BUFFALO, NY- January 7, 2025 – A new #research perspective was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 22 on December 9, 2024, entitled “Nuclear lipid droplets: a novel regulator of nuclear homeostasis and ageing.” In this article, Dr. Konstantinos Palikaras from the National and Kapodistrian University of Athens and Dr. Nektarios Tavernarakis from the University of Crete explore how tiny fat droplets, known as nuclear lipid droplets (nLDs), accumulate in the nucleus of cells as we age. Unlike regular lipid droplets, which store energy in the cytoplasm, these nuclear droplets may weaken the nucleus by disrupting critical cellular processes. The authors suggest that excessive buildup of nLDs could lead to nuclear instability and may be linked to metabolic conditions such as fatty liver disease, obesity-related disorders, and premature aging. This highlights the potential role of nLDs in cellular aging and age-related diseases. Previous research by the authors using Caenorhabditis elegans (C. elegans), a model organism commonly used to study aging, revealed the role of ATGL-1, an enzyme that regulates fat storage in the nucleus. When functioning properly, ATGL-1 helps maintain a healthy lipid balance. However, when it becomes inactive or overwhelmed, fat droplets build up around the nuclear lamina, making it more difficult for the cell to function properly. “These findings establish excessive nuclear lipid deposition as a key hallmark of aging, with profound implications for nuclear processes such as chromatin organization, DNA repair, and gene regulation.” The authors emphasize that lifestyle interventions, such as caloric restriction and better insulin regulation, can significantly reduce harmful nLD buildup, reinforcing the role of healthy metabolism in slowing cellular aging. They also call for further studies to understand how nLDs behave in human experimental models, particularly in patients with conditions like metabolic syndrome and progeria. A deeper understanding of these processes could lead to treatments designed to preserve cell health and delay age-related diseases. In summary, by presenting nuclear lipid droplets as potential therapeutic targets, this research perspective presents a new path for exploring treatments aimed at combating age-related diseases driven by lipid dysregulation. DOI - https://doi.org/10.18632/aging.206175 Corresponding authors - Konstantinos Palikaras - palikarask@med.uoa.gr, and Nektarios Tavernarakis - tavernarakis@imbb.forth.gr Video short - https://www.youtube.com/watch?v=vuSLuDk8Xjk Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206175 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, ATGL-1, HLH-30/TFEB, lipid droplet, non-linear optical phenomena, nucleus 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- January 2, 2025 – A new priority #research paper, featured as the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 22, was #published on December 29, 2024. The paper is titled “Cell-type specific epigenetic clocks to quantify biological age at cell-type resolution.” Researchers from the Chinese Academy of Sciences and Monash University developed a new way to measure biological aging in individual cell types. This new tool offers a more detailed understanding of how cells age, providing insights into diseases such as Alzheimer’s and liver pathologies, leading the way for more precise health assessments and targeted therapies. Biological age refers to how old a person’s body is biologically, which may differ from their actual age in years. Typically, biological age is estimated using “epigenetic clocks,” which rely on DNA methylation patterns—chemical marks linked to aging. Standard methods analyze all the cells from a specific tissue at once, making it difficult to understand the aging processes in the different cell types that constitute the tissue. To address this, researchers Huige Tong, Xiaolong Guo, Macsue Jacques, Qi Luo, Nir Eynon,m and Andrew E Teschendorff analyzed DNA samples from human brain and liver tissues to create a new analysis tool. With the help of advanced computer models, they studied changes in DNA methylation in samples from healthy and diseased individuals. By isolating biological aging within specific cell types, the team could better understand how these changes contribute to diseases like Alzheimer’s or liver conditions. The study revealed that certain brain cells, like neurons and glia, age faster in people with Alzheimer’s disease, suggesting that the aging of specific cell types plays a critical role in neurodegeneration. In liver diseases, such as fatty liver disease and obesity, the clock for liver cells showed signs of accelerated aging, making it a better tool than previous methods for detecting liver problems. "We find that neuron and glia specific clocks display biological age acceleration in Alzheimer’s