Aging-US

Dr. Dechao Feng from the Department of Urology, Institute of Urology, West China Hospital, Sichuan University, discusses a research paper he co-authored that was published by Aging (Aging-US) in Volume 15, Issue 18, entitled, “Identification of senescence-related lncRNA prognostic index correlating with prognosis and radiosensitivity in prostate cancer patients.” DOI - https://doi.org/10.18632/aging.204888 Corresponding authors - Dechao Feng - fdcfenix@stu.scu.edu.cn, and Ping Han - hanping@scu.edu.cn Video interview - https://www.youtube.com/watch?v=zHiWwd5RlJw Transcription - https://aging-us.net/2023/10/26/behind-the-study-senescence-related-lncrna-prognostic-index-in-prostate-cancer/ Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204888 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, prostate cancer, senescence-related lncRNA prognostic index, biochemical recurrence, radiosensitivity, androgen response About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Dr. Frank Pun, Diana Zagirova, Dr. Anatoly Urban, and Geoffrey Leung from Insilico Medicine Hong Kong Ltd., discuss a research paper they co-authored that was published by Aging (Aging-US) in Volume 15, Issue 18, entitled, “Biomedical generative pre-trained based transformer language model for age-related disease target discovery.” DOI - https://doi.org/10.18632/aging.205055 Corresponding author - Alex Zhavoronkov - alex@insilico.com Video interview - https://www.youtube.com/watch?v=kIJvrY7n3n0 Interview transcription - https://aging-us.net/2023/10/25/behind-the-study-biomedical-transformer-language-model-for-age-related-disease-discovery/ Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205055 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, transformers, deep learning, therapeutic target discovery, aging biomarkers, human aging About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- October 25, 2023 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 19, entitled, “Live while the DNA lasts. The role of autophagy in DNA loss and survival of diploid yeast cells during chronological aging.” Aging is inevitable and affects all cell types. Thus, yeast cells are often used as a model in aging studies. There are two approaches to studying aging in yeast: replicative aging, which describes the proliferative potential of cells, and chronological aging, which is used for studying post-mitotic cells. In this new study, while analyzing the chronological lifespan (CLS) of diploid Saccharomyces cerevisiae cells, researchers Tuguldur Enkhbaatar, Marek Skoneczny, Karolina Stępień, Mateusz Mołoń, and Adrianna Skoneczna from the Polish Academy of Sciences and Rzeszów University discovered a remarkable phenomenon: ploidy reduction during aging progression. “To uncover the mechanism behind this unusual process we used yeast strains undergoing a CLS assay, looking for various aging parameters.” Cell mortality, regrowth ability, autophagy induction and cellular DNA content measurements indicated that during the CLS assay, dying cells lost their DNA, and only diploids survived. The researchers demonstrated that autophagy was responsible for the gradual loss of DNA. The nucleophagy marker activation at the start of the CLS experiment correlated with the significant drop in cell viability. The activation of piecemeal microautophagy of nucleus (PMN) markers appeared to accompany the chronological aging process until the end. “Our findings emphasize the significance of maintaining at least one intact copy of the genome for the survival of post-mitotic diploid cells.” During chronological aging, cellular components, including DNA, are exposed to increasing stress, leading to DNA damage and fragmentation in aging cells. The researchers propose that PMN-dependent clearance of damaged DNA from the nucleus helps prevent genome rearrangements. However, as long as one copy of the genome can be rebuilt, cells can still survive. “The observations we made in aging research using yeast as the eukaryotic cell model may help to understand the mechanisms that prevent aneuploidy during aging or cancerogenesis in cells where chromothripsis has occurred.” DOI - https://doi.org/10.18632/aging.205102 Corresponding author - Adrianna Skoneczna - ada@ibb.waw.pl Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205102 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, genome instability, lifespan, autophagy, double-strand breaks About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- October 24, 2023 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 19, entitled, “Metabolic switch in the aging astrocyte supported via integrative approach comprising network and transcriptome analyses.” Dysregulated central-energy metabolism is a hallmark of brain aging. Supplying enough energy for neurotransmission relies on the neuron-astrocyte metabolic network. In their new study, researchers Alejandro Acevedo, Felipe Torres, Miguel Kiwi, Felipe