Aging-US

Blog summary: "Proteostatic modulation in brain aging without associated Alzheimer’s disease-and age-related neuropathological changes." ______________________________________________ A healthy brain continuously produces new proteins to support synaptic plasticity, maintain neuronal health, facilitate signaling pathways, produce neurotransmitters, enable neuroplasticity and adaptation, and meet its metabolic demands. These processes are essential for normal brain function, learning, memory, and overall cognitive abilities. Researchers believe that the dysregulation of proteins is at the core of brain aging. However, the exact recipe for protein dysregulation that leads to accelerated brain aging and neurodegenerative disorders has yet to be brought to light. Previous brain proteostasis (referring to the maintenance of protein homeostasis in brain cells) studies in individuals with Alzheimer’s disease (AD) pathology and age-related neuropathological changes have shown protein dysregulation leading to a buildup of amyloid plaques and neurofibrillary tangles. While these studies have greatly enhanced our knowledge of brain aging, gaps in our understanding remain. What proteomic characteristics do healthy brain aging individuals—without neurodegenerative disorders—have in common? “To our knowledge, whole phosphoproteomes centered on the human brain aging without AD pathology are unavailable.” In a new study, researchers Pol Andrés-Benito, Ignacio Íñigo-Marco, Marta Brullas, Margarita Carmona, José Antonio del Rio, Joaquín Fernández-Irigoyen, Enrique Santamaría, Mónica Povedano, and Isidro Ferrer from Bellvitge Institute for Biomedical Research, Universidad Pública de Navarra, Barcelona Institute for Science and Technology, and University of Barcelona aimed to shed light on the mechanisms underlying brain aging in the absence of AD pathology and age-related neuropathological changes. Their research paper was published on May 13, 2023, in Aging’s Volume 15, Issue 9, and entitled, “Proteostatic modulation in brain aging without associated Alzheimer’s disease-and age-related neuropathological changes.” Full blog - https://aging-us.org/2023/05/brain-aging-insights-from-individuals-without-neurodegeneration/ Paper DOI - https://doi.org/10.18632/aging.204698 Corresponding authors - Isidro Ferrer - 8082ifa@gmail.com, and Pol Andrés-Benito - pandres@idibell.cat Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204698 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, brain aging, cytoskeleton, membranes, synapsis, mitochondria, kinases, (phospho)proteomics, proteome 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

Impact Journals (Aging's publisher) will be participating as an exhibitor at the Society for Scholarly Publishing (SSP) 45th Annual Meeting, which convenes on May 31–June 2, 2023, at the Oregon Convention Center & Hyatt Regency Portland in Portland, Oregon, USA. This year, the SSP’s meeting theme is: “Transformation, Trust, and Transparency.” “The pace of change in our industry continues unabated, with seismic shifts in areas such as the dissemination of research, business models, and the nature of the workplace. And yet, while pressure for change has become the new normal, fundamental change has proved more elusive. We invite you to join us in highlighting the Trust and Transparency issues that underlie many of the challenges we face and exploring what it takes to create more meaningful Transformation in scholarly publishing.” (Source: sspnet.org) Visit booth No. 216 at the SSP 45th Annual Meeting to connect with members of the Impact Journals team. About Impact Journals: Impact Journals publishes scholarly journals in the biomedical sciences with a focus on all areas of cancer and aging research. Our mission is to provide scientists with the opportunity to share their exceptional discoveries, to offer services that enable rapid dissemination of results, and to present vital findings from the many fields of biomedical science. Our goal is life without disease. To learn more about Impact Journals, visit www.ImpactJournals.com. Connect with us on social media to stay updated on journals published by Impact Journals: Oncotarget Twitter – https://twitter.com/Oncotarget Aging Twitter – https://twitter.com/AgingJrnl Oncotarget Facebook – https://www.facebook.com/Oncotarget Aging Facebook – https://www.facebook.com/AgingUS Oncotarget YouTube – https://www.youtube.com/@OncotargetJournal Aging YouTube – https://www.youtube.com/@AgingJournal Oncotarget LinkedIn – https://www.linkedin.com/company/oncotarget/ Aging LinkedIn – https://www.linkedin.com/company/aging For media requests, please contact media@impactjournals.com.

