Aging-US

BUFFALO, NY- November 20, 2024 – This #review was #published by Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), in Volume 16, Issue 17, titled, “A systematic review of phenotypic and epigenetic clocks used for aging and mortality quantification in humans.” This systematic review by Brandon Warner, Edward Ratner, Anirban Datta and Amaury Lendasse from Verseon International Corporation, University of Houston and Missouri University of Science and Technology, explores how biological clocks measure aging and predict mortality. These clocks are tools scientists use to track the body's aging process by identifying specific changes over time. This review analyzes 33 biological clocks proposed over the last decade, offering key insights into their design, accuracy, and clinical applications. The study categorizes these clocks into two types: epigenetic clocks, which track cellular aging through DNA changes, and phenotypic clocks, which assess physical biomarkers like blood pressure and cholesterol. These findings highlight the transformative potential of biological clocks in aging research and preventive healthcare. Epigenetic clocks have demonstrated impressive precision in estimating chronological age by analyzing DNA methylation, a key marker of cellular aging. These tools are also linked to age-related diseases, offering valuable insights into the aging process. Phenotypic clocks, which rely on common clinical measures, have been shown to better predict mortality and health outcomes. As the study highlights: “Phenotypic clocks have shown to be better predictors of mortality than chronological age and do so using easily measurable clinical variables.” Their affordability and ease of implementation make them especially practical for healthcare settings. The review also explores how advancements in technology, such as artificial intelligence and machine learning, are enhancing the accuracy and utility of these clocks. For example, newer models now use neural networks to improve predictive performance and identify key aging biomarkers. Understanding biological age can help detect diseases earlier, tailor interventions, and encourage lifestyle changes to slow aging. By providing a clearer picture of individual aging processes, these clocks could lead the way toward personalized healthcare and improved health outcomes. The researchers call for further studies to make epigenetic clocks more affordable and expand the integration of phenotypic clocks into routine healthcare. In conclusion, this review underscores the transformative potential of biological clocks to redefine our understanding and management of aging. By addressing gaps in current research, it paves the way for future advancements in aging science and healthcare. DOI - https://doi.org/10.18632/aging.206098 Corresponding author - Brandon Warner - bwarner@verseon.com Video short - https://www.youtube.com/watch?v=rrqk5HrljQ0 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with 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/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- November 19, 2024 – A new #review was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), on October 29, 2024, Volume 16, Issue 20, titled, ”Brain aging and Alzheimer’s disease, a perspective from non-human primates.“ In the review, Ferrer Isidro from the University of Barcelona and Reial Acadèmia de Medicina de Catalunya, explores the differences in brain aging and Alzheimer’s disease between humans and their closest evolutionary relatives, such as chimpanzees, baboons, and macaques. The study highlights that while humans are uniquely susceptible to severe cognitive decline and memory loss caused by Alzheimer’s disease, non-human primates typically experience only mild changes as they age. Alzheimer’s affects over 50 million people worldwide, making it crucial to understand how aging impacts the brain. This review sheds light on the differences between humans and non-human primates and reveals that while brain aging in primates involves some structural and protein changes, it does not result in the toxic protein deposits that drive Alzheimer’s in humans. In humans, harmful tau protein deposits, known as tau tangles, appear early in life and spread widely through the brain, which damages cells and contributes to memory loss. In non-human primates, tau tangles are rare and typically confined to small regions. While primates may develop beta-amyloid deposits—fragments derived from amyloid precursor protein—these deposits are less toxic and do not interact with tau tangles to trigger Alzheimer’s-like symptoms. Aging primates experience only mild memory or behavioral changes, avoiding the severe cognitive decline and dementia often seen in humans. Humans’ unique vulnerability to Alzheimer’s may be linked