Disease with the effect being strongest for glia in the temporal lobe.” This new approach distinguishes the aging process within individual cell types from changes in the overall composition of cells in a tissue, offering a clearer view of how aging affects each specific cell type. This is crucial for identifying which cells are most affected by aging in certain diseases, guiding the development of targeted therapies. In conclusion, this study highlights the critical importance of precision in aging research, allowing deeper insights into the aging process and significant advancements in the prevention, diagnosis, and treatment of age-related diseases. DOI - https://doi.org/10.18632/aging.206184 Corresponding author - Andrew E. Teschendorff - andrew@sinh.ac.cn Video short - https://www.youtube.com/watch?v=FjJa5U2-AqQ 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

Imagine being 15 years old but having a body that shows signs of aging as if you are decades older. For some young people with sickle cell disease (SCD), this is a reality. A new study published in Volume 16, Issue 21 of Aging shows that SCD causes the body to age much faster than normal. The research not only explains why this happens but also points to new ways to help people with the disease live healthier, longer lives. What Is Sickle Cell Disease? SCD is a genetic condition that changes the shape of red blood cells. Instead of being round, like a doughnut, the cells become curved like a sickle (a farming tool). These misshapen cells struggle to move through blood vessels, often blocking blood flow and leading to pain, organ damage, and other health problems. Even with modern treatments, they can experience complications like those seen in older adults, such as weaker bones, frailty, and organ failure. In the study “Adolescents and young adults with sickle cell disease exhibit accelerated aging with elevated T-cell p16INK4a expression,” researchers wanted to understand why this happens and what it means for people with the disease. Full blog - https://aging-us.org/?p=6372 Paper DOI - https://doi.org/10.18632/aging.206152 Corresponding author - Samuel R. Wilson - samuel.wilson@med.unc.edu Video short - https://www.youtube.com/watch?v=QXVdxBikaqg Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206152 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, sickle cell disease, p16, adolescents, young adults 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- December 19, 2024 – We are pleased to announce that Dr. Marco Demaria, a leading expert in aging and cellular senescence, will join Aging (Aging-US) as Editor-in-Chief, starting January 1, 2025. Dr. Demaria will work alongside an esteemed Editorial Board. Dr. Demaria has an impressive background in aging research. He earned his PhD in Molecular Medicine from the University of Torino, Italy. In 2010, he joined the laboratory of Aging Founding Editor, the late Dr. Judith Campisi, at the Buck Institute for Research on Aging. There he developed cellular and animal models for studying cellular aging, also known as cellular senescence, and its role in tissue repair, cancer, and aging. Currently, Dr. Demaria leads DemariaLab, whose mission is “to extend human healthspan by pioneering discoveries in molecular and cellular mechanisms that regulate the aging process.” His groundbreaking research has significantly advanced our understanding of cellular senescence and its role in aging and age-related diseases. Dr. Demaria aims to develop new therapeutic approaches to create more effective treatments that mitigate the diseases and extend the healthspan. His work specifically focuses on interfering with the mechanisms of cellular senescence using genetic, pharmacological, and nutraceutical strategies. “My research is focused on understanding the molecular basis of age-related dysfunctions and disorders, and to identify new molecular and cellular targets to improve health and longevity.” - Marco Demaria He is also a Full Professor at the European Research Institute for the Biology of Ageing (ERIBA), Director of the Mechanisms of Health, Ageing and Disease (MoHAD) at the University Medical Center Groningen (UMCG), President of the International Cell Senescence Association (ICSA), and Co-Founder of Cleara Biotech. Dr. Demaria also brings valuable editorial experience from his former positions as Editor-in-Chief of npj Aging and Editorial Board member of Aging Cell. All the above, combined with Dr. Demaria’s academic contributions, commitment, and expertise, align perfectly with Aging’s mission to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population. For more information about Marco Demaria, PhD, please visit www.demarialab.com and follow him on X (Twitter) @marc_dema or on Bluesky @marcdema.bsky.social. About Aging-US Please visit our website at https://www.Aging-US.com​​ and connect with us on