inclusivity.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"4 11","pages":"1522-1523"},"PeriodicalIF":17.0,"publicationDate":"2024-10-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142515550","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
METTL3 governs thymocyte development and thymic involution by regulating ferroptosis. METTL3 通过调节铁蛋白沉积来控制胸腺细胞的发育和胸腺的消退。
IF 17
Nature aging Pub Date : 2024-10-23 DOI: 10.1038/s43587-024-00724-x
Huiru Jing, Jiayu Song, Jie Sun, Shaojun Su, Jin Hu, Haojian Zhang, Yanmin Bi, Bing Wu
{"title":"METTL3 governs thymocyte development and thymic involution by regulating ferroptosis.","authors":"Huiru Jing, Jiayu Song, Jie Sun, Shaojun Su, Jin Hu, Haojian Zhang, Yanmin Bi, Bing Wu","doi":"10.1038/s43587-024-00724-x","DOIUrl":"10.1038/s43587-024-00724-x","url":null,"abstract":"<p><p>Given its central role in immune aging, it is important to identify the regulators of thymic involution. While conventional programmed cell death has a fundamental role in thymocyte development, how cell death pathways contribute to thymic involution are unclear. In this study, we found that CD4<sup>+</sup>CD8<sup>+</sup> double-positive (DP) thymocytes acquired the characteristics of senescence in aged mice undergoing thymic involution, while expression of the m<sup>6</sup>A methyltransferase-like protein 3 (METTL3), which is enriched in DP cells from young mice, decreased with aging. By conditionally deleting METTL3 in T cells, we revealed a critical role for METTL3 in DP cell survival and in restraining the features of aging in DP thymocytes by preventing ferroptosis signaling through glutathione peroxidase 4. Mechanistically, glutathione peroxidase 4 was maintained by METTL3 at the translational level, independently of its methyltransferase activity. Furthermore, we found that pharmacological inhibition of ferroptosis promoted DP cell survival and attenuated the features of aging in DP thymocytes. These findings uncover a role for METTL3-regulated ferroptosis in thymic involution and identify strategies to restore thymic function.</p>","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":" ","pages":""},"PeriodicalIF":17.0,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142515549","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Metformin slows signs of primate aging 二甲双胍可减缓灵长类动物的衰老迹象。
IF 17
Nature aging Pub Date : 2024-10-22 DOI: 10.1038/s43587-024-00748-3
Anna Kriebs
{"title":"Metformin slows signs of primate aging","authors":"Anna Kriebs","doi":"10.1038/s43587-024-00748-3","DOIUrl":"10.1038/s43587-024-00748-3","url":null,"abstract":"","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"4 11","pages":"1518-1518"},"PeriodicalIF":17.0,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142515548","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
A hematology-based clock derived from the Study of Longitudinal Aging in Mice to estimate biological age. 根据小鼠纵向衰老研究得出的血液学时钟来估算生物年龄。
IF 17
Nature aging Pub Date : 2024-10-18 DOI: 10.1038/s43587-024-00728-7
Jorge Martinez-Romero, Maria Emilia Fernandez, Michel Bernier, Nathan L Price, William Mueller, Julián Candia, Simonetta Camandola, Osorio Meirelles, Yi-Han Hu, Zhiguang Li, Nigus Asefa, Andrew Deighan, Camila Vieira Ligo Teixeira, Dushani L Palliyaguru, Carlos Serrano, Nicolas Escobar-Velasquez, Stephanie Dickinson, Eric J Shiroma, Luigi Ferrucci, Gary A Churchill, David B Allison, Lenore J Launer, Rafael de Cabo