Baeza-Lehnert, L. Felipe Barros, Dasfne Lee-Liu, and Christian González-Billault from Universidad de Chile, Cedenna, University of California, San Diego, Centro de Estudios Científicos (CECs), Geroscience Center for Brain Health and Metabolism (GERO), Universidad San Sebastián, and the Buck Institute for Research on Aging aimed to identify genes contributing to age-associated brain functional decline. “[...] we formulated an approach to analyze the metabolic network by integrating flux, network structure and transcriptomic databases of neurotransmission and aging.” Their findings support that during brain aging: (1) The astrocyte undergoes a metabolic switch from aerobic glycolysis to oxidative phosphorylation, decreasing lactate supply to the neuron, while the neuron suffers intrinsic energetic deficit by downregulation of Krebs cycle genes, including mdh1 and mdh2 (Malate-Aspartate Shuttle); (2) Branched-chain amino acid degradation genes were downregulated, identifying dld as a central regulator; (3) Ketone body synthesis increases in the neuron, while the astrocyte increases their utilization, in line with neuronal energy deficit in favor of astrocytes. “The genes identified here are valuable candidates for future studies to understand the molecular mechanisms of healthy brain aging and prevent brain age-associated failure using energy metabolism as a target.” DOI - https://doi.org/10.18632/aging.204663 Corresponding authors - Christian González-Billault - chrgonza@uchile.cl, and Dasfne Lee-Liu - dasfne.lee@uss.cl Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204663 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, astrocyte, neuron, brain aging, flux balance analysis, network centrality About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Dr. Wenbo Yu, Stanley from the Centre for Cancer Biology, SA Pathology and University of South Australia details a #research perspective he co-authored that was #published by Aging (Aging-US) in Volume 15, Issue 17, entitled, “A Poisson distribution-based general model of cancer rates and a cancer risk-dependent theory of aging.” #author #authorinterview #interview #aging #cancer #entropy #poisson #perspective #openaccess #openscience #peerreview #journal #publication #meded #agingshort #video DOI - https://doi.org/10.18632/aging.205016 Corresponding author - Wenbo Yu - stanley.yu@sa.gov.au Video interview - https://www.youtube.com/watch?v=1n7puuJrido Transcription - https://aging-us.net/2023/10/23/behind-the-study-poisson-distribution-based-model-of-cancer-rates-cancer-risk-dependent-theory-of-aging/ Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205016 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, cancer incidence model, poisson distribution, entropy About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- October 18, 2023 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 19, entitled, “Reduction of double-strand DNA break repair exacerbates vascular aging.” Advanced age is the greatest risk factor for cardiovascular disease (CVD), the leading cause of death. Arterial function is impaired in advanced age which contributes to the development of CVD. One underexplored hypothesis is that DNA damage within arteries leads to this dysfunction, yet evidence demonstrating the incidence and physiological consequences of DNA damage in arteries, and in particular, in the microvasculature, in advanced age is limited. In their new study, researchers Samuel I. Bloom, Jordan R. Tucker, Daniel R. Machin, Hossein Abdeahad, AdeLola O. Adeyemo, Tyler G. Thomas, R. Colton Bramwell, Lisa A. Lesniewski, and Anthony J. Donato from The University of Utah, Florida State University and the Veterans Affairs Medical Center-Salt Lake City began by assessing the abundance of DNA damage in human and mouse lung microvascular endothelial cells and found that aging increases the percentage of cells with DNA damage. “To explore the physiological consequences of increases in arterial DNA damage, we evaluated measures of endothelial function, microvascular and glycocalyx properties, and arterial stiffness in mice that were lacking or heterozygous for the double-strand DNA break repair protein ATM kinase.” Surprisingly, in young mice, vascular function remained unchanged which led the researchers to rationalize that perhaps aging is required to accumulate DNA damage. Indeed, in comparison to wild type littermate controls, mice heterozygous for ATM that were aged to ~18 mo (Old ATM +/−) displayed an accelerated vascular aging phenotype characterized by increases in arterial DNA damage, senescence signaling, and impairments in endothelium-dependent dilation due to elevated oxidative stress. Furthermore, old ATM +/− mice had reduced microvascular density and glycocalyx thickness as well as increased arterial stiffness. “Collectively, these data demonstrate that DNA damage that accumulates in arteries in advanced age contributes to arterial dysfunction that