social media at: 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- December 18, 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 21 on November 22, 2024, entitled, “Anti-aging effect of extracellular vesicles from mesenchymal stromal cells on senescence-induced chondrocytes in osteoarthritis.” The study, authored by Jérémy Boulestreau, Marie Maumus, Giuliana Bertolino Minani, Christian Jorgensen, and Danièle Noël from the Institute for Regenerative Medicine and Biotherapy and Centre Hospitalier Universitaire de Montpellier, introduces a potential new therapy for osteoarthritis. This therapy uses tiny particles called extracellular vesicles (EVs), derived from fat tissue, to repair damage caused by aging cells in the joints, slowing the progression of osteoarthritis and restoring joint health. Osteoarthritis, the most common joint disorder in older adults, occurs when cartilage breaks down, leading to inflammation, stiffness, and pain. One major contributor to it is cellular senescence, a process where cells stop dividing and release harmful substances that worsen inflammation and damage joint tissues. In this study, the researchers showed that EVs from fat-derived mesenchymal stromal cells (ASC-EVs) decreased the harmful effects of senescent cells. ASC-EVs showed strong therapeutic effects in both cellular and mouse preclinical studies. They reduced inflammation and DNA damage markers in cells derived from human joints and improved cellular health. In mice with osteoarthritis, the vesicles restored joint balance, reduced cartilage damage, and preserved joint function for weeks. The findings highlight the potential of regenerative medicine, which uses the body’s own mechanisms to repair damage. By targeting the aging process in joint cells, this therapy offers a breakthrough for osteoarthritis treatment. Millions of people suffering from joint pain, inflammation, and reduced mobility could benefit from this innovative approach. In the future, the researchers plan to explore ways to enhance the therapy, including whether repeated treatments could provide even longer-lasting benefits. These could lead to new options in treating osteoarthritis and other age-related conditions. “In addition to their anti-inflammatory and regenerative properties, our study confirms that ASC-EVs may be a relevant option for future clinical applications in degenerative diseases, such as OA, which are increasing with the population aging.” In conclusion, this research offers a promising regenerative therapy for osteoarthritis, with the potential to improve the quality of life for millions of older adults. DOI - https://doi.org/10.18632/aging.206158 Corresponding author - Danièle Noël - daniele.noel@inserm.fr Video short - https://www.youtube.com/watch?v=06qw2nR3ovY Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206158 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- December 17, 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 21 on November 29, 2024, entitled, “Thermotherapy has sexually dimorphic responses in APP/PS1 mice.” Researchers Samuel A. McFadden, Mackenzie R. Peck, Lindsey N. Sime, MaKayla F. Cox, Erol D. Ikiz, Caleigh A. Findley, Kathleen Quinn, Yimin Fang, Andrzej Bartke, Erin R. Hascup, and Kevin N. Hascup from Southern Illinois University School of Medicine, found that raising body temperature through heat therapy improved memory in male mice with Alzheimer’s disease but worsened memory in females. These findings emphasize the importance of personalized treatments based on sex-specific responses to therapy. Alzheimer’s disease (AD) is a progressive brain disorder characterized by memory loss and confusion. It is caused by the buildup of harmful proteins like beta-amyloid, which damages brain cells over time. In this study, genetically modified mice predisposed to develop Alzheimer disease (APP/PS1 mice) were kept in warmer environments for six months to explore the effects of heat therapy on memory and metabolism. The results revealed that male mice benefited from the therapy, with improved memory and reduced levels of beta-amyloid in their brains. Female mice, however, experienced a worsening of memory, likely due to increased inflammation triggered by the heat therapy. Inflammation, where the immune system is hyperactivated, can harm brain cells and worsen Alzheimer's disease symptoms. “Thermotherapy improved spatial navigation in male C57BL/6 and APP/PS1 mice, with the later attributed to reduced hippocampal soluble amyloid-β (Aβ)42. Female APP/PS1 mice exhibited worse spatial memory recall after chronic thermotherapy.” Heat therapy is already known to provide general health benefits, such as improving heart health and regulating blood sugar. This study suggests it could also offer a simple, non-drug approach to slowing Alzheimer’s progression, particularly for men. Unlike exercise, which offers