BUFFALO, NY — April 3, 2025 — Aging (Aging-US) is pleased to announce a special Call for Papers for a commemorative collection honoring the legacy of Dr. Mikhail (Misha) Blagosklonny, the founding editor of the journal and a pioneer in aging biology. His groundbreaking work shaped fundamental concepts in the field, particularly regarding the role of mTOR in aging and cancer, the use of rapamycin, bypassing senescence during the process of transformation, personalized medicine, and theories on why we age. This special collection will explore key themes central to Dr. Blagosklonny’s scientific contributions, with a focus on mechanistic insights, translational approaches, and theoretical perspectives. We invite original research, reviews, and perspective articles covering topics such as: The role of mTOR in aging and age-related diseases Rapamycin and other pharmacological strategies to extend lifespan Senescence bypass and its implications for cancer and regenerative medicine Personalized medicine approaches in aging and longevity research Theoretical models and evolutionary perspectives on aging The special issue will be guest-edited by leading scientist in the field, David Gems, who will oversee the selection of high-quality contributions that reflect the depth and impact of Dr. Blagosklonny’s work. We encourage researchers working on these topics to submit their manuscripts and contribute to this tribute to one of the most influential figures in aging research. SUBMISSION DETAILS: Submission Deadline: December 1, 2025 Manuscript Format: Please follow the journal’s submission guidelines Peer Review: All submissions will undergo a rigorous peer-review process Submission Link: https://aging.msubmit.net/cgi-bin/main.plex We look forward to your contributions to this special issue and to honoring Dr. Blagosklonny’s enduring impact on the field of aging research. To learn more about Aging (Aging-US), 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

Could a class of drugs that clear aging cells also help treat Alzheimer’s disease? A recent study, featured as the cover for Aging (Volume 17, Issue 3), titled “Differential senolytic inhibition of normal versus Aβ-associated cholinesterases: implications in aging and Alzheimer’s disease,” suggests they might—and with remarkable precision. Understanding Alzheimer’s Disease Alzheimer’s disease is a progressive neurological disorder that gradually steals memory, independence, and a person’s sense of identity. A defining feature of Alzheimer’s is the buildup of amyloid-β (Aβ) plaques—sticky protein clumps that interfere with communication between brain cells. This disruption is closely linked to changes in a group of enzymes called cholinesterases, especially acetylcholinesterase (AChE) and butyrylcholinesterase (BChE). These enzymes normally play a vital role in regulating neurotransmitters critical for memory, learning, and cognitive function. In Alzheimer’s, however, their behavior changes significantly, particularly when they interact with Aβ plaques. The Study: Exploring Senolytics for Alzheimer’s Enzyme Inhibition A research team from Dalhousie University in Canada looked into whether senolytic compounds—a class of drugs that eliminate damaged, aging cells often referred to as “zombie” cells—could also target the harmful forms of cholinesterase enzymes found in Alzheimer’s disease. Their goal was to see if these compounds could selectively inhibit the disease-associated versions of AChE and BChE, without affecting the healthy forms that are essential for normal brain function. Full blog - https://aging-us.org/2025/04/senolytic-compounds-show-promise-in-targeted-alzheimers-treatments/ DOI - https://doi.org/10.18632/aging.206227 Corresponding author - Sultan Darvesh - sultan.darvesh@dal.ca Video short - https://www.youtube.com/watch?v=CJQFpG9Jn6Y Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206227 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, cellular senescence, β-amyloid, acetylcholinesterase, butyrylcholinesterase, cholinesterase inhibitors 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 — April 1, 2025 — A new #research paper was #published in Aging (Aging-US) on March 29, 2025, as the #cover of Volume 17, Issue 3, titled “Differential senolytic inhibition of normal versus Aβ-associated cholinesterases: implications in aging and Alzheimer’s disease.” In this study, a research team from Dalhousie University, led by Sultan Darvesh, discovered that certain anti-aging compounds, known as senolytics, can block harmful brain enzymes linked to Alzheimer’s disease (AD) without affecting healthy ones. Senolytics are compounds that help clear out damaged or “zombie” cells that build up with age and contribute to inflammation and tissue dysfunction. This work provides new insight into how AD-related damage can be precisely targeted, leading the way for safer treatments that protect memory and brain health in older adults. Alzheimer’s disease is one of the most common causes of memory loss and dementia. A hallmark of the disease is the buildup of sticky protein clumps in the brain, known as amyloid-beta plaques. Two enzymes—acetylcholinesterase (AChE) and butyrylcholinesterase (BChE)—are found near these plaques. While these