to traits that emerged through evolution, including larger brains, longer lifespans, and higher cognitive abilities. These adaptations may have come at a cost, making human brains more susceptible to aging-related damage. This review also suggests that tau tangles play a more critical role in Alzheimer’s progression than previously thought. While traditional treatments focus on targeting beta-amyloid deposits, this research highlights the need to shift attention to tau pathology. The work challenges the widely accepted amyloid cascade hypothesis, which suggests that beta-amyloid is the main driver of Alzheimer’s. Instead, it points to tau tangles as the initial and most damaging change in human brains. This insight could encourage new treatments that focus on preventing or reducing tau deposits. The findings also emphasize the value of studying non-human primates to understand why their brains are more resistant to severe aging-related damage. By identifying protective mechanisms in primates, researchers may discover new strategies to delay or prevent Alzheimer’s in humans. “These observations show that human brain aging differs from brain aging in non-human primates, and humans constitute the exception among primates in terms of severity and extent of brain aging damage.” In conclusion, this review not only improves our understanding of why humans are uniquely vulnerable to Alzheimer’s disease but also opens new avenues for exploring innovative strategies to combat aging-related brain damage in humans. DOI - https://doi.org/10.18632/aging.206143 Corresponding author - Ferrer Isidro - 8082ifa@gmail.com Video short - https://www.youtube.com/watch?v=kUN88OSsJes About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. Please visit our website at https://www.Aging-US.com​​ and connect with us on social media. MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- November 13, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), on October 25, 2024, Volume 16, Issue 20, titled, ”Canonical ligand-dependent and non-canonical ligand-independent EphA2 signaling in the eye lens of wild-type, knockout, and aging mice.“ Researchers from the School of Optometry and Vision Science Program at Indiana University have uncovered important new insights into how the aging affects the eye lens and contributes to cataract formation, a condition impacting millions worldwide. This study focuses on the EphA2 protein, traditionally associated with cancer, which researchers have now identified as essential for maintaining the lens’s clarity and function as it ages. Cataracts are the leading cause of blindness worldwide, primarily affecting older adults, yet the precise biological mechanisms behind their formation remain unclear. This research sheds light on the role of the EphA2 protein receptor in the eye lens, revealing that it operates through two distinct signaling pathways: a canonical (ligand-dependent) and a non-canonical (ligand-independent) pathway. By studying various groups of mice, including those lacking the EphA2 protein receptor and its ligand partner ephrin-A5, scientists observed how these signaling pathways change with age, affecting the organization and maturation of lens cells. Researchers Jenna L. Horner, Michael P. Vu, Jackson T. Clark, Isaiah J. Innis, and Catherine Cheng observed that EphA2’s canonical signaling, which organizes lens cells, remains stable in aging lens tissue, particularly in epithelial cells. They found that the non-canonical signaling pathway—previously associated primarily with aggressive cancer cells—increases with age in normal lens cells. This increase suggests that non-canonical signaling plays a crucial role in helping lens fiber cells mature and maintain their structure over time. “Here, we report that canonical ligand-mediated EphA2 activation is restricted to the lens epithelial cells and show the first evidence of physiological non-canonical EphA2 activity in a normal tissue.” This understanding could lead to new therapies targeting EphA2 to delay or prevent cataracts. In conclusion, this study represents a significant advance in understanding the cellular mechanisms behind lens aging and cataract development, potentially paving the way for new non-surgical cataract treatments. DOI - https://doi.org/10.18632/aging.206144 Corresponding author - Catherine Cheng - ckcheng@iu.edu Video short - https://www.youtube.com/watch?v=3ScKLgOxQvA Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206144 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, fiber cells, epithelial cells, Y588, Y589, S897, phosphorylation, maturation, ephrin About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with 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/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- November 12, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), on October 24, 2024, Volume 16, Issue 20, titled, "Development and validation of an electronic frailty index in a national health maintenance organization." The study, led by researchers Fabienne Hershkowitz Sikron, Rony Schenker, Yishay Koom, Galit Segal, Orit Shahar, Idit Wolf, Bawkat Mazengya, Maor Lewis, Irit Laxer and Dov Albukrek from Meuhedet Health Maintenance Organization (HMO) in collaboration with colleagues from the Joint-Eshel Organization and the Israeli Ministry of Health, introduces the Meuhedet Electronic Frailty Index (MEFI)—a digital tool designed to assess frailty in older people and identify those most at risk for serious health outcomes, such as hospitalization or death. As people live longer, identifying those at higher risk for health complications is essential to maintaining quality of life in older age. Frailty, a condition marked by increased vulnerability to adverse health outcomes, has emerged as a crucial predictor of health deterioration in older people. While frailty assessment tools exist, this study adapts and validates an Electronic Frailty Index (EFI) tailored specifically to Israeli data and healthcare infrastructure, enabling more targeted and culturally relevant assessments. The MEFI was developed using data from 120,986 individuals aged 65 and older, comprising different indicators, including physical, social, and cognitive deficits. The index classifies individuals as "fit," "mildly frail," "moderately frail," or "severely frail" and is integrated into Israel’s electronic health records system. Researchers found that patients with higher MEFI scores faced significantly increased risks of hospitalization or mortality within one year, with risk levels rising fourfold for the most frail compared to those classified as fit. According to the authors, “The findings also showed that the MEFI version we created is valid in predicting mortality or hospitalization and had better predictive accuracy compared to CCI,” underscoring its reliability in assessing health risks. This integration enables Meuhedet HMO to implement proactive and preventive care measures across its network. Beyond predicting hospitalization and mortality, the MEFI’s alignment with Israel’s National Social Security benefit system reinforces its validity and practical use. As the authors note, “As a health maintenance organization, our mandate is to help our patients live longer and better. Using the MEFI as part of routine primary care may help us achieve this goal.” By focusing on early intervention for those most at risk, MEFI could significantly impact health maintenance costs and enable clinicians to allocate resources more effectively. This new EFI version positions Israel at the forefront of frailty research, and its success could pave the way for other countries with similar healthcare systems to adopt or adapt the approach. Future steps include integrating MEFI as a routine part of primary care in Israel to ensure timely intervention and support as patients age. In summary, MEFI is a powerful tool that empowers Israel’s healthcare system to identify and support older adults most in need, marking a significant advancement in caring for an aging population. DOI - https://doi.org/10.18632/aging.206141 Corresponding Author - Fabienne Hershkowitz Sikron - fabian_hershkowitz@meuhedet.co.il Video short - https://www.youtube.com/watch?v=HxIDuGI1cGc Please visit our website at https://www.Aging-US.com​​. MEDIA@IMPACTJOURNALS.COM

Imagine a future where we not only live longer but stay healthy throughout those extra years. Thanks to recent breakthroughs in biotechnology and artificial intelligence (AI) in healthcare, this vision is closer to becoming a reality. Advancements in Aging Research Aging research has made significant progress in recent years by combining disciplines like biology, technology, and medicine to tackle the challenges of extending healthspans and reducing age-related diseases. While people today live longer than ever before, extending our “healthspan”—the years we stay active and illness-free—remains challenging. AI and health biomarkers (biological indicators of our body’s condition) are now key tools in the pursuit of longer, healthier lives. In a recent paper, led by corresponding authors Yu-Xuan Lyu from Southern University of Science and Technology Shenzhen; Alex Zhavoronkov from Insilico Medicine AI Limited, Masdar City, Abu Dhabi; Morten Scheibye-Knudsen and Daniela Bakula from the Center for Healthy Aging, University of Copenhagen, along with numerous other collaborators, the transformative potential of AI in aging research was explored. The research paper, titled “Longevity biotechnology: bridging AI, biomarkers, geroscience and clinical applications for healthy longevity,” was published as the cover paper in Aging’s Volume 16, Issue 20. Full blog - https://aging-us.org/2024/11/how-ai-and-longevity-biotechnology-are-revolutionizing-healthcare-for-healthier-longer-lives/ Paper DOI - https://doi.org/10.18632/aging.206135 Corresponding authors - Yu-Xuan Lyu - lvyx@sustech.edu.cn, Alex Zhavoronkov - alex@insilico.com, Morten Scheibye-Knudsen - mscheibye@sund.ku.dk, and Daniela Bakula - bakula@sund.ku.dk Video short - https://www.youtube.com/watch?v=Hpfe5WJ5g7I Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206135 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, biotechnology, artificial intelligence, healthy longevity About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with 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/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- November 6, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 20 on October 24, 2024, entitled “On the lifespan of Enchytraeus crypticus - impact of iron (nanomaterial and salt) on aging.” This recent study reveals important insights into how iron oxide nanoparticles (Fe3O4 NMs)—tiny particles with unique magnetic properties widely used in medicine and environmental procedures—may affect soil health over time. Led by Susana I.L. Gomes, Janeck J. Scott-Fordsmand, and Mónica J.B. Amorim from the University of Aveiro in Portugal and Aarhus University in Denmark, the research focuses on how these particles interact with the soil-dwelling worm Enchytraeus crypticus, which plays an essential role in breaking down organic matter and supporting soil structure. Iron oxide nanoparticles are increasingly used in applications like magnetic resonance imaging, drug delivery, and environmental cleanup. Their effects on soil ecosystems remain largely unexplored. In this study, the team selected Enchytraeus crypticus, a globally present soil-dwelling worm, as an indicator species to assess potential risks to soil health. Over a 202-day period, they examined how iron oxide nanoparticles and traditional iron salt (FeCl3) impact the worm’s lifespan, aging, and reproductive ability. Findings revealed that prolonged exposure to iron oxide nanoparticles reduced the lifespan, longevity, and reproductive success of Enchytraeus crypticus, particularly in isolated conditions. Worms in lower-density groups experienced greater harm, with shorter lifespans and fewer offspring, while those in larger groups faced less severe impacts. This suggests that population density and environmental factors may influence nanoparticle toxicity. Although iron chloride also showed toxic effects, iron oxide nanoparticles posed higher risks over time, likely due to a slower release of iron ions that extends exposure. In conclusion, this research highlights the importance of comprehensive studies on the long-term effects of nanoparticles on the environment. As iron oxide nanoparticles become more prevalent, understanding their impact on soil ecosystems is crucial to protecting biodiversity and ensuring the sustainability of natural resources. DOI - https://doi.org/10.18632/aging.206134 Corresponding author - Mónica J.B. Amorim - mjamorim@ua.pt Video short - https://www.youtube.com/watch?v=ElhbSAhMeXw Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206134 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, long-term, magnetite, nanobiomaterial, survival About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with 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/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- November 5, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 20 on October 17, 2024, entitled, “Werner syndrome RECQ helicase participates in and directs maintenance of the protein complexes of constitutive heterochromatin in proliferating human cells.” Researchers from the Department of Laboratory Medicine and Pathology at the University of Washington have discovered that the Werner syndrome gene (WRN), linked to premature aging, plays a crucial role in maintaining cellular organization and DNA stability. Their study shows that loss of WRN function disrupts essential protein interactions, potentially accelerating aging as cells lose structural integrity. Werner syndrome is a rare genetic disorder that causes accelerated aging due to mutations in the WRN gene, which disrupts normal cell functions. The WRN gene is typically responsible for essential tasks like DNA repair, replication, and maintaining telomeres—the protective caps on DNA that shorten with age. However, exactly how WRN loss leads to faster aging is still not fully understood. In this study, researchers Pavlo Lazarchuk, Matthew Manh Nguyen, Crina M. Curca, Maria N. Pavlova, Junko Oshima, and Julia M. Sidorova found that beyond its known roles, the WRN gene is also essential for maintaining