similar benefits, heat therapy is accessible for people who are weak or unable to engage in physical activity. While these findings are promising, the researchers emphasize the need for more studies to understand why men and women respond so differently to heat therapy. Future research should also investigate whether the results can be replicated in humans and how the therapy can be tailored to individual needs. In conclusion, heat therapy could present a safe and practical option for managing Alzheimer’s disease, particularly in men. However, the observed gender differences highlight the importance of further research to refine its therapeutic potential and ensure it benefits everyone. DOI - https://doi.org/10.18632/aging.206156 Corresponding author - Kevin N. Hascup - khascup49@siumed.edu Video short - https://www.youtube.com/watch?v=IeMPHss4vj8 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- December 11, 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 21 on November 14, 2024, entitled, “Adolescents and young adults with sickle cell disease exhibit accelerated aging with elevated T-cell p16INK4a expression.” Researchers Samuel R. Wilson, Natalia Mitin, Vanessa L. Ayer Miller, Andrew B. Smitherman, and Marcus A. Carden, from the University of North Carolina at Chapel Hill, Sapere Bio, Campbell University, and Cogent Biosciences have discovered that young people with sickle cell disease (SCD) exhibit signs of accelerated biological aging compared to those without the disease. By measuring levels of p16INK4a, a key marker of cellular aging, the team found significantly higher levels in individuals with SCD. Remarkably, some participants showed biological aging equivalent to an additional 43 years. These findings suggest that SCD may drive faster aging in the body, offering new insights into the disease's long-term impact. Sickle cell disease (SCD) is a genetic condition primarily affecting individuals of African or Mediterranean descent. While treatments have advanced, people with SCD often face significant health challenges, including complications that mimic the effects of aging. Cellular aging, or senescence, occurs when cells stop dividing yet continue to send harmful signals that damage surrounding tissues. Researchers believe this process happens at an accelerated rate in people with SCD, underscoring the importance of finding ways to slow it down and mitigate its impact. The study compared p16INK4a levels in 18 adolescents and young adults with SCD to 27 healthy people of the same age. The results showed that even the youngest participant with SCD had higher levels of this aging marker than anyone in the non-SCD group. “Our youngest participant, a 15-year-old with SCD, had a higher p16 expression than all the comparators, underscoring the early rise of p16 expression in this population.” The researchers believe this faster aging could be caused by the chronic inflammation, lack of oxygen, and stress on the body associated with SCD. Along with managing the symptoms of the disease, SCD patients also face a higher risk of aging-related problems like organ damage and physical decline much earlier in life. The findings suggest that measuring p16INK4a levels could help clinicians identify patients at risk for these problems earlier and offer targeted care. The study also opens the door to new treatments, such as drugs that aim to remove old, damaged cells. These therapies could potentially slow down the aging process. Further research is essential to confirm these findings and to gain a deeper understanding of how to support SCD patients effectively. Larger, long-term studies could investigate whether therapies targeting cell aging can help prevent complications and improve the quality of life for individuals with SCD. In conclusion, this study marks an important step in understanding how SCD accelerates aging and offers new ways to improve the lives of those living with the condition. DOI - https://doi.org/10.18632/aging.206152 Corresponding author - Samuel R. Wilson - samuel.wilson@med.unc.edu Video short - https://www.youtube.com/watch?v=QXVdxBikaqg 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​​. MEDIA@IMPACTJOURNALS.COM