is known to drive CVD.” DOI - https://doi.org/10.18632/aging.205066 Corresponding author - Anthony J. Donato - tony.donato@utah.edu Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.20506 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, DNA damage, vascular function, endothelial cell, senescence, oxidative stress, arterial stiffness About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- October 16, 2023 – A new research paper was published on the cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 19, entitled, “BMAL1 modulates senescence programming via AP-1.” Cellular senescence and circadian dysregulation are biological hallmarks of aging. Whether they are coordinately regulated has not been thoroughly studied. In this new study, researchers Sarah K. Jachim, Jian Zhong, Tamas Ordog, Jeong-Heon Lee, Aditya V. Bhagwate, Nagaswaroop Kengunte Nagaraj, Jennifer J. Westendorf, João F. Passos, Aleksey V. Matveyenko, and Nathan K. LeBrasseur from the Mayo Clinic in Rochester, Minnesota, hypothesized that BMAL1, a pioneer transcription factor and master regulator of the molecular circadian clock, plays a role in the senescence program. “Here, we demonstrate BMAL1 is significantly upregulated in senescent cells and has altered rhythmicity compared to non-senescent cells.” Through BMAL1-ChIP-seq, they showed that BMAL1 is uniquely localized to genomic motifs associated with AP-1 in senescent cells. Integration of BMAL1-ChIP-seq data with RNA-seq data revealed that BMAL1 presence at AP-1 motifs is associated with active transcription. Finally, the researchers showed that BMAL1 contributes to AP-1 transcriptional control of key features of the senescence program, including altered regulation of cell survival pathways, and confers resistance to drug-induced apoptosis. “Overall, these results highlight a previously unappreciated role of the core circadian clock component BMAL1 on the molecular phenotype of senescent cells.” DOI - https://doi.org/10.18632/aging.205112 Corresponding authors - Nathan K. LeBrasseur - lebrasseur.nathan@mayo.edu Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205112 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, AP-1, circadian clock, cellular senescence, senolytic, transcription regulation About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Sleep is vital for our health and well-being, but as we age, we tend to experience less and less of it. In particular, we lose some of the deep sleep stages, known as slow wave sleep (SWS), that are crucial for memory consolidation and brain maintenance. This can affect cognitive performance and increase our risk of developing dementia. Not everyone is equally vulnerable to the negative effects of poor sleep quality. Some people seem to be more resilient and able to cope with less SWS without compromising their mental abilities. What makes them different? One possible factor is cognitive reserve (CR). CR is a concept that refers to the brain’s ability to adapt and compensate for age-related changes or brain damage. It is influenced by various aspects of our life experiences, such as education, occupation, leisure activities, social interactions, and mental stimulation. People with higher CR are thought to have more efficient brain networks, more cognitive strategies, and more brain reserve (i.e., more neurons and connections) that can buffer the impact of aging or pathology on cognition. In a new study, researchers Valentin Ourry, Stéphane Rehel, Claire André, Alison Mary, Léo Paly, Marion Delarue, Florence Requier, Anne Hendy, Fabienne Collette, Natalie L. Marchant, Francesca Felisatti, Cassandre Palix, Denis Vivien, Vincent de la Sayette, Gaël Chételat, Julie Gonneaud, and Géraldine Rauchs from Normandie University, UNI – ULB Neuroscience Institute, University of Liege, University College London, and CHU de Caen aimed to identify individuals in whom sleep disturbances might have greater behavioral consequences. On September 28, 2023, their research paper was published in Aging’s Volume 15, Issue 18, entitled, “Effect of cognitive reserve on the association between slow wave sleep and cognition in community-dwelling older adults.” Full blog - Paper DOI -https://doi.org/10.18632/aging.204943 Corresponding author - Géraldine Rauchs - geraldine.rauchs@inserm.fr Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204943 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, sleep, cognitive reserve, cognition About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- October 11, 2023 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 18, entitled, “Pathways explaining racial/ethnic and socio-economic disparities in dementia incidence: the UK Biobank study.” Pathways explaining racial/ethnic disparities in dementia risk are under-evaluated. In their new study, researchers May A. Beydoun, Hind A. Beydoun, Marie T. Fanelli-Kuczmarski, Jordan Weiss, Michael F. Georgescu, Osorio Meirelles, Donald M. Lyall, Michele