a specialized structure in the cell nucleus called constitutive heterochromatin (CH). CH is a densely packed form of DNA that keeps certain parts of the genome stable and “switched off,” protecting against unwanted changes. In cells lacking WRN, the CH structure becomes disorganized, leading to DNA instability and accelerating cellular aging. Another important finding was that WRN loss affects the nuclear envelope, the membrane surrounding DNA, which houses essential proteins like Lamin B1 and Lamin B receptor (LBR). These proteins anchor constitutive heterochromatin (CH) to the nuclear membrane, helping keep DNA compact and stable. Without WRN, this anchoring weakens, and the cell’s internal structure begins to resemble that of aging cells. “Our study highlights WRN as a contributor to the integrity of CH and points at the altered levels and distribution of LBR as a mediating mechanism.” By identifying WRN’s role in organizing the cell’s interior, this study provides a new perspective on age-related genomic instability, where DNA becomes more prone to damage. In conclusion, this research highlights the importance of stable cell structures in slowing aging, potentially paving the way for future treatments targeting WRN pathways to protect DNA integrity and combat premature aging. This new insight may also inform therapies for age-related diseases. DOI - https://doi.org/10.18632/aging.206132 Corresponding Author - Julia M. Sidorova - julias@uw.edu Video short - https://www.youtube.com/watch?v=N4m6QFJhQNA Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206132 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, Werner progeria, heterochromatin, senescence, nuclear lamina, satellite repeats About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. Please visit our website at https://www.Aging-US.com​​ and connect with 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/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- October 31, 2024 – A new #research paper was #published as the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 20, entitled, “Longevity biotechnology: bridging AI, biomarkers, geroscience and clinical applications for healthy longevity.” This paper summarizes recent advances in healthspan biotechnology discussed at the 2023 Aging Research and Drug Discovery Meeting (ARDD), where leading experts reviewed breakthroughs in artificial intelligence (AI), biomarkers, aging clocks, geroscience, and clinical trials that support healthier, longer lives. The authors present a comprehensive view of how these technologies are shaping research and industry approaches to aging, focusing on targeting aging itself to reduce multiple age-related diseases and extend the healthy years of life. With people living longer, addressing age-related health issues is more critical than ever. Traditional healthcare often treats age-related diseases individually, overlooking aging as a core issue. Longevity biotechnology seeks to change this by combining AI with biomarker analysis to detect early signs of aging, enabling targeted interventions that not only delay disease but also promote longer, healthier lives. Led by corresponding authors Yu-Xuan Lyu from Southern University of Science and Technology Shenzhen; Alex Zhavoronkov from Insilico Medicine AI Limited, Masdar City, Abu Dhabi; Morten Scheibye-Knudsen and Daniela Bakula from the Center for Healthy Aging, University of Copenhagen, this research synthesizes the potential of AI to identify precise biomarkers of aging, supporting the development of "aging clocks"—tools that use biological data to estimate a person’s biological age and health risks. These tools help clinicians tailor prevention and treatment to individual needs. Additionally, AI speeds up the discovery of drugs that target primary aging drivers, such as cellular damage and decreased cellular energy, offering the potential to slow, prevent, or even reverse certain effects of aging and enhance quality of life. “The fusion of AI with biomarker research has markedly revolutionized the way biomarkers are identified and validated in the field of ageing.” This approach not only promises to slow, prevent, or even reverse certain effects of aging but also emphasizes the potential for AI-driven methods to extend healthspans. In conclusion, the authors emphasize the need for continued investment in AI-driven therapies and biomarker research, which hold the potential to redefine aging care and improve health outcomes as people grow older. DOI - https://doi.org/10.18632/aging.206135 Corresponding Authors - Yu-Xuan Lyu - lvyx@sustech.edu.cn, Alex Zhavoronkov - alex@insilico.com, Morten Scheibye-Knudsen - mscheibye@sund.ku.dk, and Daniela Bakula - bakula@sund.ku.dk Video short - https://www.youtube.com/watch?v=Hpfe5WJ5g7I Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206135 