enzymes play important roles in brain function, they can also contribute to AD progression when they attach to plaques. Drugs that target these enzymes are already used to help with memory, but they often block both harmful and healthy forms, which can cause unwanted side effects. To investigate a better solution, researchers tested six compounds that are known for their anti-aging or brain-boosting properties. They wanted to know if these compounds could block only the harmful AChE and BChE enzymes forms linked to Alzheimer’s disease. Using brain tissue samples from AD patients and enzyme activity assays, they discovered that compounds such as dasatinib and nintedanib, both senolytics, were able to block the forms of AChE and BChE associated with amyloid-beta plaques. These compounds did not affect normal brain enzymes, though. “We show that the selected senolytics and nootropic inhibit ChEs associated with plaques but not the enzymes associated with normal neural elements.” The study also used computer modeling to explore how these compounds interact with the enzymes. The models showed that the enzymes change shape when near plaques, making them easier for certain compounds to target. This change may explain how the drugs can selectively affect only the diseased areas of the brain. While not all compounds worked equally well, the findings offer a new strategy for treating AD. By focusing on the differences between healthy and diseased enzyme forms, researchers may be able to design more precise and effective therapies. This selective approach could improve memory, reduce inflammation, and avoid the side effects of AD’s current treatments. In summary, this research opens new possibilities for treating Alzheimer’s disease in a more targeted way. It also highlights how discoveries in aging and brain health can work together to create better therapies for neurodegenerative diseases. DOI - https://doi.org/10.18632/aging.206227 Corresponding author - Sultan Darvesh - sultan.darvesh@dal.ca Video short - https://www.youtube.com/watch?v=CJQFpG9Jn6Y Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206227 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts 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 — March 26, 2025 — A new #research paper was #published in Aging (Aging-US) on January 29, 2025, in Volume 17, Issue 2, titled “Diet, lifestyle and telomere length: using Copula Graphical Models on NHANES data.” Researchers Angelo M. Tedaldi, Pariya Behrouzi, and Pol Grootswagers from Wageningen University and Research used data from the National Health and Nutrition Examination Survey (NHANES) to explore how diet and lifestyle affect telomere length, a key marker of cellular aging. They found that inflammation—rather than diet, exercise, or smoking—had the strongest and most consistent association to telomere shortening. The findings suggest that reducing inflammation may be more effective than dietary changes in slowing down the aging process at the cellular level. Telomeres are protective caps at the ends of chromosomes that get shorter as we age. When they become too short, cells lose the ability to divide properly, which can contribute to aging and age-related diseases. Previous studies suggested that healthy habits might protect telomeres, but many focused on a small number of factors and did not account for important elements like inflammation or differences in blood cell composition. This study aimed to take a more complete, data-driven approach. The research team analyzed health data from over 7,000 U.S. adults collected between 1999 and 2002. Using a method called Copula Graphical Modeling, they examined more than 100 variables—such as diet, physical activity, smoking, and blood biomarkers—across three age groups: Young (20–39 years), Middle (40–59 years), and Old (60–84 years). They found that telomere length was most strongly associated to age, levels of C-reactive protein (CRP)—a common marker of inflammation—and gamma-tocopherol, a form of vitamin E found in the blood. Higher CRP levels were consistently associated with shorter telomeres, especially in younger and middle-aged adults. The results suggest that while lifestyle factors like diet and exercise still play a role, their impact on aging may be indirect—mainly through their influence on inflammation. This finding shifts the focus toward managing chronic inflammation as a potentially more effective way to preserve telomere length and promote healthy aging. “The central role played by CRP and the marginal role of antioxidants suggests that telomeres are particularly vulnerable not to oxidative stress, but to inflammation; and they should be protected against it.” The study challenges earlier research that looked at individual lifestyle factors isolated. By using a more advanced and inclusive method, this analysis offers a clearer picture of how health behaviors, biological markers, and aging are connected. Although this research cannot prove a cause-and-effect relationship, it strongly supports the idea that inflammation plays a key role in cellular aging. The authors recommend further long-term studies to better understand how inflammation affects telomere length over time. In the meantime, reducing chronic inflammation