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104. NIH SenNet Consortium to map senescent cells throughout the human lifespan to understand physiological health

Author

Lee, Patty J., Benz, Christopher C., Blood, Philip, Börner, Katy, Campisi, Judith, Chen, Feng, Daldrup-Link, Heike, De Jager, Phil, Ding, Li, Duncan, Francesca E., Eickelberg, Oliver, Fan, Rong, Finkel, Toren, Furman, David, Garovic, Vesna, Gehlenborg, Nils, Glass, Carolyn, Heckenbach, Indra, Joseph, Ziv Bar, Katiyar, Pragati, Kim, So Jin, Königshoff, Melanie, Kuchel, George A., Lee, Haesung, Lee, Jun Hee, Ma, Jian, Ma, Qin, Melov, Simon, Metis, Kay, Mora, Ana L., Musi, Nicolas, Neretti, Nicola, Passos, João F., Rahman, Irfan, Rivera-Mulia, Juan Carlos, Robson, Paul, Rojas, Mauricio, Roy, Ananda L., Scheibye-Knudsen, Morten, Schilling, Birgit, Shi, Pixu, Silverstein, Jonathan C., Suryadevara, Vidyani, Xie, Jichun, Wang, Jinhua, Wong, A. Ian, Niedernhofer, Laura J., Wang, Siyuan, Anvari, Hannah, Balough, Julia, Lee, Patty J., Benz, Christopher C., Blood, Philip, Börner, Katy, Campisi, Judith, Chen, Feng, Daldrup-Link, Heike, De Jager, Phil, Ding, Li, Duncan, Francesca E., Eickelberg, Oliver, Fan, Rong, Finkel, Toren, Furman, David, Garovic, Vesna, Gehlenborg, Nils, Glass, Carolyn, Heckenbach, Indra, Joseph, Ziv Bar, Katiyar, Pragati, Kim, So Jin, Königshoff, Melanie, Kuchel, George A., Lee, Haesung, Lee, Jun Hee, Ma, Jian, Ma, Qin, Melov, Simon, Metis, Kay, Mora, Ana L., Musi, Nicolas, Neretti, Nicola, Passos, João F., Rahman, Irfan, Rivera-Mulia, Juan Carlos, Robson, Paul, Rojas, Mauricio, Roy, Ananda L., Scheibye-Knudsen, Morten, Schilling, Birgit, Shi, Pixu, Silverstein, Jonathan C., Suryadevara, Vidyani, Xie, Jichun, Wang, Jinhua, Wong, A. Ian, Niedernhofer, Laura J., Wang, Siyuan, Anvari, Hannah, and Balough, Julia

Abstract

Cells respond to many stressors by senescing, acquiring stable growth arrest, morphologic and metabolic changes, and a proinflammatory senescence-associated secretory phenotype. The heterogeneity of senescent cells (SnCs) and senescence-associated secretory phenotype are vast, yet ill characterized. SnCs have diverse roles in health and disease and are therapeutically targetable, making characterization of SnCs and their detection a priority. The Cellular Senescence Network (SenNet), a National Institutes of Health Common Fund initiative, was established to address this need. The goal of SenNet is to map SnCs across the human lifespan to advance diagnostic and therapeutic approaches to improve human health. State-of-the-art methods will be applied to identify, define and map SnCs in 18 human tissues. A common coordinate framework will integrate data to create four-dimensional SnC atlases. Other key SenNet deliverables include innovative tools and technologies to detect SnCs, new SnC biomarkers and extensive public multi-omics datasets. This Perspective lays out the impetus, goals, approaches and products of SenNet.

Published
2022

108. Improving the Approach to Defining, Classifying, Reporting and Monitoring Adverse Events in Seriously Ill Older Adults: Recommendations from a Multi-stakeholder Convening

Author

Baim-Lance, Abigail, primary, Ferreira, Katelyn B., additional, Cohen, Harvey Jay, additional, Ellenberg, Susan S., additional, Kuchel, George A., additional, Ritchie, Christine, additional, Sachs, Greg A., additional, Kitzman, Dalane, additional, Morrison, R. Sean, additional, and Siu, Albert, additional

Published
2022
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110. Additional file 1 of Markers of systemic inflammation are positively associated with influenza vaccine antibody responses with a possible role for ILT2(+)CD57(+) NK-cells

Author

Picard, Emilie, Armstrong, Sarah, Andrew, Melissa K., Haynes, Laura, Loeb, Mark, Pawelec, Graham, Kuchel, George A., McElhaney, Janet E., and Verschoor, Chris P.

Abstract

Additional file 1: Table S1. Summary of antibody and cell-mediated immune responses pre- and 4-weeks post-influenza vaccination. Table S2. Results from multivariable analysis of vaccine antibody responses in older adults where plasma TNF, IL-6 and CRP were simultaneously included as fixed effects. Table S3. Summary of participants enrolled in the follow-up cohort, including pre-vaccination levels of inflammatory mediators and antibody responses pre- and 4-weeks post-influenza vaccination. Figure S1. Associations between inflammatory mediator levels and antibody responses of high-dose vaccine recipients are independent of frailty. Figure S2. Joint effects of TNF and IL-6 in the association with post-vaccination antibody titres in standard- dose (SD) and high-dose (HD) older recipients. Figure S3. Sex-stratified models of systemic inflammation and the response to influenza vaccination in young (YA) and older (OA) adults vaccinated with either standard (SD) or high (HD) dose vaccine. Figure S4. ILT2+CD57+ Dim NK-cells mediate a significant proportion of the effect of frailty on post-vaccination A/H3N2 antibody titres in older high-dose recipients.

Published
2022
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111. Additional file 1 of Advanced biological age is associated with improved antibody responses in older high-dose influenza vaccine recipients over four consecutive seasons

Author

Verschoor, Chris P., Belsky, Daniel W., Andrew, Melissa K., Haynes, Laura, Loeb, Mark, Pawelec, Graham, McElhaney, Janet E., and Kuchel, George A.

Abstract

Additional file 1: Supplementary Table 1. Regression table describing the association between standardized, natural-log 4-week antibody titres and ΔBA in high-dose recipients, including a two-way interaction between ΔBA and CMV serostatus. Supplementary Table 2. KDM training parameters derived from the CLSA and used calculate biological aging in the vaccination cohort. Supplementary Figure 1. Characteristics of KDM biological age (BA) in the CLSA training cohort and associations with the frailty index (FI). A) Pearson’s correlation (R) for BA with chronological age and significance (p) for females (red asterisk) and males (blue dots). B) Distribution of ΔBA in females and males, including the mean and standard deviation. C) Differences in years for ΔBA (and 95% confidence interval) for pre-frail (0.10=FI

Published
2022
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120. Urinary Incontinence and Voiding Dysfunction with Aging: A Multifaceted Geriatric Syndrome in Search of Multidisciplinary Research Solutions.

Author

Kuchel, George A

Subjects
*URINATION disorders, *BACTERIURIA, *URINARY incontinence, *INAPPROPRIATE prescribing (Medicine), *AGING, *INTERDISCIPLINARY research, *OLDER people, *NATURAL history
Abstract

Urinary incontinence and voiding dysfunction are common issues that significantly impact the quality of life and independence of older adults. Despite advancements in research, these problems are often underdiagnosed and undertreated, with medications that have adverse effects being used as a suboptimal solution. Various challenges contribute to the difficulty in managing these conditions, including social stigma, lack of education among clinicians, and misconceptions about treatment options. However, there is hope for the future as multidisciplinary research is being conducted to better understand and address the complex factors involved in geriatric voiding issues and incontinence. This research aims to develop effective and safe interventions for these common conditions. [Extracted from the article]

Published
2024
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126. Analysis ofCYP2C19genetic variants with ischaemic events in UK patients prescribed clopidogrel in primary care: a retrospective cohort study

Author

Pilling, Luke C, primary, Türkmen, Deniz, additional, Fullalove, Hannah, additional, Atkins, Janice L, additional, Delgado, Joao, additional, Kuo, Chia-Ling, additional, Kuchel, George A, additional, Ferrucci, Luigi, additional, Bowden, Jack, additional, Masoli, Jane A H, additional, and Melzer, David, additional

Published
2021
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134. Intermittent clearance of p21-highly-expressing cells extends lifespan and confers sustained benefits to health and physical function.

