Our bodies are quite miraculous machines. We are born with a genome that contains the code for every protein necessary for survival. We develop and produce hormones that allow us to reproduce and have children. But what happens to us as we age? This question has puzzled scientists for years while they offer theory after theory.

In 1957, evolutionary biologist George Williams proposed what he called the antagonistic pleiotropy hypothesis as a theory of how and why we age. He claimed that our bodies express a gene that has benefits for our early life, but that same gene will harm us later on. His hypothesis has inspired aging research and led to a story about a chemical discovered deep within the dirt of an island floating in the Pacific.

In 1964, Canadian researchers, led by Stanley Skoryna from McGill University, set sail out of Halifax for Easter Island—a speck of land floating 2,000 miles off the coast of Chile, where the human population is small but life is diverse. They were hoping to retrieve precious specimens from the island before its land was tarnished with the building of a new airport. Stanley and his team collected hundreds of plant samples, countless animal specimens, and took blood and saliva from all 949 of the island’s residents.

What they found buried in the dirt on Easter Island would turn out to be the biggest treasure of all: a bacteria that would mystify scientists for the next 50 years. This bacteria was found to create a chemical now known as rapamycin, cleverly named after Easter Island’s native name, Rapa Nui.

Read the full article: https://www.impactjournals.com/journals/blog/aging/rapamycin-miracle-chemical-discovered-easter-islands-dirt/

About Aging

Launched in 2009, 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. 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 http://www.Aging-US.com​​ or connect with us on:

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Aging

Rapamycin: The Miracle Compound From Easter Island

BUFFALO, NY- May 11, 2022 – A new research perspective was published in Oncoscience journal by Mikhail Blagosklonny, M.D., Ph.D., entitled, “Altos Labs and the quest for immortality: but can we live longer right now?”

“Here I discuss how combining rapamycin with other modalities may let us live long enough to benefit from future discoveries in cellular reprogramming and what needs to be done at Altos Labs to make this happen.”

Altos Labs—a new anti-aging biotechnology company funded by multiple billionaire investors, including Jeff Bezos and Yuri Milner—has reported a focus on reprogramming cells in order to reverse the trajectory of diseases, and thus, reverse aging.

In his research perspective, Dr. Blagosklonny writes that potential life-extension with rapamycin may allow us to win time while awaiting future discoveries that will reverse aging.

“Rapamycin treatment is rapidly becoming a mainstream anti-aging intervention.” 

However, Dr. Blagosklonny also writes that rapamycin alone is unlikely to extend lifespan sufficiently to benefit from Altos Labs’ future discoveries in our lifetime.

“If Altos Labs would allocate a small percentage of its funding to develop rapamycin based drug combinations, then additional decades of life extension may be available 3–5 years from now.”

“The number of potential combinations with rapamycin is enormous.” 

Read Dr. Blagosklonny’s research perspective: https://www.oncoscience.us/article/552/text/ 

Correspondence to: Mikhail V. Blagosklonny 

Email: Blagosklonny@oncotarget.com, Blagosklonny@rapalogs.com 

Keywords: aging, longevity, lifespan, geroscience, rapalogs, gerostatics

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Aging (Aging-US)

Press Release: Altos Labs Research Perspective by Dr. Blagosklonny

Crossref is a non-profit organization that logs and updates citations for scientific publications. Each month, Crossref identifies a list of the most popular Aging (Aging-US) papers based on the number of times a DOI is successfully resolved. 

Below are Crossref’s Top 10 Aging DOIs in 2023.