may be one of the most important steps to help support healthy aging and reduce the risk of age-related diseases. DOI - https://doi.org/10.18632/aging.206194 Corresponding author - Angelo M. Tedaldi - angelomt1999@gmail.com Video short - https://www.youtube.com/watch?v=C2yXfF7iY6c Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts 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 — March 25, 2025 — A new #research paper was #published in Aging (Aging-US) on January 31, 2025, in Volume 17, Issue 2, titled “Cysteinyl leukotriene receptor 1 modulates retinal immune cells, vascularity and proteolytic activity in aged mice.” The study, led by first author and corresponding author Andreas Koller from the University Hospital of the Paracelsus Medical University, found that blocking an inflammatory receptor called CysLTR1 in the retinas of aging mice improved retinal health. These findings suggest a new approach to slowing age-related vision loss and protecting eye health in older adults. Age-related vision problems are a growing concern worldwide, and inflammation plays a key role in damaging the retina over time. The retina is the part of the eye that captures light and sends visual signals to the brain, making it vital for clear eyesight. In this study, scientists focused on the CysLTR1 receptor, which is known to promote inflammation and is found in high amounts in the retina. They explored whether blocking this receptor could reduce the harmful effects of aging in the eye. To achieve this, researchers treated aged mice with montelukast (MTK), a drug commonly used for asthma, which specifically blocks CysLTR1. The oral treatment lasted eight weeks and results were compared with both untreated aged mice and healthy young mice. After treatment, the older mice showed major improvements in retinal health. One key finding was a reduction in immune cells called microglia, which tend to increase with age and contribute to chronic inflammation in the retina. With CysLTR1 blocked, the number of these immune cells dropped significantly, suggesting reduced retinal inflammation. Lower inflammation is linked to a lower risk of age-related eye diseases like macular degeneration. “The reduction in immune cells caused by Cysltr1 suppression may dampen neuroinflammation, a known promoter of tissue aging.” Another important result was the restoration of blood vessel function. The tiny blood vessels in the retina had narrowed in aging mice, reducing blood flow and oxygen supply to the eye. MTK treatment increased the diameter of these vessels, improving circulation and possibly helping the retina work more efficiently. The study also indicated that blocking CysLTR1 helped boost the retina’s natural ability to clear out waste proteins. As we age, this cleaning process slows down, allowing harmful material to build up in the eye. After treatment, the aged mice had stronger proteasome activity—the system responsible for breaking down cellular waste—and fewer signs of waste accumulation. Importantly, the treatment did not harm retinal nerve cells, which are essential for vision. This evidence indicates that the therapy was not only effective but also safe. While more research is needed to confirm these results in humans, this study highlights the potential of repurposing MTK to protect against age-related vision decline. Because it is already an approved drug, testing it for age-related eye diseases like macular degeneration or diabetic retinopathy could move forward more quickly. Blocking inflammation and supporting the eye’s natural cleaning systems may be a promising new way to preserve healthy vision in aging populations. DOI - https://doi.org/10.18632/aging.206193 Corresponding author - Andreas Koller - a.koller@salk.at Video short - https://www.youtube.com/watch?v=ngnrPJzHlpI 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

In this installment of the Longevity & Aging Series, Dr. Julia Sidorova from the Department of Laboratory Medicine and Pathology at the University of Washington (Seattle, WA) joined host Dr. Evgeniy Galimov to discuss her co-authored research paper from Volume 16, Issue 20 of Aging (Aging-US), titled “Werner syndrome RECQ helicase participates in and directs maintenance of the protein complexes of constitutive heterochromatin in proliferating human cells.” DOI - https://doi.org/10.18632/aging.206132 Corresponding Author - Julia M. Sidorova - julias@uw.edu Video interview - https://www.youtube.com/watch?v=3yn8O-JA6GE Abstract Werner syndrome of premature aging is caused by mutations in the WRN RECQ helicase/exonuclease, which functions in DNA replication, repair, transcription, and telomere maintenance. How the loss of WRN accelerates aging is not understood in full. Here we show that WRN is necessary for optimal constitutive heterochromatin levels in proliferating human fibroblasts. Locally, WRN deficiency derepresses SATII pericentromeric satellite repeats but does not reduce replication fork progression on SATII repeats. Globally, WRN loss reduces a subset of protein-protein interactions responsible for the organization of constitutive heterochromatin in the nucleus, namely, the interactions involving Lamin B1 and Lamin B receptor, LBR. Both the mRNA level and subcellular distribution of LBR are affected by WRN deficiency, and unlike the former, the latter phenotype does not require WRN catalytic activities. The phenotypes of heterochromatin disruption seen in WRN-deficient proliferating fibroblasts are also observed in WRN-proficient fibroblasts undergoing replicative or oncogene-induced senescence. WRN interacts with histone deacetylase 2, HDAC2; WRN/HDAC2 association is mediated by heterochromatin protein alpha, HP1α, and WRN complexes with HP1α and HDAC2 are downregulated in senescing cells. The data suggest that the effect of WRN loss on heterochromatin is separable from senescence program, but mimics at least some of the heterochromatin changes associated with it. 