Author

Wang, Binsheng, Wang, Lichao, Gasek, Nathan S., Kuo, Chia-Ling, Nie, Jia, Kim, Taewan, Yan, Pengyi, Zhu, Junyu, Torrance, Blake L., Zhou, Yueying, Flores, Lisa C., Allen, Colton, Andrade, Allison M., Guo, Chun, Cohn, Rachel L., Jellison, Evan R., Bartley, Jenna M., Kuchel, George A., Li, Sheng, and Pirtskhalava, Tamar

Abstract

A key challenge in aging research is extending lifespan in tandem with slowing down functional decline so that life with good health (healthspan) can be extended. Here, we show that monthly clearance, starting from 20 months, of a small number of cells that highly express p21 Cip1 (p21 high) improves cardiac and metabolic function and extends both median and maximum lifespans in mice. Importantly, by assessing the health and physical function of these mice monthly until death, we show that clearance of p21 high cells improves physical function at all remaining stages of life, suggesting healthspan extension. Mechanistically, p21 high cells encompass several cell types with a relatively conserved proinflammatory signature. Clearance of p21 high cells reduces inflammation and alleviates age-related transcriptomic signatures of various tissues. These findings demonstrate the feasibility of healthspan extension in mice and indicate p21 high cells as a therapeutic target for healthy aging. [Display omitted] • p21 high cells, distinct from p16 high cells, accumulate in various tissues with aging • Intermittent p21 high cell clearance extends both median and maximum lifespans in mice • Intermittent p21 high cell clearance results in sustained health improvement • Intermittent p21 high cell clearance alleviates age-related transcriptomic signatures Wang et al. identify a distinct senescent cell population (p21 high cells) in various tissues with aging. p21 high cells encompass numerous cell types with a conserved proinflammatory signature. Intermittent clearance of p21 high cells reduces inflammation, extends lifespan, and results in sustained benefits to health and physical function in old mice. [ABSTRACT FROM AUTHOR]

Published
2024
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136. A Cellular Reference Resource for the Mouse Urinary Bladder

Author

Baker, Dylan, primary, Al-Naggar, Iman M., additional, Sivajothi, Santhosh, additional, Flynn, William F., additional, Amiri, Anahita, additional, Luo, Diane, additional, Hardy, Cara C., additional, Kuchel, George A., additional, Smith, Phillip P., additional, and Robson, Paul, additional

Published
2021
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139. Extending human healthspan and longevity: a symposium report

Author

DeVito, Loren M., primary, Barzilai, Nir, additional, Cuervo, Ana Maria, additional, Niedernhofer, Laura J., additional, Milman, Sofiya, additional, Levine, Morgan, additional, Promislow, Daniel, additional, Ferrucci, Luigi, additional, Kuchel, George A., additional, Mannick, Joan, additional, Justice, Jamie, additional, Gonzales, Mitzi M., additional, Kirkland, James L., additional, Cohen, Pinchas, additional, and Campisi, Judith, additional

Published
2021
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141. Fisetin for COVID ‐19 in skilled nursing facilities: Senolytic trials in the COVID era

Author

Verdoorn, Brandon P., primary, Evans, Tamara K., additional, Hanson, Gregory J., additional, Zhu, Yi, additional, Langhi Prata, Larissa G. P., additional, Pignolo, Robert J., additional, Atkinson, Elizabeth J., additional, Wissler‐Gerdes, Erin O., additional, Kuchel, George A., additional, Mannick, Joan B., additional, Kritchevsky, Stephen B., additional, Khosla, Sundeep, additional, Rizza, Stacey A., additional, Walston, Jeremy D., additional, Musi, Nicolas, additional, Lipsitz, Lewis A., additional, Kiel, Douglas P., additional, Yung, Raymond, additional, LeBrasseur, Nathan K., additional, Singh, Ravinder J., additional, McCarthy, Teresa, additional, Puskarich, Michael A., additional, Niedernhofer, Laura J., additional, Robbins, Paul D., additional, Sorenson, Matthew, additional, Tchkonia, Tamara, additional, and Kirkland, James L., additional

Published
2021
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142. Network Topology of Biological Aging and Geroscience-Guided Approaches to COVID-19

Author

Landay, Alan, primary, Bartley, Jenna M., additional, Banerjee, Dishary, additional, Hargis, Geneva, additional, Haynes, Laura, additional, Keshavarzian, Ali, additional, Kuo, Chia-Ling, additional, Kwon, Oh Sung, additional, Li, Sheng, additional, Li, Shuzhao, additional, Oh, Julia, additional, Ozbolat, Ibrahim Tarik, additional, Ucar, Duygu, additional, Xu, Ming, additional, Yao, Xudong, additional, Unutmaz, Derya, additional, and Kuchel, George A., additional

Published
2021
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143. Sarcopenia and Variation in the Human Leukocyte Antigen Complex

Author

Jones, Garan, Pilling, Luke C, Kuo, Chia-Ling, Kuchel, George, Ferrucci, Luigi, and Melzer, David

Subjects
Inflammation, Male, UK Biobank, Sarcopenia, Genotype, Hand Strength, THE JOURNAL OF GERONTOLOGY: Medical Sciences, Articles, Middle Aged, musculoskeletal system, Polymorphism, Single Nucleotide, United Kingdom, Autoimmune Diseases, body regions, Phenotype, HLA Antigens, Surveys and Questionnaires, Muscle, Humans, Female, human activities, Autoimmune, Aged, Genome-Wide Association Study
Abstract

Background Aging is characterized by chronic inflammation plus loss of muscle mass and strength, termed sarcopenia. Human leukocyte antigen (HLA) types are drivers of autoimmune disease, although with limited penetrance. We tested whether autoimmune diagnoses are associated with sarcopenia, and whether HLA types and related genetic variants are associated with sarcopenia in autoimmune disease-free older people. Methods Data were collected from 181,301 UK Biobank European descent volunteers aged 60–70 with measured hand grip strength and impedance. Logistic regression analysis estimated HLA type and sarcopenia associations, adjusted for confounders and multiple testing. Results Having any autoimmune diagnosis was associated with sarcopenia (odds ratio [OR] 1.83, 95% confidence interval (CI) 1.74–1.92, p = 4.0*10−125). After excluding autoimmune diagnoses, 6 of 100 HLA types (allele frequency >1%) were associated with sarcopenia (low grip strength and muscle mass). Having two HLA-DQA1*03:01 alleles increased odds of sarcopenia by 19.3% (OR 1.19, CI 1.09–1.29, p = 2.84*10–5), compared to no alleles. Having ≥6 of the 12 HLA alleles increased sarcopenia odds by 23% (OR 1.23, CI 1.12–1.35, p = 7.28*10–6). Of 658 HLA region non-coding genetic variants previously implicated in disease, 4 were associated with sarcopenia, including rs41268896 and rs29268645 (OR 1.08, CI 1.05–1.11, p = 1.06*10–8 and 1.07, CI 1.04–1.09, p = 1.5*10–6, respectively). Some HLA associations with sarcopenia were greater in female participants. Conclusion Autoimmune diagnoses are strongly associated with sarcopenia in 60- to 70-year olds. Variation in specific HLA types and non-coding single nucleotide polymorphisms is also associated with sarcopenia in older carriers free of diagnosed autoimmune diseases. Patients with sarcopenia might benefit from targeted treatment of autoimmune processes.

Published
2019

145. The American Geriatrics Society/National Institute on Aging Bedside-to-Bench Conference: Research Agenda on Delirium in Older Adults

Author

Alessi, Cathy, Auerbach, Andrew, Avelino-Silva, Thiago J., Boustani, Malaz, Brown, Emery, Brummel, Nathan E., Campbell, Noll, Cunningham, Colm, Davis, Daniel, Deiner, Stacie, Dugan, Laura, Eldadah, Basil, Ely, Wesley E., Fick, Donna, Gould, Robert, Hansen, Jennie Chin, Han, Jin Ho, Hayden, Kathleen M., Hopkins, Ramona O., Hughes, Christopher G., Hung, William W., Inouye, Sharon K., Jeste, Dilip V., Jones, Richard, Kennedy, Maura, Khan, Babar A., Kimchi, Eyal, Nadkarni, Neelesh K., Kuchel, George, Lee, Hochang Benjamin, Marcantonio, Edward, Nana, Arvind, Oh, Esther, Pandharipande, Pratik, Resnick, Neil, Robinson, Thomas, Saczynski, Jane, Sieber, Frederick, Silverstein, Jeffrey H., Spanjevic, Lily, Tate, Judith, Vasunilashorn, Sarinnapha (Fah), Walston, Jeremy, and Xie, Zhongcong

Published
2015
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