Dean Bunnell, PhD candidate from the Department of Biological Sciences at the University of Alabama, describes a research paper he co-authored that was published by Aging (Aging-US) in Volume 15, Issue 6, entitled, “RNA virus-mediated changes in organismal oxygen consumption rate in young and old Drosophila melanogaster males.” DOI - https://doi.org/10.18632/aging.204593 Corresponding author - Stanislava Chtarbanova - schtarbanova@ua.edu Abstract Aging is accompanied by increased susceptibility to infections including with viral pathogens resulting in higher morbidity and mortality among the elderly. Significant changes in host metabolism can take place following virus infection. Efficient immune responses are energetically costly, and viruses divert host molecular resources to promote their own replication. Virus-induced metabolic reprogramming could impact infection outcomes, however, how this is affected by aging and impacts organismal survival remains poorly understood. RNA virus infection of Drosophila melanogaster with Flock House virus (FHV) is an effective model to study antiviral responses with age, where older flies die faster than younger flies due to impaired disease tolerance. Using this aged host-virus model, we conducted longitudinal, single-fly respirometry studies to determine if metabolism impacts infection outcomes. Analysis using linear mixed models on Oxygen Consumption Rate (OCR) following the first 72-hours post-infection showed that FHV modulates respiration, but age has no significant effect on OCR. However, the longitudinal assessment revealed that OCR in young flies progressively and significantly decreases, while OCR in aged flies remains constant throughout the three days of the experiment. Furthermore, we found that the OCR signature at 24-hours varied in response to both experimental treatment and survival status. FHV-injected flies that died prior to 48- or 72-hours measurements had a lower OCR compared to survivors at 48-hours. Our findings suggest the host’s metabolic profile could influence the outcome of viral infections. Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204593 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Drosophila melanogaster, virus infection, single-fly respirometry, metabolism 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

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 9, entitled, “Increased expression of musashi 1 on breast cancer cells has implication to understand dormancy and survival in bone marrow.” Breast cancer (BC) stem cells (CSCs) resist treatment and can exist as dormant cells in tissues such as the bone marrow (BM). Years before clinical diagnosis, BC cells (BCCs) could migrate from the primary site where the BM niche cells facilitate dedifferentiation into CSCs. Additionally, dedifferentiation could occur by cell autonomous methods. In this new study, researchers George R. Nahas, Lauren S. Sherman, Garima Sinha, Markos H. El Far, Andrew Petryna, Steven M. Munoz, Kimberly A. Silverio, Maran Shaker, Pujan Neopane, Veronica Mariotti, and Pranela Rameshwar from Rutgers New Jersey Medical School studied the role of the RNA-binding protein, Musashi I (Msi 1). They also analyzed its relationship with the T-cell inhibitory molecule programmed death-ligand 1 (PD-L1) in CSCs. “We validated the link between Msi 1 and PD-L1 in CSCs [cancer stem cells] based on significant reduction of CSCs following Msi 1 knockdown.” PD-L1 is expressed on triple negative BC and other cancers. Therefore, PD-L1 is an immune checkpoint that is a target in immune therapy for cancers. Msi 1 can support BCC growth through stabilization of oncogenic transcripts and modulation of stem cell-related gene expression. The researchers reported on a role for Msi 1 to maintain CSCs. They found that it seemed to occur by the differentiation of CSCs to more matured BCCs. This correlated with increased transition from cycling quiescence and reduced expression of stem cell-linked genes. CSCs co-expressed Msi 1 and PD-L1. Msi 1 knockdown led to a significant decrease in CSCs with undetectable PD-L1. “This study has implications for Msi 1 as a therapeutic target, in combination with [an] immune checkpoint inhibitor. Such treatment could also prevent dedifferentiation of breast cancer to CSCs, and to reverse tumor dormancy. The proposed combined treatment might be appropriate for other solid tumors.” DOI - https://doi.org/10.18632/aging.204620 Corresponding author - Pranela Rameshwar - rameshwa@njms.rutgers.edu Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204620 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, cancer stem cell, breast cancer, musashi 1, bone marrow, dormancy 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