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. 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

Could the air we breathe, the food we eat, or the chemicals in our everyday environment be accelerating our aging process? A recent study published in Aging suggests that exposure to certain environmental chemicals may be linked to faster biological aging through changes in DNA. These findings could have major implications for public health and longevity. Understanding How Scientists Measure Aging at the DNA Level Aging is not just about wrinkles and gray hair—it happens at the molecular level too. Scientists use epigenetic clocks to measure biological aging, which can differ from a person’s actual chronological age. These clocks track DNA methylation, a type of chemical modification that can change over time due to environmental factors like diet, pollution, and chemical exposure. Until now, there has been little research into how widespread environmental chemicals impact these aging markers. The Study: Investigating the Impact of Environmental Pollutants on Aging A research team led by first author Dennis Khodasevich and corresponding author Andres Cardenas from Stanford University, conducted an exposome-wide association study to examine how different environmental pollutants affect epigenetic aging. Using data from the National Health and Nutrition Examination Survey (NHANES), they analyzed blood and urine samples from 2,346 adults aged 50 to 84. The study measured 64 environmental chemicals, including heavy metals, pesticides, plastics, and tobacco-related compounds, to identify potential links to accelerated aging. The study titled “Exposome-wide association study of environmental chemical exposures and epigenetic aging in the national health and nutrition examination survey,” was published in Aging on February 11, 2025. Full blog - https://aging-us.org/2025/03/how-environmental-chemicals-may-accelerate-biological-aging/ Paper DOI - https://doi.org/10.18632/aging.206201 Corresponding author - Andres Cardenas - andresca@stanford.edu Video short - https://www.youtube.com/watch?v=WcL-K399a7M Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.206201 Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts Keywords - aging, epigenetic aging, environmental exposures, exposome, epigenetics 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 — March 19, 2025 — A new #research paper was #published in Aging (Aging-US) on February 27, 2025, in Volume 17, Issue 2, titled “Age, sex, and mitochondrial-haplotype influence gut microbiome composition and metabolites in a genetically diverse rat model.” The research team, led by first author Hoang Van M. Nguyen and corresponding author Archana Unnikrishnan from the University of Oklahoma Health Sciences, studied how aging affects gut bacteria in a special group of rats generated to have genetic diversity similar to humans. Their research found that both biological sex and mitochondrial DNA—the small set of genes inherited only from mothers—play a key role in how gut bacteria change over time. The gut microbiome, a collection of bacteria in the intestines, affects digestion, metabolism, and even brain function. As people age, these bacteria shift, and some of these changes are linked to diseases like Alzheimer’s, Parkinson’s, and metabolic disorders. However, most studies have looked at either men or women without comparing differences between sexes, and few have explored how mitochondrial DNA might influence these changes. To better understand these factors, researchers analyzed fecal samples from the genetically diverse rats to assess gut bacteria composition and metabolic byproducts. The results showed that aging affects gut bacteria differently in males and females. More bacterial species changed with age in female rats than in males, and only a few changes were consistent across both sexes. These findings suggest that men and women may experience aging differently at the microbial level, which could impact nutrition and disease risk. “Five microbial species changed significantly with age in male rats compared to nine microbial species in female rats. Only three of these microbes changed with age in both male and female rats.” Another key discovery was that mitochondrial DNA influences how gut bacteria evolve with age. These effects were different in males and females, suggesting a deeper connection between mitochondrial function and gut health, with potential implications for personalized medicine and aging research. In addition to studying