10: Old-age-induced obesity reversed by a methionine-deficient diet or oral administration of recombinant methioninase-producing Escherichia coli in C57BL/6 mice

DOI: https://doi.org/10.18632/aging.204783

Authors: Yutaro Kubota, Qinghong Han, Jose Reynoso, Yusuke Aoki, Noriyuki Masaki, Koya Obara, Kazuyuki Hamada, Michael Bouvet, Takuya Tsunoda, and Robert M. Hoffman

9: Metformin use history and genome-wide DNA methylation profile: potential molecular mechanism for aging and longevity

DOI: https://doi.org/10.18632/aging.204498 

Authors: Pedro S. Marra, Takehiko Yamanashi, Kaitlyn J. Crutchley, Nadia E. Wahba, Zoe-Ella M. Anderson, Manisha Modukuri, Gloria Chang, Tammy Tran, Masaaki Iwata, Hyunkeun Ryan Cho, and Gen Shinozaki

8: Age prediction from human blood plasma using proteomic and small RNA data: a comparative analysis

DOI: https://doi.org/10.18632/aging.204787 

Authors: Jérôme Salignon, Omid R. Faridani, Tasso Miliotis, Georges E. Janssens, Ping Chen, Bader Zarrouki, Rickard Sandberg, Pia Davidsson, and Christian G. Riedel

7: Characterization of the HDAC/PI3K inhibitor CUDC-907 as a novel senolytic

DOI: https://doi.org/10.18632/aging.204616 

Authors: Fares Al-Mansour, Abdullah Alraddadi, Buwei He, Anes Saleh, Marta Poblocka, Wael Alzahrani, Shaun Cowley, and Salvador Macip

6: Potential reversal of biological age in women following an 8-week methylation-supportive diet and lifestyle program: a case series

DOI: https://doi.org/10.18632/aging.204602 

Authors: Kara N. Fitzgerald, Tish Campbell, Suzanne Makarem, and Romilly Hodges

5: Leukocyte telomere length, T cell composition and DNA methylation age

DOI: https://doi.org/10.18632/aging.101293 

Authors: Brian H. Chen, Cara L. Carty, Masayuki Kimura, Jeremy D. Kark, Wei Chen, Shengxu Li, Tao Zhang, Charles Kooperberg, Daniel Levy, Themistocles Assimes, Devin Absher, Steve Horvath, Alexander P. Reiner, and Abraham Aviv

4: DNA methylation GrimAge strongly predicts lifespan and healthspan

DOI: https://doi.org/10.18632/aging.101684 

Authors: Ake T. Lu, Austin Quach, James G. Wilson, Alex P. Reiner, Abraham Aviv, Kenneth Raj, Lifang Hou, Andrea A. Baccarelli, Yun Li, James D. Stewart, Eric A. Whitsel, Themistocles L. Assimes, Luigi Ferrucci, and Steve Horvath

3: Deep biomarkers of aging and longevity: from research to applications

DOI: https://doi.org/10.18632/aging.102475 

Authors: Alex Zhavoronkov, Ricky Li, Candice Ma, and Polina Mamoshina

2: An epigenetic biomarker of aging for lifespan and healthspan

DOI: https://doi.org/10.18632/aging.101414 

Authors: Morgan E. Levine, Ake T. Lu, Austin Quach, Brian H. Chen, Themistocles L. Assimes, Stefania Bandinelli, Lifang Hou, Andrea A. Baccarelli, James D. Stewart, Yun Li, Eric A. Whitsel, James G Wilson, Alex P Reiner, Abraham Aviv, Kurt Lohman, Yongmei Liu, Luigi Ferrucci, and Steve Horvath

1: Chemically induced reprogramming to reverse cellular aging

DOI: https://doi.org/10.18632/aging.204896

Authors: Jae-Hyun Yang, Christopher A. Petty, Thomas Dixon-McDougall, Maria Vina Lopez, Alexander Tyshkovskiy, Sun Maybury-Lewis, Xiao Tian, Nabilah Ibrahim, Zhili Chen, Patrick T. Griffin, Matthew Arnold, Jien Li, Oswaldo A. Martinez, Alexander Behn, Ryan Rogers-Hammond, Suzanne Angeli, Vadim N. Gladyshev, and David A. Sinclair

Aging is an open-access, traditional, peer-reviewed journal that has published high-impact papers in all fields of aging research since 2009. All papers are available to readers (at no cost and free of subscription barriers) in bi-monthly issues at Aging-US.com.

For media inquiries, please contact media@impactjournals.com.