A new research paper was published on the cover of Aging (Aging-US) Volume 15, Issue 9, entitled, “In vitro and in vivo effects of zoledronic acid on senescence and senescence-associated secretory phenotype markers.” Zoledronic acid has been found to reduce fracture risk and, in some studies, to decrease mortality in humans and extend lifespan and healthspan in animals. Because senescent cells accumulate with aging and contribute to multiple comorbidities, the non-skeletal actions of zoledronic acid could be due to senolytic (killing of senescent cells) or senomorphic (inhibition of the secretion of the senescence-associated secretory phenotype (SASP)) actions. In this new study, researchers Parinya Samakkarnthai, Dominik Saul, Lei Zhang, Zaira Aversa, Madison L. Doolittle, Jad G. Sfeir, Japneet Kaur, Elizabeth J. Atkinson, James R. Edwards, Graham G. Russell, Robert J. Pignolo, James L. Kirkland, Tamar Tchkonia, Laura J. Niedernhofer, David G. Monroe, Nathan K. Lebrasseur, Joshua N. Farr, Paul D. Robbins, and Sundeep Khosla from the Mayo Clinic, Phramongkutklao Hospital and College of Medicine, Eberhard Karls University, University of Minnesota, University of Oxford, and University of Sheffield tested the above hypothesis using multiple complementary approaches (in vitro, in vivo, and in silico) to evaluate possible effects of zoledronic acid on modulating cellular senescence. The researchers first performed in vitro senescence assays using human lung fibroblasts and DNA repair-deficient mouse embryonic fibroblasts, which demonstrated that zoledronic acid killed senescent cells with minimal effects on non-senescent cells. Next, in aged mice treated with zoledronic acid or vehicle for 8 weeks, zoledronic acid significantly reduced circulating SASP factors, including CCL7, IL-1β, TNFRSF1A, and TGFβ1 and improved grip strength. Analysis of publicly available RNAseq data from CD115+ (CSF1R/c-fms+) pre-osteoclastic cells isolated from mice treated with zoledronic acid demonstrated a significant downregulation of senescence/SASP genes (SenMayo). To establish that these cells are potential senolytic/senomorphic targets of zoledronic acid, the team used single cell proteomic analysis (cytometry by time of flight [CyTOF]) and demonstrated that zoledronic acid significantly reduced the number of pre-osteoclastic (CD115+/CD3e-/Ly6G-/CD45R-) cells and decreased protein levels of p16, p21, and SASP markers in these cells without affecting other immune cell populations. “Collectively, our findings demonstrate that zoledronic acid has senolytic effects in vitro and modulates senescence/SASP biomarkers in vivo. These data point to the need for additional studies testing zoledronic acid and/or other bisphosphonate derivatives for senotherapeutic efficacy.” DOI - https://doi.org/10.18632/aging.204701 Corresponding author - Sundeep Khosla - khosla.sundeep@mayo.edu 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

A new editorial paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 8, entitled, “The senescence-associated secretory phenotype induces neuroendocrine transdifferentiation.” In this editorial, researchers Anda Huna, Nadine Martin and David Bernard from the Université de Lyon discuss the senescence-associated secretory phenotype (SASP). SASP, in addition to stable proliferation arrest, is one of the most remarkable characteristics of senescent cells. Indeed, these cells secrete a variety of factors including cytokines, growth factors and matrix metalloproteases among others. In response to stress, through their SASP, senescent cells are able to modify and instruct their microenvironment. “The SASP is known to have several, sometimes contradictory, effects on phenotypes, including the induction or reinforcement of senescence in neighboring cells, promotion or inhibition of stemness, modification of extracellular matrix, activation or inhibition of immune responses and induction of epithelial-mesenchymal transition and cell migration.” Although cellular senescence and its SASP can initially display some beneficial effects, for instance favoring wound healing or blocking tumor initiation, accumulation of senescent cells and their secretome during aging or chronic stresses (tobacco, obesity, alcohol among others) plays a significant role in promoting aging-associated features and pathologies, like fibrosis, steatosis, chronic inflammation or cancer. In the context of cancer, senescence initially has an antitumoral role, as it promotes proliferation arrest and favors an anti-tumoral immune surveillance in response to oncogenic stress or DNA damage accumulation. However, SASP plays a dual role in tumor initiation and progression, as it first has a tumor suppressive action by reinforcing senescence in neighboring cells and recruiting immune cells, but also plays a tumor promoting role by promoting stemness, epithelial-mesenchymal transition and cell migration and by inhibiting immune responses. “Overall our work reveals a new effect of senescent cells and their SASP in tumors and offers new insights into NED [neuroendocrine transdifferentiation] in breast and prostate cancer biology. It also provides a new vision of the contribution of senescent cells and their SASP to aging-related pathologies, which could involve NED induction in some contexts.” DOI - https://doi.org/10.18632/aging.204669 Corresponding author - David Bernard - david.bernard@lyon.unicancer.fr Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204669 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, cellular senescence, aging, cancer, NF-κB, calcium signaling 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