{"title":"A hematology-based clock derived from the Study of Longitudinal Aging in Mice to estimate biological age.","authors":"Jorge Martinez-Romero, Maria Emilia Fernandez, Michel Bernier, Nathan L Price, William Mueller, Julián Candia, Simonetta Camandola, Osorio Meirelles, Yi-Han Hu, Zhiguang Li, Nigus Asefa, Andrew Deighan, Camila Vieira Ligo Teixeira, Dushani L Palliyaguru, Carlos Serrano, Nicolas Escobar-Velasquez, Stephanie Dickinson, Eric J Shiroma, Luigi Ferrucci, Gary A Churchill, David B Allison, Lenore J Launer, Rafael de Cabo","doi":"10.1038/s43587-024-00728-7","DOIUrl":"https://doi.org/10.1038/s43587-024-00728-7","url":null,"abstract":"<p><p>Biological clocks and other molecular biomarkers of aging are difficult to implement widely in a clinical setting. In this study, we used routinely collected hematological markers to develop an aging clock to predict blood age and determine whether the difference between predicted age and chronologic age (aging gap) is associated with advanced aging in mice. Data from 2,562 mice of both sexes and three strains were drawn from two longitudinal studies of aging. Eight hematological variables and two metabolic indices were collected longitudinally (12,010 observations). Blood age was predicted using a deep neural network. Blood age was significantly correlated with chronological age, and aging gap was positively associated with mortality risk and frailty. Platelets were identified as the strongest age predictor by the deep neural network. An aging clock based on routinely collected blood measures has the potential to provide a practical clinical tool to better understand individual variability in the aging process.</p>","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":" ","pages":""},"PeriodicalIF":17.0,"publicationDate":"2024-10-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142484582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
LGBTQ older adults deserve safe and affirming housing 男女同性恋、双性恋、变性者和跨性别者中的老年人理应获得安全、平等的住房。
IF 17
Nature aging Pub Date : 2024-10-15 DOI: 10.1038/s43587-024-00739-4
Philippe Saad
{"title":"LGBTQ older adults deserve safe and affirming housing","authors":"Philippe Saad","doi":"10.1038/s43587-024-00739-4","DOIUrl":"10.1038/s43587-024-00739-4","url":null,"abstract":"LGBTQ older adults have historically lacked safe, affordable or community-affirming housing opportunities. Philippe Saad, an architect and founding board member at LGBTQ Senior Housing, describes the importance of these housing initiatives and introduces The Pryde, the first LGBTQ-affirming income-restricted senior-housing option in New England.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"4 11","pages":"1511-1511"},"PeriodicalIF":17.0,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142484583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
SEA-AD is a multimodal cellular atlas and resource for Alzheimer’s disease SEA-AD 是阿尔茨海默病的多模态细胞图谱和资源
IF 17
Nature aging Pub Date : 2024-10-14 DOI: 10.1038/s43587-024-00719-8
Michael Hawrylycz, Eitan S. Kaplan, Kyle J. Travaglini, Mariano I. Gabitto, Jeremy A. Miller, Lydia Ng, Jennie L. Close, Rebecca D. Hodge, Brian Long, Tyler Mollenkopf, Shoaib Mufti, Nicole M. Gatto, Eric B. Larson, Paul K. Crane, Thomas J. Grabowski, C. Dirk Keene, Ed S. Lein
{"title":"SEA-AD is a multimodal cellular atlas and resource for Alzheimer’s disease","authors":"Michael Hawrylycz,&nbsp;Eitan S. Kaplan,&nbsp;Kyle J. Travaglini,&nbsp;Mariano I. Gabitto,&nbsp;Jeremy A. Miller,&nbsp;Lydia Ng,&nbsp;Jennie L. Close,&nbsp;Rebecca D. Hodge,&nbsp;Brian Long,&nbsp;Tyler Mollenkopf,&nbsp;Shoaib Mufti,&nbsp;Nicole M. Gatto,&nbsp;Eric B. Larson,&nbsp;Paul K. Crane,&nbsp;Thomas J. Grabowski,&nbsp;C. Dirk Keene,&nbsp;Ed S. Lein","doi":"10.1038/s43587-024-00719-8","DOIUrl":"10.1038/s43587-024-00719-8","url":null,"abstract":"The Seattle Alzheimer’s Disease Brain Cell Atlas (SEA-AD) is a multifaceted open-data resource that is designed to identify cellular and molecular pathologies that underlie Alzheimer’s disease. Integrating neuropathology, single-cell and spatial genomics, and longitudinal clinical metadata, SEA-AD is a unique resource for studying the pathogenesis of Alzheimer’s disease and related dementias.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"4 10","pages":"1331-1334"},"PeriodicalIF":17.0,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142443624","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Francisco Lopera (1951–2024) 弗朗西斯科-洛佩拉(1951-2024)。