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, biotechnology, artificial intelligence, healthy longevity About Aging-US The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with 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/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- October 29, 2024 – A new #editorial was #published in Aging (listed by MEDLINE/PubMed as “Aging (Albany NY)” and “Aging-US” by Web of Science) Volume 16, Issue 19 on October 14, 2024, entitled “Integrating cardiovascular risk biomarkers in the context of inflammaging.” Cardiovascular diseases (CVD) remain the leading cause of death worldwide, accounting for nearly one-third of all global mortalities. Risk assessment for CVD has traditionally focused on well-known factors linked to atherosclerosis, including demographics, lifestyle choices like smoking and physical activity, and conditions such as diabetes, hypertension, and obesity. Biomarkers, such as non-HDL cholesterol, have also played a key role in identifying those at risk. However, significant residual cardiovascular risk persists despite managing these established risk factors, suggesting additional, unaddressed contributors to cardiovascular health. In their paper, researchers Jacopo Sabbatinelli, Matilde Sbriscia, Fabiola Olivieri, and Angelica Giuliani from Università Politecnica delle Marche and IRCCS INRCA in Ancona, Italy, explore how integrating specific cardiovascular biomarkers could help assess this residual inflammatory risk, particularly in the context of aging-related inflammation, or “inflammaging.” The biomarkers investigated—high-sensitivity C-reactive protein (hs-CRP), high-sensitivity cardiac troponin (hs-cTn), and natriuretic peptides—serve as valuable indicators of both inflammatory burden and early cardiovascular risk. In conclusion, the authors demonstrate that combining markers of chronic inflammation with cardiac health indicators offers a more complete understanding of cardiovascular risk and reveals the impact of aging-related inflammation, or “inflammaging,” on heart health. Researchers suggest that this approach opens new avenues for targeted interventions in aging populations. DOI - https://doi.org/10.18632/aging.206136 Corresponding author - Jacopo Sabbatinelli - j.sabbatinelli@staff.univpm.it Video short - https://www.youtube.com/watch?v=yJJXbwHj6hs Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206136 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, cardiovascular disease, inflammaging, cardiac biomarkers, residual inflammatory risk About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with 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/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM

BUFFALO, NY- October 24, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 19 on October 3, 2024, entitled “A new model and precious tool to study molecular mechanisms of macrophage aging.” As highlighted in the abstract, the accumulation of senescent cells, marked by a senescence-associated secretory phenotype (SASP), plays a role in chronic inflammation and age-related diseases (ARD). During aging, macrophages can develop a senescent-like phenotype with altered functions, promoting the buildup of senescent cells. In the context of aging and ARD, controlling the resolution of inflammation and preventing chronic inflammation—particularly by targeting macrophages—should be a priority. In their paper, researchers Rémy Smith, Kévin Bassand, Ashok Dussol, Christophe Piesse, Eric Duplus, and Khadija El Hadri from Sorbonne Université in Paris and Université Sorbonne Paris Nord in Bobigny, France, developed an in vitro model of murine peritoneal macrophage aging. Using this model, they demonstrated that chronic treatment with CB3, a thioredoxin-1 mimetic anti-inflammatory peptide, completely prevents the increase of p21CIP1 and allows day 14 macrophages to maintain their proliferative activity. "We describe a new model of macrophage aging with a senescence-like phenotype associated with inflammatory, metabolic and functional perturbations.” DOI - https://doi.org/10.18632/aging.206124 Corresponding authors - Eric Duplus - eric.duplus@sorbonne-universite.fr, and Khadija El Hadri - khadija.zegouagh@sorbonne-universite.fr Video short - https://www.youtube.com/watch?v=LfN78LR-CYU Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206124 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, macrophage, inflammation, senescence, thioredoxin-1 mimetic peptide About Aging-US The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.) Please visit our website at https://www.Aging-US.com​​ and connect with 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/ Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc MEDIA@IMPACTJOURNALS.COM