A new review paper was published in Aging (Aging-US) Volume 15, Issue 8, entitled, “How can we modulate aging through nutrition and physical exercise? An epigenetic approach.” The World Health Organization predicts that by 2050, 2.1 billion people worldwide will be over 60 years old, a drastic increase from only 1 billion in 2019. Considering these numbers, strategies to ensure an extended “healthspan” or healthy longevity are urgently needed. In this new review, researchers Ana Teresa Rajado, Nádia Silva, Filipa Esteves, David Brito, Alexandra Binnie, Inês M. Araújo, Clévio Nóbrega, José Bragança, and Pedro Castelo-Branco from the ALFA Score Consortium, University of Algarve Campus Gambelas, William Osler Health System, and Champalimaud Centre for the Unknown discuss their present study that approaches the promotion of healthspan from an epigenetic perspective. Epigenetic phenomena are modifiable in response to an individual’s environmental exposures, and therefore link an individual’s environment to their gene expression pattern. Epigenetic studies demonstrate that aging is associated with decondensation of the chromatin, leading to an altered heterochromatin structure, which promotes the accumulation of errors. “In this article we explore aging and its associated epigenetic changes as well as how these changes may be delayed or reversed through nutrition, caloric restriction and sustained physical activity, as schematized in Figure 2.” Canonical histones are replaced by histone variants, concomitant with an increase in histone post-translational modifications (PTMs). A slight increase in DNA methylation at promoters has been observed, which represses transcription of previously active genes, in parallel with global genome hypomethylation. Aging is also associated with deregulation of gene expression - usually provided by non-coding RNAs - leading to both the repression of previously transcribed genes and to the transcription of previously repressed genes. “Age-associated epigenetic events are less common in individuals with a healthy lifestyle, including balanced nutrition, caloric restriction and physical exercise. Healthy aging is associated with more tightly condensed chromatin, fewer PTMs and greater regulation by ncRNAs.” DOI: https://doi.org/10.18632/aging.204668 Corresponding Author: Pedro Castelo-Branco - pjbranco@ualg.pt Sign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204666 Subscribe for free publication alerts from Aging: https://www.aging-us.com/subscribe-to-toc-alerts Keywords: epigenetics, aging, nutrition, caloric restriction, physical exercise 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

A new research paper was published in Aging (Aging-US) Volume 15, Issue 8, entitled, “Single-cell transcriptomic analysis uncovers diverse and dynamic senescent cell populations.” Senescence is a state of enduring growth arrest triggered by sublethal cell damage. Given that senescent cells actively secrete proinflammatory and matrix-remodeling proteins, their accumulation in tissues of older persons has been linked to many diseases of aging. Despite intense interest in identifying robust markers of senescence, the highly heterogeneous and dynamic nature of the senescent phenotype has made this task difficult. In this new study, researchers Noah Wechter, Martina Rossi, Carlos Anerillas, Dimitrios Tsitsipatis, Yulan Piao, Jinshui Fan, Jennifer L. Martindale, Supriyo De, Krystyna Mazan-Mamczarz, and Myriam Gorospe from the National Institute on Aging set out to comprehensively analyze the senescent transcriptome of human diploid fibroblasts at the individual-cell scale by performing single-cell RNA-sequencing analysis through two approaches. “Here, we used single-cell RNA sequencing (scRNA-seq) analysis to document both the diverse transcriptomes of human senescent fibroblasts at an individual-cell scale, and the changes in the transcriptome over time during etoposide-triggered senescence.” First, the researchers characterized the different cell states in cultures undergoing senescence triggered by different stresses, and found distinct cell subpopulations that expressed mRNAs encoding proteins with roles in growth arrest, survival and the secretory phenotype. Second, they characterized the dynamic changes in the transcriptomes of cells as they developed etoposide-induced senescence; by tracking cell transitions across this process, the researchers found two different senescence programs that developed divergently, one in which cells expressed traditional senescence markers such as p16 (CDKN2A) mRNA, and another in which cells expressed long noncoding RNAs and splicing was dysregulated. Finally, they obtained evidence that the proliferation status at the time of senescence initiation affected the path of senescence, as determined based on the expressed RNAs. “We propose that a deeper understanding of the transcriptomes during the progression of different senescent cell phenotypes will help develop more effective interventions directed at this detrimental cell population.” DOI - https://doi.org/10.18632/aging.204666 Corresponding authors - Krystyna Mazan-Mamczarz - krystyna.mazan-mamczarz@nih.gov, and Myriam Gorospe - myriam-gorospe@nih.gov Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204666 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, senescence, single-cell analysis, transcriptome 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