IF 17
Nature aging Pub Date : 2024-10-09 DOI: 10.1038/s43587-024-00735-8
Agustín Ibáñez, Randall Bateman, Hernando Santamaria-García
{"title":"Francisco Lopera (1951–2024)","authors":"Agustín Ibáñez,&nbsp;Randall Bateman,&nbsp;Hernando Santamaria-García","doi":"10.1038/s43587-024-00735-8","DOIUrl":"10.1038/s43587-024-00735-8","url":null,"abstract":"A trailblazing Latin American leader in Alzheimer’s disease research and a compassionate patient advocate","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"4 11","pages":"1516-1517"},"PeriodicalIF":17.0,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.nature.com/articles/s43587-024-00735-8.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142396462","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
The brain–body energy conservation model of aging 脑-体能量守恒衰老模型。
IF 17
Nature aging Pub Date : 2024-10-08 DOI: 10.1038/s43587-024-00716-x
Evan D. Shaulson, Alan A. Cohen, Martin Picard
{"title":"The brain–body energy conservation model of aging","authors":"Evan D. Shaulson,&nbsp;Alan A. Cohen,&nbsp;Martin Picard","doi":"10.1038/s43587-024-00716-x","DOIUrl":"10.1038/s43587-024-00716-x","url":null,"abstract":"Aging involves seemingly paradoxical changes in energy metabolism. Molecular damage accumulation increases cellular energy expenditure, yet whole-body energy expenditure remains stable or decreases with age. We resolve this apparent contradiction by positioning the brain as the mediator and broker in the organismal energy economy. As somatic tissues accumulate damage over time, costly intracellular stress responses are activated, causing aging or senescent cells to secrete cytokines that convey increased cellular energy demand (hypermetabolism) to the brain. To conserve energy in the face of a shrinking energy budget, the brain deploys energy conservation responses, which suppress low-priority processes, producing fatigue, physical inactivity, blunted sensory capacities, immune alterations and endocrine ‘deficits’. We term this cascade the brain–body energy conservation (BEC) model of aging. The BEC outlines (1) the energetic cost of cellular aging, (2) how brain perception of senescence-associated hypermetabolism may drive the phenotypic manifestations of aging and (3) energetic principles underlying the modifiability of aging trajectories by stressors and geroscience interventions. The authors offer a new energy-focused perspective on aging by introducing a brain–body model that positions the brain’s response to cytokine signals of hypermetabolism as a mechanistic link between the cellular hallmarks and organismal manifestations of aging.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"4 10","pages":"1354-1371"},"PeriodicalIF":17.0,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142396467","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Senescent stromal fibroblasts in bladder tumors support cancer progression 膀胱肿瘤中的衰老基质成纤维细胞支持癌症进展。
IF 17
Nature aging Pub Date : 2024-10-08 DOI: 10.1038/s43587-024-00738-5
{"title":"Senescent stromal fibroblasts in bladder tumors support cancer progression","authors":"","doi":"10.1038/s43587-024-00738-5","DOIUrl":"10.1038/s43587-024-00738-5","url":null,"abstract":"Aging is associated with biological processes (such as the accumulation of senescent cells) that are relevant to the development of cancer. Using genetically modified mouse models, we discovered that p16high senescent cells with a secretory phenotype accumulate in the bladder during aging, which leads to cancer progression.","PeriodicalId":94150,"journal":{"name":"Nature aging","volume":"4 11","pages":"1527-1528"},"PeriodicalIF":17.0,"publicationDate":"2024-10-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142396466","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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