Aging’s Top 10 Papers in 2023 (Crossref Data)

Missing data in aging studies, especially in the assessment of gait speed (the time it takes individuals to cover a set distance), presents a significant challenge. The elderly are more prone to health and functional issues, which often interfere with data collection efforts. Given that gait speed is a key indicator of functional status and overall health in older individuals, ensuring its availability and accurate measurement is essential for the integrity of aging research.

In a new study, researchers Robert Thiesmeier, Ahmad Abbadi, Debora Rizzuto, Amaia Calderón-Larrañaga, Scott M. Hofer, and Nicola Orsini from Karolinska Institutet, Stockholm University, Stockholm Gerontology Research Center, and Oregon Health and Science University address the systematic challenge of missing gait speed data in aging research and explore the application of multiple imputation (MI), a statistical technique that has emerged as a constructive approach to handle such gaps in data. The team critically examined the implementation strategies, methodologies, and the impact that these missing variables could have on the outcomes of aging studies, thereby offering a framework to manage and interpret incomplete datasets in aging research. On February 14, 2024, their research paper was published in Aging’s Volume 16, Issue 4, entitled, “Multiple imputation of systematically missing data on gait speed in the Swedish National Study on Aging and Care.”

“[...] this study aims to investigate and assess the performance of different MI strategies specifically targeting the systematically missing discrete variable of gait speed in the SNAC [Swedish National Study on Aging and Care] IPDMA [individual participant data meta-analyses] with only four large cohort studies.”

Full blog - https://aging-us.org/2024/03/overcoming-missing-data-in-the-swedish-national-study-on-aging/

Paper DOI - https://doi.org/10.18632/aging.205552

Corresponding authors - Robert Thiesmeier - robert.thiesmeier@ki.se

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Keywords - aging, simulation, systematically missing values, individual participant data, meta-analysis, gait speed

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.

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Overcoming Missing Data in the Swedish National Study on Aging

The human brain is a complex organ, and its aging process is influenced by a plethora of factors, both genetic and environmental. Aging-related changes in the brain can lead to cognitive decline and susceptibility to neurodegenerative diseases. Therefore, understanding the molecular mechanisms underlying these changes is crucial for developing therapeutic strategies to delay or prevent age-related cognitive decline.

Over the past few years, a myriad of scientific studies have been conducted to understand the intricate relationship between our genes and the aging process. In a new study, researchers Joseph A. Zarrella and Amy Tsurumi from Harvard T.H. Chan School of Public Health, Massachusetts General Hospital, Harvard Medical School, and Shriner’s Hospitals for Children-Boston explored the concept of genome brain age prediction, a groundbreaking area of study that employs advanced bioinformatics tools to analyze changes in gene expression associated with aging. On February 28, 2024, their research paper was published and chosen as the cover paper for Aging’s Volume 16, Issue 5, entitled, “Genome-wide transcriptome profiling and development of age prediction models in the human brain.”

“[…] we aimed to profile transcriptome changes in the aging PFC [prefrontal cortex] overall and compare females and males, and develop prediction models for age.”

Full blog - https://aging-us.org/2024/03/predicting-brain-age-with-machine-learning-and-transcriptome-profiling/

Paper DOI - https://doi.org/10.18632/aging.205609

Corresponding author - Amy Tsurumi - atsurumi@mgh.harvard.edu

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Keywords - aging, machine learning, prediction model, biomarker, transcriptome

About Aging-US

Launched in 2009, Aging-US publishes papers of general interest and biological significance in all fields of aging research and age-related diseases, including cancer—and now, with a special focus on COVID-19 vulnerability as an age-dependent syndrome. Topics in Aging-US go beyond traditional gerontology, including, but not limited to, cellular and molecular biology, human age-related diseases, pathology in model organisms, signal transduction pathways (e.g., p53, sirtuins, and PI-3K/AKT/mTOR, among others), and approaches to modulating these signaling pathways.

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Predicting Brain Age With Machine Learning and Transcriptome Profiling

Menopause marks the beginning of the next biological chapter in a woman’s life. Characterized by the natural ebb of reproductive hormones (particularly estrogen), menopause ushers in a new season of aging. This hormonal shift not only signifies a transition in fertility but also influences systemic health. The menopause-associated decline in estrogen has been associated with various health issues, including alterations in brain structure and function. However, the mechanics of this phenomenon are still poorly understood. A greater understanding of how menopause alters the brain could aid in the early detection, and possible prevention, of neurodegenerative disease.