Geoffrey Leung and Dr. Doris Leung, Senior Application Scientists from Insilico Medicine Hong Kong Ltd., detail a research paper they co-authored that was published by Aging (Aging-US) in Volume 15, Issue 8, entitled, "Identification of dual-purpose therapeutic targets implicated in aging and glioblastoma multiforme using PandaOmics - an AI-enabled biological target discovery platform.” #openaccess #aging #glioblastoma #research #ai #artificialintelligence #peerreview #openscience #researchpaper #journal #publication #meded #targetdiscovery #gbm DOI - https://doi.org/10.18632/aging.204678 Corresponding author - Mikhail Korzinkin - mike@insilicomedicine.com Abstract Glioblastoma Multiforme (GBM) is the most aggressive and most common primary malignant brain tumor. The age of GBM patients is considered as one of the disease's negative prognostic factors and the mean age of diagnosis is 62 years. A promising approach to preventing both GBM and aging is to identify new potential therapeutic targets that are associated with both conditions as concurrent drivers. In this work, we present a multi-angled approach of identifying targets, which takes into account not only the disease-related genes but also the ones important in aging. For this purpose, we developed three strategies of target identification using the results of correlation analysis augmented with survival data, differences in expression levels and previously published information of aging-related genes. Several studies have recently validated the robustness and applicability of AI-driven computational methods for target identification in both cancer and aging-related diseases. Therefore, we leveraged the AI predictive power of the PandaOmics TargetID engine in order to rank the resulting target hypotheses and prioritize the most promising therapeutic gene targets. We propose cyclic nucleotide gated channel subunit alpha 3 (CNGA3), glutamate dehydrogenase 1 (GLUD1) and sirtuin 1 (SIRT1) as potential novel dual-purpose therapeutic targets to treat aging and GBM. Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204678 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, target discovery, GBM, glioblastoma, PandaOmics 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

Blog summary of an editorial published in Aging’s Volume 15, Issue 8, on April 3, 2023, entitled, “Artificial intelligence and the aging mind.” _________________________________________ Aging is a risk factor for many diseases, including Alzheimer’s disease (AD). While scientists have made some progress in understanding the physiology of aging and its relationship to AD and related disorders, our understanding remains incomplete (to say the least). It is possible that civilization is currently in the midst of an artificial intelligence (AI) and machine learning (ML) “boom.” Researchers are now using AI and ML technologies to elevate our comprehension of aging and aging-related diseases. “Artificial intelligence (AI) and machine learning (ML) technologies can help us better understand these diseases and aging itself by using biological data from the brain or other sources to create a mapping between age and biological data.” In a new editorial paper, researchers Jeyeon Lee, Leland R. Barnard and David T. Jones from the Mayo Clinic in Rochester, Minnesota, discuss a recent study they conducted and explore the potential of AI to revolutionize the field of geriatrics. Their editorial was published in Aging’s Volume 15, Issue 8, on April 3, 2023, entitled, “Artificial intelligence and the aging mind.” Full blog - https://aging-us.org/2023/05/the-brain-age-gap/ Paper DOI - https://doi.org/10.18632/aging.204644 (PDF) Corresponding author - David T. Jones - Jones.David@mayo.edu Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204644 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, brain age, artificial intelligence, Alzheimer’s dementia, neurodegenerative disease, biomarker 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