bacteria, the researchers analyzed metabolic compounds such as short-chain fatty acids and bile acids, which help with digestion. They found that aging altered these compounds based on both sex and mitochondrial DNA. For example, older female rats had higher levels of short-chain fatty acids in their feces, possibly due to differences in nutrient absorption. This study highlights new factors that shape the gut microbiome in aging populations. Understanding how biological sex and mitochondrial DNA influence these changes could lead to targeted approaches for maintaining gut health and preventing age-related diseases. These findings reinforce the importance of personalized health strategies that consider both genetic and biological differences. DOI - https://doi.org/10.18632/aging.206211 Corresponding author - Archana Unnikrishnan - archana-unnikrishnan@ouhsc.edu Video short - https://www.youtube.com/watch?v=RtsqRi2_uAI 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. 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 — March 18, 2025 — A new #research paper was #published by Aging (Aging-US) on March 7, 2025, titled “Accelerated aging associated with cancer characteristics and treatments among breast cancer survivors.” Led by first author Cong Wang and corresponding author Xiao-Ou Shu from Vanderbilt University, this study examines how breast cancer and its treatments contribute to accelerated aging in survivors. Their study revealed that breast cancer patients show signs of faster biological aging compared to cancer-free individuals, with long-term effects lasting up to ten years post-diagnosis. This finding raises concerns about the potential lasting impact of cancer therapies on aging and overall health. Breast cancer is one of the most common cancers in women worldwide, with improved treatments leading to longer survival rates. However, emerging evidence suggests that these treatments may also accelerate aging. The study used Phenotypic Age Acceleration (PAA), a biological marker that estimates a person’s aging rate based on blood tests. Researchers compared data from 1,264 breast cancer patients and 429 cancer-free controls. The results indicated that breast cancer survivors had significantly higher PAA at diagnosis and continued to show signs of accelerated aging up to ten years later. “This is the first large study with 10 years of follow-up to evaluate PAA among BC survivors.” The study found that tumor severity played a role in aging acceleration. Women with advanced-stage (Stage III/IV) or high-grade tumors showed the highest levels of aging acceleration. Additionally, treatments such as chemotherapy and endocrine therapy were linked to increased biological aging. One year after diagnosis, chemotherapy was associated with the most significant rise in PAA, while endocrine therapy had long-term effects, increasing aging markers even ten years after treatment. Interestingly, not all cancer treatments had the same effect. Surgery and radiation therapy were associated with lower aging acceleration over time. These findings suggest that systemic therapies, which affect the whole body, may contribute more to aging-related changes than localized treatments. The findings highlight the need for ongoing monitoring of breast cancer survivors beyond their initial recovery. Understanding how cancer treatments influence aging can help improve post-treatment care and potentially lead to strategies that reduce these effects. Further research is needed to explore whether lifestyle changes, medications, or other interventions could slow down aging in cancer survivors. As the number of breast cancer survivors continues to grow, addressing the long-term health consequences of cancer treatment is crucial. This study provides valuable insights into how different factors contribute to accelerated aging, helping to shape future research and healthcare approaches for breast cancer survivors. DOI - https://doi.org/10.18632/aging.206218 Corresponding author - Xiao-Ou Shu - xiao-ou.shu@vumc.org Video short - https://www.youtube.com/watch?v=cfuyzVyDeHY 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. 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 — March 17, 2025 — Impact Journals (Aging’s publisher) is pleased to announce its participation as an exhibitor at theAmerican Association for Cancer Research (AACR) Annual Meeting 2025. The meeting is scheduled for April 25-30, 2025, at the McCormick Place Convention Center in Chicago, Illinois. This 2025 AACR Annual Meeting theme, “Unifying Cancer Science and Medicine: A Continuum of Innovation for Impact,” highlights significant advancements and groundbreaking discoveries in cancer research. Aging closely aligns with this mission, dedicated to disseminating impactful scientific research at the intersection of oncology and gerontology. Visit Booth 2815 to meet directly with members of the Aging team, explore the latest research publications, and discuss opportunities for collaboration and manuscript submissions. Aging, supported by its publisher Impact Journals, remains dedicated to promoting innovation, collaboration, and advancing scientific knowledge in aging-related cancer research. 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