In a new study, researchers Gwang-Won Kim, Kwangsung Park, Yun-Hyeon Kim, and Gwang-Woo Jeong from Chonnam National University used neuroimaging to shed light on how menopause alters brain morphology and functional connectivity in postmenopausal women. On March 23, 2024, their research paper was published as the cover of Aging’s Volume 16, Issue 6, entitled, "Altered brain morphology and functional connectivity in postmenopausal women: automatic segmentation of whole-brain and thalamic subnuclei and resting-state fMRI."

Full blog - https://aging-us.org/2024/04/how-menopause-changes-brain-structure-and-connectivity/

Paper DOI - https://doi.org/10.18632/aging.205662

Corresponding author - Gwang-Woo Jeong - gwjeong@jnu.ac.kr

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Keywords - aging, brain morphology, functional connectivity, sex hormones, thalamic subnuclei

About Aging-US

Aging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.

Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).

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How Menopause Changes Brain Structure and Connectivity

Aging is still shrouded in proverbial darkness. But, some researchers hypothesize that aging may be linked to stem cell exhaustion. Stemness, the ability of a cell to differentiate into various cell types, is an essential characteristic defining the functionality of stem cells. It has been observed that stem cells seem to diminish with age, although the precise role of stem cells in human aging remains to be elucidated. 

“Among the biological pathways associated with aging, we can highlight stem cell exhaustion, which argues that during normal aging, the decrease in the number or activity of these cells contributes to physiological dysfunction in aged tissues [4].”

In a new study, researchers Gabriel Arantes dos Santos, Gustavo Daniel Vega Magdaleno and João Pedro de Magalhães from the Universidade de Sao Paulo, University of Birmingham and the University of Liverpool applied a machine learning method to detect stemness signatures from transcriptome data of healthy human tissues. Their research paper was published on April 4, 2024, and chosen as the cover of Aging’s Volume 16, Issue 7, entitled, “Evidence of a pan-tissue decline in stemness during human aging.”

Full blog - https://aging-us.org/2024/04/first-evidence-of-a-pan-tissue-decline-in-stemness-during-human-aging/

Paper DOI - https://doi.org/10.18632/aging.205717

Corresponding author - João Pedro de Magalhães - jp@senescence.info

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Keywords - aging, longevity, stem cells, transcriptomics, senescence

About Aging-US

Aging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.

Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).

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First Evidence of a Pan-tissue Decline in Stemness During Human Aging

With an ever-increasing global population grappling with age-related ocular ailments like cataracts, dry eyes, glaucoma, and macular degeneration, the need for new research in this domain is more pressing than ever. 

In a new study, researchers Kohsaku Numa, Sandip Kumar Patel, Zhixin A. Zhang, Jordan B. Burton, Akifumi Matsumoto, Jun-Wei B. Hughes, Chie Sotozono, Birgit Schilling, Pierre-Yves Desprez, Judith Campisi (1948-2024), and Koji Kitazawa from the Buck Institute for Research on Aging, Kyoto Prefectural University of Medicine, University of Cambridge, and California Pacific Medical Center shed light on a pivotal aspect of corneal health – the impact of ultraviolet-A (UV-A) radiation on corneal endothelial cells. Their research paper was published on the cover of Aging’s Volume 16, Issue 8, entitled, “Senescent characteristics of human corneal endothelial cells upon ultraviolet-A exposure.”

“The objective of this study was to investigate the senescent phenotypes of human corneal endothelial cells (hCEnCs) upon treatment with ultraviolet (UV)-A.”

Full blog - https://aging-us.org/2024/05/uv-a-exposure-cellular-senescence-and-vision-impairment/

Paper DOI - https://doi.org/10.18632/aging.205761

Corresponding author - Koji Kitazawa - kkitazaw@koto.kpu-m.ac.jp

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Keywords - aging, cellular senescence, senescence-associated secretory phenotype, RNA-Seq, proteomics, gene ontology analysis

About Aging-US

Aging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.

Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).

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UV-A Exposure, Cellular Senescence, and Vision Impairment

For centuries, the question of when human life commences has perplexed philosophers, theologians, and scientists alike. With the advent of modern reproductive technologies and groundbreaking scientific advancements, this profound inquiry has taken on renewed urgency and complexity. 

In a fascinating new review paper, researchers Polina A. Loseva and Vadim N. Gladyshev from Harvard Medical School delved into this intricate subject, exploring the multifaceted perspectives that have shaped our understanding of life’s origins. On May 6, 2024, their review was published on the cover of Aging’s Volume 16, Issue 9, entitled, “The beginning of becoming a human.” 

Below, this article breaks down their chronological review of the various ways life has been defined: movement, fusion, self-sufficiency, uniqueness, and now, aging.

Full blog - https://aging-us.org/2024/05/when-does-human-life-truly-begin/

Paper DOI - https://doi.org/10.18632/aging.205824

Corresponding authors - Polina A. Loseva - polina.loseva89@gmail.com, and Vadim N. Gladyshev - vgladyshev@rics.bwh.harvard.edu

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Keywords - aging, human, life, 14-day rule

About Aging-US

Aging publishes research papers in all fields of aging research, including but not limited to aging processes (from yeast to mammals), cellular senescence, age-related diseases (such as cancer and Alzheimer’s disease) and their prevention and treatment, anti-aging strategies and drug development, and, importantly, the role of signal transduction pathways in aging (such as mTOR) and potential approaches to modulate these signaling pathways to extend lifespan.

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.).

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When Does Human Life Truly Begin?

Werner syndrome (WS) is a rare genetic disorder marked by the premature onset of features typically associated with normal aging. This autosomal recessive condition manifests in individuals who generally develop normally until adolescence. As the syndrome progresses, affected individuals are predisposed to age-related diseases much earlier in life. These conditions include cataracts, type 2 diabetes, atherosclerosis, osteoporosis, and various cancers. The underlying cause of Werner syndrome is believed to be mutations in the WRN gene, which encodes a RecQ helicase crucial for DNA repair and replication.

Despite the accelerated aging, cognitive function remains unaffected in individuals with WS, providing a unique model for studying the mechanisms of aging and exploring potential therapeutic interventions. Although extensive research has been conducted, the precise mechanisms underlying these effects remain elusive.

On May 24, 2024, researchers Lucie Aumailley, Marie Julie Dubois, André Marette, and Michel Lebel from Université Laval published research paper chosen as the cover of Aging’s Volume 16, Issue 10, entitled, “Integrated liver and serum proteomics uncover sexual dimorphism and alteration of several immune response proteins in an aging Werner syndrome mouse model.” Recognizing the limitations of traditional investigative approaches, Aumailley et al. utilized advanced proteomics in their study. Proteomics allows the simultaneous identification and quantification of hundreds of proteins, providing a comprehensive analysis of liver and serum proteome profiles from wild-type and WRN mutant mice at different ages to uncover biological processes influenced by age and genotype.

Full blog - https://aging-us.org/2024/06/werner-syndrome-and-the-power-of-proteomics/

Paper DOI - https://doi.org/10.18632/aging.205866

Corresponding author - Michel Lebel - michel.lebel@crchudequebec.ulaval.ca

Video short - https://www.youtube.com/watch?v=uP6deANWgP4

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Keywords - aging, proteomics, Werner syndrome, fatty liver, sexual dimorphism, immunoglobulins

About Aging-US

Aging publishes research papers in all fields of aging research, including but not limited to aging processes (from yeast to mammals), cellular senescence, age-related diseases (such as cancer and Alzheimer’s disease) and their prevention and treatment, anti-aging strategies and drug development, and, importantly, the role of signal transduction pathways in aging (such as mTOR) and potential approaches to modulate these signaling pathways to extend lifespan.

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:

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Werner Syndrome and the Power of Proteomics

BUFFALO, NY- June 25, 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 11, entitled, “Associations of childhood, adolescence, and midlife cognitive function with DNA methylation age acceleration in midlife.”