K. Evans, and Alan B. Zonderman from the National Institute on Aging, Fort Belvoir Community Hospital, Stanford University, and the University of Glasgow examined those disparities and their related pathways among UK Biobank study respondents (50–74 y, N = 323,483; 3.6% non-White minorities) using a series of Cox proportional hazards and generalized structural equations models (GSEM). “The present study examines pathways that might explain racial, ethnic, and socio-economic disparities in AD or all-cause dementia in a large cohort study, the UK Biobank. Our study used several methodologies, including structural equation modeling coupled with survival analysis techniques to examine complex mediating effects between race, ethnicity, socioeconomic status, and dementia or AD [Alzheimer’s disease] risk in a sex-specific manner focusing on lifestyle, biological and cognitive pathways. It is also an attempt at replicating a previous study conducted among US older adults [24].” Results: After ≤15 years, 5,491 all-cause dementia cases were diagnosed. Racial minority status (RACE_ETHN, Non-White vs. White) increased dementia risk by 24% (HR = 1.24, 95% CI: 1.07–1.45, P = 0.005), an association attenuated by socio-economic status (SES), (HR = 1.12, 95% CI: 0.96–1.31). Total race-dementia effect was mediated through both SES and Life’s Essential 8 lifestyle sub-score (LE8LIFESTYLE), combining diet, smoking, physical activity, and sleep factors. SES was inversely related to dementia risk (HR = 0.69, 95% CI: 0.67, 0.72, P < 0.001). Pathways explaining excess dementia risk among racial minorities included ‘RACE_ETHN(−) → SES(−) → DEMENTIA’, ‘RACE_ETHN(−) → SES(−) → Poor cognitive performance, COGN(+) → DEMENTIA’ and ‘RACE_ETHN(−) → SES(+) → LE8LIFESTYLE(−) → DEMENTIA’. “Pending future interventions, lifestyle factors including diet, smoking, physical activity, and sleep are crucial for reducing racial and socio-economic disparities in dementia.” DOI - https://doi.org/10.18632/aging.205058 Corresponding author - May A. Beydoun - baydounm@mail.nih.gov Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, dementia, Alzheimer’s disease, health disparities, socio-economic status, structural equations modeling About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ X - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- October 10, 2023 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 18, entitled, “High-throughput single-cell profiling of B cell responses following inactivated influenza vaccination in young and older adults.” Seasonal influenza contributes to a substantial disease burden, resulting in approximately 10 million hospital visits and 50 thousand deaths in a typical year in the United States. 70 - 85% of the mortality occurs in people over the age of 65. Influenza vaccination is the best protection against the virus, but it is less effective for the elderly, which may be in part due to differences in the quantity or type of B cells induced by vaccination. In their new study, researchers Meng Wang, Ruoyi Jiang, Subhasis Mohanty, Hailong Meng, Albert C. Shaw, and Steven H. Kleinstein from Yale University / Yale School of Medicine investigated this possibility. “[...] we sorted pre- and post-vaccination peripheral blood B cells from three young and three older adults with strong antibody responses to the inactivated influenza vaccine and employed single-cell technology to simultaneously profile the gene expression and the B cell receptor (BCR) of the B cells.” Prior to vaccination, the researchers observed a higher somatic hypermutation frequency and a higher abundance of activated B cells in older adults than in young adults. Following vaccination, young adults mounted a more clonal response than older adults. The expanded clones included a mix of plasmablasts, activated B cells, and resting memory B cells in both age groups, with a decreased proportion of plasmablasts in older adults. Differential abundance analysis identified additional vaccine-responsive cells that were not part of expanded clones, especially in older adults. “To summarize, we showed a quantitative difference in B cell response following vaccination between age groups, with expansion dominated by plasmablasts in the young, and activated B cells in older adults. [...] Overall, this study provides insights into the B cell vaccine response differences between young and older adults and may be beneficial to design more effective vaccines in the older age groups.” DOI - https://doi.org/10.18632/aging.204778 Corresponding authors - Albert C. Shaw - albert.shaw@yale.edu, and Steven H. Kleinstein - steven.kleinstein@yale.edu Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204778 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, B cell receptor, repertoire, clonal expansion, single-cell RNA-seq About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/@AgingJournal LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM