Aging-US

Scientific integrity is a crucial component of scholarly publishing for any credible journal. Peer-reviewed, open-access journal Aging (listed as “Aging (Albany NY)” by Medline/PubMed and “Aging-US” by Web of Science) has recently presented its Scientific Integrity process. Launched in 2009, Aging is an open-access biomedical journal dedicated to publishing high-quality, aging-focused research. Aging publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Aging has a scientific integrity process to ensure that publications meet a number of scrupulous criteria for authenticity and integrity. Each published paper is thoroughly analyzed by diligent reviewers and services, including multiple in-house developed image forensics softwares. A growing industry of digital technologies, tools and ideas are constantly being added to Aging’s scientific integrity toolbox. Aging’s Scientific Integrity process is built upon six critical components: 1-Easily Accessible Ethics Statements 2-Devotion to Industry Standards for Scientific Publishing 3-Rigorous and Insightful Peer Review 4-Detection and Zero-Tolerance of Plagiarism 5-Leading-Edge Image Forensics 6-Post-Publication Investigations (if needed) The new webpage also depicts publishing statistics in a detailed graph —showcasing a visual representation of the number of post-publication corrections and retractions by Aging compared to the industry average, between 2010 and 2022. As of September 2022, Aging’s average rate of corrections/retractions since 2009 is a low 2.33%. The industry average correction/retraction rate is 3.80%. Aging’s highly-effective scientific integrity process allows researchers to read, share and cite Aging papers with confidence. Learn more about Aging’s Scientific Integrity Process: https://www.aging-us.com/scientific-integrity Video: https://www.youtube.com/watch?v=5wbStfARUlI Please visit our website at www.Aging-US.com​​ and connect with us socially: SoundCloud – https://soundcloud.com/Aging-Us Facebook – https://www.facebook.com/AgingUS/ Twitter – https://twitter.com/AgingJrnl Instagram – https://www.instagram.com/agingjrnl/ YouTube – https://www.youtube.com/agingus​ LinkedIn – https://www.linkedin.com/company/aging/ Reddit – https://www.reddit.com/user/AgingUS Pinterest – https://www.pinterest.com/AgingUS/ For media inquiries, please contact media@impactjournals.com

A new research perspective was published in Aging (listed as "Aging (Albany NY)" by MEDLINE/PubMed and "Aging-US" by Web of Science) Volume 14, Issue 20, entitled, “Rapamycin treatment early in life reprograms aging: hyperfunction theory and clinical practice.” On October 24, 2022, Mikhail Blagosklonny, M.D., Ph.D. from Roswell Park Comprehensive Cancer Center published a riveting research perspective discussing the clinical application of early-life rapamycin treatment and its ability to reprogram aging, based on the hyperfunction theory. “Making provocative headlines, three outstanding publications demonstrated that early-life treatment with rapamycin, including treatments during developmental growth, extends lifespan in animals, confirming predictions of hyperfunction theory, which views aging as a quasi-program (an unintended continuation of developmental growth) driven in part by mTOR. Despite their high theoretical importance, clinical applications of two of these studies in mice, Drosophila and Daphnia cannot be implemented in humans because that would require growth retardation started at birth. A third study demonstrated that a transient (around 20% of total lifespan in Drosophila) treatment with rapamycin early in Drosophila adult life is as effective as lifelong treatment, whereas a late-life treatment is not effective. However, previous studies in mice demonstrated that a transient late-life treatment is highly effective. Based on hyperfunction theory, this article attempts to reconcile conflicting results and suggests the optimal treatment strategy to extend human lifespan.” DOI: https://doi.org/10.18632/aging.204354 Corresponding Author: Mikhail V. Blagosklonny - Corresponding Email: Blagosklonny@oncotarget.com Video - https://www.youtube.com/watch?v=Br7iD48fKF4 Keywords: senescence, gerostatics, geroscience, sirolimus, healthspan Sign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204354 About Aging-US: Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at www.Aging-US.com​​ and connect with us: SoundCloud – https://soundcloud.com/Aging-Us Facebook – https://www.facebook.com/AgingUS/ Twitter – https://twitter.com/AgingJrnl Instagram – https://www.instagram.com/agingjrnl/ YouTube – https://www.youtube.com/agingus​ LinkedIn – https://www.linkedin.com/company/aging/ Reddit – https://www.reddit.com/user/AgingUS Pinterest – https://www.pinterest.com/AgingUS/ For media inquiries, please contact media@impactjournals.com Aging (Aging-US) Journal Office 6666 E. Quaker Str., Suite 1B Orchard Park, NY 14127 Phone: 1-800-922-0957, option 1

Dr. Ya-Jen Chiu from the Department of Life Science at National Taiwan Normal University in Taipei, discusses a research paper she co-authored that was published by Aging (Aging-US) in Volume 14, Issue 18, entitled, “Novel TRKB agonists activate TRKB and downstream ERK and AKT signaling to protect Aβ-GFP SH-SY5Y cells against Aβ toxicity.” DOI - https://doi.org/10.18632/aging.204306 Corresponding authors - Chiung-Mei Chen - cmchen@cgmh.org.tw, Ying-Chieh Sun - sun@ntnu.edu.tw, Guey-Jen Lee-Chen - t43019@ntnu.edu.tw Video - https://www.youtube.com/watch?v=1rT96K9VeZw Transcript - https://aging-us.net/2022/11/01/behind-the-study-novel-trkb-agonists-activate-trkb-and-downstream-erk-and-akt-signaling/ Abstract Decreased BDNF and impaired TRKB signaling contribute to neurodegeneration in Alzheimer's disease (AD). We have shown previously that coumarin derivative LM-031 enhanced CREB/BDNF/BCL2 pathway. In this study we explored if LM-031 analogs LMDS-1 to -4 may act as TRKB agonists to protect SH-SY5Y cells against Aβ toxicity. By docking computation for binding with TRKB using 7,8-DHF as a control, all four LMDS compounds displayed potential of binding to domain d5 of TRKB. In addition, all four LMDS compounds exhibited anti-aggregation and neuroprotective efficacy on SH-SY5Y cells with induced Aβ-GFP expression. Knock-down of TRKB significantly attenuated TRKB downstream signaling and the neurite outgrowth-promoting effects of these LMDS compounds. Among them, LMDS-1 and -2 were further examined for TRKB signaling. Treatment of ERK inhibitor U0126 or PI3K inhibitor wortmannin decreased p-CREB, BDNF and BCL2 in Aβ-GFP cells, implicating the neuroprotective effects are via activating TRKB downstream ERK, PI3K-AKT and CREB signaling. LMDS-1 and -2 are blood-brain barrier permeable as shown by parallel artificial membrane permeability assay. Our results demonstrate how LMDS-1 and -2 are likely to work as TRKB agonists to exert neuroprotection in Aβ cells, which may shed light on the potential application in therapeutics of AD. Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204306 Keywords - aging, Alzheimer’s disease, TRKB agonists, Aβ, neuroprotection, therapeutics About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

A new research paper was published on the cover of Aging (listed as "Aging (Albany NY)" by Medline/PubMed and "Aging-US" by Web of Science) Volume 14, Issue 20, entitled, “Downregulation of senescence-associated secretory phenotype by knockdown of secreted frizzled-related protein 4 contributes to the prevention of skin aging.” There is growing evidence that the appearance and texture of the skin that is altered during the aging process are considerably enhanced by the accumulation of senescent dermal fibroblasts. These senescent cells magnify aging via an inflammatory, histolytic, and senescence-associated secretory phenotype (SASP). Secreted frizzled-related protein 4 (SFRP4) was previously determined to be expressed in dermal fibroblasts of aging skin, and its increased expression has been shown to promote cellular senescence. However, its role in the SASP remains unknown. In this new study, researchers Kento Takaya, Toru Asou and Kazuo Kishi from Keio University School of Medicine’s Department of Plastic and Reconstructive Surgery investigated the classical model of skin fibroblasts based on Hayflick’s mitotic limit, the observation of SFRP4 expression in replicating senescent cells, and the effect of regulating this on the suppression of SASP and aging skin. “These results may contribute to the development of new therapies to ameliorate skin aging.” The researchers found that SFRP4 was significantly expressed in p16ink4a-positive human skin fibroblasts and that treatment with recombinant SFRP4 promoted SASP and senescence, whereas siRNA knockdown of SFRP4 suppressed SASP. They also found that knockdown of SFRP4 in mouse skin ameliorates age-related reduction of subcutaneous adipose tissue, panniculus carnosus muscle layer, and thinning and dispersion of collagen fibers. These findings suggest a potential candidate for the development of new skin rejuvenation therapies that suppress SASP. “This study shows that SFRP4, which is specifically expressed in aged p16ink4a-positive skin fibroblasts, contributes to SASP, and that treatment with SFRP4 causes worsening of this phenotype. To the best of our knowledge, the present study is the first to report that the suppression of SFRP4 expression in vivo ameliorates skin aging-related phenotypes, that is, adipose tissue atrophy and collagen fiber thinning, via SASP suppression.” DOI: https://doi.org/10.18632/aging.204273 Corresponding Author: Kento Takaya - Email: kento-takaya312@keio.jp Keywords: skin, fibroblast, SASP, SFRP4 Sign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204273 About Aging-US: Launched in 2009, Aging (Aging-US) publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at www.Aging-US.com​​ and connect with us: SoundCloud – https://soundcloud.com/Aging-Us Facebook – https://www.facebook.com/AgingUS/ Twitter – https://twitter.com/AgingJrnl Instagram – https://www.instagram.com/agingjrnl/ YouTube – https://www.youtube.com/agingus​ LinkedIn – https://www.linkedin.com/company/aging/ Reddit – https://www.reddit.com/user/AgingUS Pinterest – https://www.pinterest.com/AgingUS/ For media inquiries, please contact media@impactjournals.com. Aging (Aging-US) Journal Office 6666 E. Quaker Str., Suite 1B Orchard Park, NY 14127 Phone: 1-800-922-0957, option 1

Dr. Takushi Namba, Associate Professor at Kochi University in Japan, discusses a research paper he co-authored that was published by Aging (Aging-US) in Volume 14, Issue 19, entitled, “Lotus germ extract rejuvenates aging fibroblasts via restoration of disrupted proteostasis by the induction of autophagy.” DOI - https://doi.org/10.18632/aging.204303 Corresponding author - Takushi Namba - t-namba@kochi-u.ac.jp Video - https://www.youtube.com/watch?v=sXDw80HrqzM Abstract Cell aging attenuates cellular functions, resulting in time-dependent disruption of cellular homeostasis, which maintains the functions of proteins and organelles. Mitochondria are important organelles responsible for cellular energy production and various metabolic processes, and their dysfunction is strongly related to the progression of cellular aging. Here we demonstrate that disruption of proteostasis attenuates mitochondrial function before the induction of DNA damage signaling by proliferative and replicative cellular aging. We found that lotus (Nelumbo nucifera Gaertn.) germ extract clears abnormal proteins and agglutinates via autophagy-mediated restoration of mitochondrial function and cellular aging phenotypes. Pharmacological analyses revealed that DAPK1 expression was suppressed in aging cells, and lotus germ extract upregulated DAPK1 expression by stimulating the acetylation of histones and then induced autophagy by activating the DAPK1-Beclin1 signaling pathway. Furthermore, treatment of aging fibroblasts with lotus germ extract stimulated collagen production and increased contractile ability in three-dimensional cell culture. Thus, time-dependent accumulation of abnormal proteins and agglutinates suppressed mitochondrial function in cells in the early stage of aging, and reactivation of mitochondrial function by restoring proteostasis rejuvenated aging cells. Lotus germ extract rejuvenates aging fibroblasts via the DAPK1-Beclin1 pathway-induced autophagy to clear abnormal proteins and agglutinates. Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204303 Keywords - aging, mitochondria, autophagy, proteostasis About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

A new review paper was published in Aging (listed as "Aging (Albany NY)" by MEDLINE/PubMed and "Aging-US" by Web of Science) Volume 14, Issue 19, entitled, “RNA modifications in aging-associated cardiovascular diseases.” Cardiovascular disease (CVD) is a leading cause of morbidity and mortality worldwide that bears an enormous healthcare burden. Aging is a major contributing factor to CVDs. Functional gene expression network during aging is regulated by mRNAs transcriptionally and by non-coding RNAs epi-transcriptionally. RNA modifications alter the stability and function of both mRNAs and non-coding RNAs and are involved in differentiation, development and diseases. In this new review paper, researchers Xinyu Yang, Priyanka Gokulnath, H. Immo Lehmann, Zhitao Hou, Sun Yang, Liangzhen You, Guoxia Zhang, Yanwei Xing, Ji Lei, Guoping Li, Shuwen Guo, and Hongcai Shang from Fangshan Hospital and Dongzhimen Hospital (affiliated with Beijing University of Chinese Medicine), Massachusetts General Hospital, Harvard Medical School, Heilongjiang University of Chinese Medicine, and Chinese Academy of Chinese Medical Sciences reviewed major chemical RNA modifications on mRNAs and non-coding RNAs, including N6-adenosine methylation, N1-adenosine methylation, 5-methylcytidine, pseudouridylation, 2′ -O-ribose-methylation, and N7-methylguanosine, in the aging process with an emphasis on cardiovascular aging. They also summarize the currently available methods to detect RNA modifications and the bioinformatic tools to study RNA modifications. “More importantly, we discussed the specific implication of the RNA modifications on mRNAs and non-coding RNAs in the pathogenesis of aging-associated CVDs, including atherosclerosis, hypertension, coronary heart diseases, congestive heart failure, atrial fibrillation, peripheral artery disease, venous insufficiency, and stroke.” DOI: https://doi.org/10.18632/aging.204311 Corresponding Authors: Guoping Li; Shuwen Guo; Hongcai Shang - Corresponding Emails: gli21@mgh.harvard.edu; guo1163@163.com; shanghongcai@bucm.edu.cn Keywords: RNA modifications, aging, aging-related cardiovascular diseases, epitranscriptome Sign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204311 About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Listen to a blog summary of a trending research paper published by Aging (Aging-US) in Volume 14, Issue 19, entitled, “Natural variation in macrophage polarization and function impact pneumocyte senescence and susceptibility to fibrosis.” ______________________________________ Radiation is an effective treatment for many types of cancer. Unfortunately, this treatment has the potential to cause long-term side effects in some patients, including the thickening or scarring of lung tissue, known as pulmonary fibrosis. Radiation-induced pulmonary fibrosis (RIPF) is a serious complication that can occur after radiation therapy and can lead to death. Predicting an individual’s risk of developing RIPF remains challenging for clinicians, as little is known about the underlying mechanisms that cause it. “Differential susceptibility to lung injury from radiation and other toxic insults across mouse strains is well described but poorly understood.” Previous studies in mouse models have shown that there are natural variations in susceptibility to RIPF among different strains of mice. The mechanism(s) underlying this difference in susceptibility is still unknown. In a new study, researchers Eun Joo Chung, Seokjoo Kwon, Uma Shankavaram, Ayla O. White, Shaoli Das, and Deborah E. Citrin from the National Institutes of Health’s National Cancer Institute investigated differences in macrophage function across mouse strains and their potential contribution to varied RIPF susceptibility. On September 28, 2022, their research paper was published in Aging’s Volume 14, Issue 19, “Natural variation in macrophage polarization and function impact pneumocyte senescence and susceptibility to fibrosis.” Full blog - https://aging-us.org/2022/10/investigating-susceptibility-to-radiation-induced-pulmonary-fibrosis/ DOI - https://doi.org/10.18632/aging.204309 Corresponding author - Deborah E. Citrin - citrind@mail.nih.gov Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204309 Keywords - aging, senescence, macrophage, alveolar epithelial cell Type II, strain About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

Fedor Galkin, Scientific Director at Deep Longevity, Inc. in Hong Kong, discusses a research paper he co-authored that was published by Aging (Aging-US) as the cover for Volume 14, Issue 18, entitled, “Psychological factors substantially contribute to biological aging: evidence from the aging rate in Chinese older adults.” DOI - https://doi.org/10.18632/aging.204264 Corresponding author - Fedor Galkin - fedor@deeplongevity.com Video - https://www.youtube.com/watch?v=WBxTe1fGPxI Abstract We have developed a deep learning aging clock using blood test data from the China Health and Retirement Longitudinal Study, which has a mean absolute error of 5.68 years. We used the aging clock to demonstrate the connection between the physical and psychological aspects of aging. The clock detects accelerated aging in people with heart, liver, and lung conditions. We demonstrate that psychological factors, such as feeling unhappy or being lonely, add up to 1.65 years to one’s biological age, and the aggregate effect exceeds the effects of biological sex, living area, marital status, and smoking status. We conclude that the psychological component should not be ignored in aging studies due to its significant impact on biological age. Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204264 Press release - https://www.aging-us.com/news_room/Psychological-factors-substantially-contribute-to-biological-aging-evidence-from-the-aging-rate-in-Chinese-older-adults Keywords - aging, psychological aging, lifespan psychology, aging clocks, longevity About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM

A new research paper was published on the cover of Aging (listed as "Aging (Albany NY)" by Medline/PubMed and "Aging-US" by Web of Science) Volume 14, Issue 19, entitled, “Centenarians consistently present a younger epigenetic age than their chronological age with four epigenetic clocks based on a small number of CpG sites.” Aging is a progressive time-dependent biological process affecting differentially individuals, who can sometimes present exceptional longevity. Epigenetic alterations are one of the hallmarks of aging, which comprise the epigenetic drift and clock at DNA methylation level. In a new study, researchers Antoine Daunay, Lise M. Hardy, Yosra Bouyacoub, Mourad Sahbatou, Mathilde Touvier, Hélène Blanché, Jean-François Deleuze, and Alexandre How-Kit from Foundation Jean Dausset – CEPH, Laboratory of Excellence GenMed, Sorbonne Paris Nord University, University of Paris (CRESS), and Institut François Jacob investigated the DNA methylation-based age (DNAmage) of long-lived French individuals in the CEPH Aging Cohort using four epigenetic clocks. “In the present study, we estimated the DNA methylation-based age (DNAmage) using four epigenetic clocks based on a small number of CpGs in French centenarians and semi-supercentenarians (CSSC, n=214) as well as nonagenarians' and centenarians' offspring (NCO, n=143) compared to individuals from the French general population (CG, n=149).” DNA methylation analysis of the nine CpGs included in the epigenetic clocks showed high correlation with chronological age (-0.66>R>0.54) and also the presence of an epigenetic drift for four CpGs that was only visible in CSSC. DNAmage analysis showed that CSSC and to a lesser extend NCO present a younger DNAmage than their chronological age (15-28.5 years for CSSC, 4.4-11.5 years for NCO and 4.2-8.2 years for CG), which were strongly significant in CSSC compared to CG (p-values<2.2e-16). These differences suggest that epigenetic aging and potentially biological aging are slowed in exceptionally long-lived individuals and that epigenetic clocks based on a small number of CpGs are sufficient to reveal alterations of the global epigenetic clock. “This suggests a decelerated epigenetic and biological aging in these two groups of individuals, confirming the results of three other studies performed on Italian, Australian and Israeli long-lived individuals. In addition, our study also demonstrated the possibility of using epigenetic clocks based on a small number of CpG sites to reveal DNAmage and chronological age differences between individuals with different life expectancy.” DOI: https://doi.org/10.18632/aging.204316 Corresponding Author: Alexandre How-Kit - Email: alexandre.how-kit@fjd-ceph.org Keywords: epigenetic clock, DNAmage, centenarians, DNA methylation, pyrosequencing, longevity Sign up for free Altmetric alerts about this article: https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204316 About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/

Blog summary of a trending research paper published in Volume 14, Issue 18, entitled, "The association between continuous ambulatory heart rate, heart rate variability, and 24-h rhythms of heart rate with familial longevity and aging." ______________________________________ A normal resting heart rate (HR) for adults should be anywhere between 60 and 100 beats per minute. A low resting heart rate has been associated with better overall health and fitness. Crosswise, a higher resting heart rate appears to have a strong correlation with mortality. Heart rate variability (HRV), the beat-to-beat changes in heart rate, is indicative of the heart’s ability to respond to changes in physical and emotional stress. Low HRV has been shown to be a risk factor for heart disease, while high HRV has been associated with good heart health. Although HR and HRV are frequently studied, these parameters are not often investigated continuously or over long periods of time in healthy, middle-aged individuals. “Parameters of HR and HRV are often investigated during a short electrocardiogram (ECG) measurement at the study center or in the hospital, but not continuously over a longer period while individuals continue with their daily lives.” In a new study, researchers Janneke M. Wiersema, Annelies E.P. Kamphuis, Jos H.T. Rohling, Laura Kervezee, Abimbola A. Akintola, Steffy W. Jansen, P. Eline Slagboom, Diana van Heemst, and Evie van der Spoel from Leiden University Medical Center and Catharina Hospital used continuous ambulatory ECG measurements collected over a period of 24 to 90 hours to investigate the relationship between heart rate parameters and familial longevity and chronological age. On August 16, 2022, their research paper was published in Aging’s Volume 14, Issue 18, and entitled, “The association between continuous ambulatory heart rate, heart rate variability, and 24-h rhythms of heart rate with familial longevity and aging.” Full blog - https://aging-us.org/2022/10/does-a-link-exist-between-longevity-aging-and-heart-rate-parameters/ DOI - https://doi.org/10.18632/aging.204219 Corresponding author - Evie van der Spoel - e.van_der_spoel@lumc.nl Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.204219 Keywords - aging, longevity, continuous ambulatory measurements, heart rate, heart rate variability About Aging-US Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways. Please visit our website at https://www.Aging-US.com​​ and connect with us: SoundCloud - https://soundcloud.com/Aging-Us Facebook - https://www.facebook.com/AgingUS/ Twitter - https://twitter.com/AgingJrnl Instagram - https://www.instagram.com/agingjrnl/ YouTube - https://www.youtube.com/agingus​ LinkedIn - https://www.linkedin.com/company/aging/ Pinterest - https://www.pinterest.com/AgingUS/ Media Contact 18009220957 MEDIA@IMPACTJOURNALS.COM