Prior studies showed increased age acceleration (AgeAccel) is associated with worse cognitive function among old adults. In this new study, researchers Junyu Chen, Leah Moubadder, Elizabeth S. Clausing, Katrina L. Kezios, Karen N. Conneely, Anke Hüls, Andrea Baccarelli, Pam Factor-Litvak, Piera Cirrillo, Rachel C. Shelton, Bruce G. Link, and Shakira F. Suglia from Emory University, University of Nebraska, Columbia University, Public Health Institute, Washington, DC, and the University of California Riverside examined the associations of childhood, adolescence and midlife cognition with AgeAccel based on DNA methylation (DNAm) in midlife.

“To the best of our knowledge, this is the first study to show the association of cognition at younger age with midlife age acceleration, and associations between midlife age acceleration measures and cognitive function that are independent of childhood and adolescent cognition.”

Data are from 359 participants who had cognition measured in childhood and adolescence in the Child Health and Development study, and had cognition, blood based DNAm measured during midlife in the Disparities study. Childhood cognition was measured by Raven’s Progressive Matrices and Peabody Picture Vocabulary Test (PPVT). Adolescent cognition was measured only by PPVT. Midlife cognition included Wechsler Test of Adult Reading (WTAR), Verbal Fluency (VF), Digit Symbol (DS). AgeAccel measures including Horvath, Hannum, PhenoAge, GrimAge and DunedinPACE were calculated from DNAm. Linear regressions adjusted for potential confounders were utilized to examine the association between each cognitive measure in relation to each AgeAccel.

There are no significant associations between childhood cognition and midlife AgeAccel. A 1-unit increase in adolescent PPVT, which measures crystalized intelligence, is associated with 0.048-year decrease of aging measured by GrimAge and this association is attenuated after adjustment for adult socioeconomic status. Midlife crystalized intelligence measure WTAR is negatively associated with PhenoAge and DunedinPACE, and midlife fluid intelligence measure (DS) is negatively associated with GrimAge, PhenoAge and DunedinPACE. AgeAccel is not associated with VF in midlife.

“In conclusion, our study showed the potential role of cognitive functions at younger ages in the process of biological aging. We also showed a potential relationship of both crystalized and fluid intelligence with aging acceleration.”

DOI - https://doi.org/10.18632/aging.205943

Corresponding author - Junyu Chen - junyu.chen@emory.edu

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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.

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Childhood, Adolescence, and Midlife Cognitive Function Linked to Age Acceleration in Midlife

BUFFALO, NY- June 26, 2024 – A new editorial paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 11, entitled, “Global consensus for sarcopenia.”

In this new editorial, researchers Ben Kirk, Peggy M. Cawthon, and Alfonso J. Cruz-Jentoft from the University of Melbourne and Western Health discuss the global societal issue of skeletal muscle loss and weakness, termed Sarcopenia. Low muscle mass or low strength/function increases the susceptibility to poor outcomes such as fragility, hip fractures, disability, and low quality of life in older people [1–4]. Skeletal muscle also acts as an endocrine organ and interacts with local and distal tissues; for instance, muscle cells secrete molecules involved in bone fracture healing and the same molecules help regulate distal tissues such as the brain, heart, and kidneys [5, 6]. This may partially explain why low muscle mass is a strong predictor of disease-specific mortality (dementia, cancer, heart failure, kidney/liver disease) as well as all-cause mortality in aging [7]. 

“Until now, there has been no universal agreement on a definition for Sarcopenia.”

Previous definitions were continent- and region-specific: Asia, Europe, North America, and Australia/New Zealand [8]. These definitions were certainly important in drawing attention to, and understanding of, this muscle disease. However, these definitions led to wide estimates in disease prevalence/incidence as well as heterogeneity when comparing treatments results of randomised trials [9]. The lack of a single definition likely impacted the identification of or treatment for sarcopenia in research and clinical practice (i.e., caused confusion for scientists, physicians and health care professionals on which definition, cutpoints, and muscle assessment tools to employ). 