Sleep is essential for everyone, but for those living with dementia, it is vital for better health and quality of life. Addressing sleep problems in dementia care is a crucial step toward improving life for both patients and caregivers. Dementia and Sleep Sleep is critical for brain health and well-being, but it is often a struggle for people with dementia. Dementia, a condition that affects memory, thinking, and daily life, is frequently complicated by other health issues like heart disease, diabetes, and anxiety. On top of these challenges, sleep problems such as insomnia and sleep apnea are common, making life even harder for patients and their caregivers. Addressing sleep issues is key to improving the lives of people with dementia and easing the burden on their support systems. Recognizing this need, researchers Upasana Mukherjee, Ujala Sehar, Malcolm Brownell, and P. Hemachandra Reddy from Texas Tech University Health Sciences Center conducted an extensive review. Published in Aging, Volume 16, Issue 21, their work aims to update healthcare professionals on these issues and promote new practices in dementia care. The Study: Update on Sleep and Dementia’s Connection “Sleep deprivation in dementia comorbidities: focus on cardiovascular disease, diabetes, anxiety/depression and thyroid disorders” is a comprehensive review that explores the connections between sleep disturbances, dementia, and related conditions like heart disease, diabetes, and anxiety. Full blog - https://aging-us.org/2024/12/the-hidden-link-between-sleep-and-dementia-how-better-rest-can-improve-lives/ Paper DOI - https://doi.org/10.18632/aging.206157 Corresponding author - P. Hemachandra Reddy - hemachandra.reddy@ttuhsc.edu Video short - https://www.youtube.com/watch?v=lrrrXabMjjM Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206157 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, dementia and comorbidities, sleep disturbances, cardiovascular disease, diabetes, thyroid disorders, anxiety, insomnia, sleep apnea 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- December 10, 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 21 on November 18, 2024, entitled, “Prostaglandin E2 regulates senescence and post-senescence neoplastic escape in primary human keratinocytes.” Researchers Elise Srour, Nathalie Martin, Claire Drullion, Clémentine De Schutter, Joëlle Giroud, Adrien Pioger, Julie Deslé, Laure Saas, Joe Nassour, Julien Théry, Gauthier Decanter, Nicolas Penel, Chantal Vercamer, Clara Salazar-Cardozo, Corinne Abbadie, and Olivier Pluquet from CNRS, University of Lille, the Oscar Lambret Center, and the University of Colorado School of Medicine have revealed how a molecule called Prostaglandin E2 (PGE2) influences skin aging and cancer risk. Their study shows that PGE2 not only drives skin cells to age but also enables some of these aging cells to bypass natural limits and develop into pre-cancerous cells. This process provides insights into why older skin is more susceptible to cancer. The study focused on keratinocytes, the primary cells in the outer layer of the skin. As these cells age, they enter a state called senescence, where they stop dividing to prevent damaged cells from turning cancerous. While this process typically serves as a protective mechanism, the researchers found that, in certain cases, some senescent cells can escape this state, re-enter the cell cycle, and acquire characteristics of early cancer. By examining keratinocytes from donors of different ethnicities and ages, the researchers identified the PTGS2/PGE2/EP4 pathway as a key driver of this escape process. The researchers show that blocking PGE2 or its associated pathway reduced the chances of aged cells becoming precancerous. This suggests that drugs targeting this pathway, including some anti-inflammatory medications already in use, might be repurposed to slow skin aging and prevent early-stage skin cancers. Additionally, the study also found that PGE2 levels increase in the skin as it ages, further supporting its role in skin health and disease. "These results indicate that the PTGS2/PGE2/EP4 pathway is required to induce and maintain the senescent phenotype of NHEKs, and that PGE2 level is a potential determinant of the initial steps of the age-related oncogenic process." The team also highlighted the broader implications of their work. The PTGS2/PGE2/EP4 pathway is not only linked to skin health but also to age-related inflammation, a condition that contributes to several diseases. By addressing this pathway, researchers hope to address not only skin aging but other health challenges linked to aging and chronic inflammation. In conclusion, this study reveals important molecular drivers of skin aging and early cancer, leading the way for new approaches that can promote healthier skin. DOI - https://doi.org/10.18632/aging.206149 Corresponding author - Olivier Pluquet - olivier.pluquet@ibl.cnrs.fr Video short - https://www.youtube.com/watch?v=4aNf3X2RJSw 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

Discover how megakaryocytes, a type of bone marrow cell, can boost blood vessel growth to aid bone healing. The research reveals that younger megakaryocytes outperform older ones in stimulating endothelial cells. This finding sheds light on the reasons behind slower healing in older adults and opens the door to potential treatments that could dramatically improve recovery from fractures. Enhancing the healing process could have a profound impact on the quality of life for millions facing age-related complications.