“To address this, the Global Leadership Initiative in Sarcopenia (GLIS) [9] was formed to create a unified global definition for use in research and clinical settings.”

DOI - https://doi.org/10.18632/aging.205919

Corresponding author - Ben Kirk - ben.kirk@unimelb.edu.au

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Keywords - aging, sarcopenia, global definition, GLIS, skeletal muscle

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Global Consensus for Sarcopenia

Cellular quality control mechanisms like mitophagy, a specialized form of autophagy that eliminates dysfunctional mitochondria, play a pivotal role in various physiological processes. Defects in mitophagy have been linked to neurodegeneration, heart failure, cancer, and aging.

A recent study, by researchers Marta Mauro-Lizcano, Federica Sotgia, and Michael P. Lisanti from the University of Salford, has shed light on the intricate link between mitophagy and cancer stem cells (CSCs). In this study, the researchers developed an innovative fluorescence-based approach to enrich subpopulations of cancer cells exhibiting high basal levels of mitophagy. Their findings reveal that elevated mitophagy activity enhances CSC properties, including self-renewal, ATP production, proliferation, and cell migration, underscoring the potential of targeting mitophagy as a therapeutic strategy for cancer treatment. 

On June 4, 2024, their research paper was published on the cover of Aging’s Volume 16, Issue 11, entitled, “Mitophagy and cancer: role of BNIP3/BNIP3L as energetic drivers of stemness features, ATP production, proliferation, and cell migration.”

Full blog - https://aging-us.org/2024/06/targeting-mitophagy-as-a-therapeutic-strategy-for-cancer-treatment/

Paper DOI - https://doi.org/10.18632/aging.205939

Corresponding authors - Federica Sotgia - fsotgia@gmail.com, and Michael P. Lisanti - michaelp.lisanti@gmail.com

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Keywords - aging, mitophagy, BNIP3, BNIP3L(NIX), cancer stem cells (CSCs), flow cytometry (FACS)

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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.

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Targeting Mitophagy as a Therapeutic Strategy for Cancer Treatment

BUFFALO, NY- July 1, 2024 – A new #review paper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 12, entitled, “Senescent cell-derived vaccines: a new concept towards an immune response against cancer and aging?”

Two recent seminal works have untangled the intricate role of tumor-associated senescent cells in cancer progression, or regression, by guiding our immune system against cancer cells. The characterization of these unique, yet diverse cell populations, should be considered, particularly when contemplating the use of senolytics, which are drugs that selectively eliminate senescent cells, in a cancer framework. In this new review, researchers João Pessoa, Sandrina Nóbrega-Pereira, and Bruno Bernardes de Jesus from the University of Aveiro describe the current knowledge in this field. 

“In particular, we will discuss how the presence of senescent cells in tumors could be used as a therapeutic target in immunogenic cancers and how we may hypothetically design an adaptive anti-aging vaccine.”

DOI - https://doi.org/10.18632/aging.205975

Corresponding authors - Bruno Bernardes de Jesus - brunob.jesus@ua.pt

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Keywords - aging, cancer, immunotherapy, tumor-associated senescent cells, senescence, antigen, vaccine

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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.
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Senescent Cell-derived Vaccines: A New Concept Towards an Immune Response Against Cancer and Aging?

BUFFALO, NY- July 9, 2024 – A new #editorial paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 12, entitled, “Aging retinal pigmented epithelium: omics-based insights into vision decline.”

In this new editorial, researchers Ioan V. Matei and Luminita Paraoan from Edge Hill University discuss vision decline with aging. Of all senses affected by aging, vision decline arguably has the most impactful relationship with overall wellbeing, health and personal autonomy. However, while the ensuing importance of vision loss has long been recognised from a public health perspective given an increasingly aging population, understanding the molecular and cellular mechanisms driving age-related pathological changes is still in its infancy. 

“This matter is, therefore, critical for tackling sensory impairment and ensuring healthy aging.” 

The retinal pigmented epithelium (RPE), the cellular monolayer located between the neuroretina and the highly vascularized choroid, from which it is separated by Bruch’s membrane (BrM), has a critical role in human vision and performs essential functions throughout life for maintaining the retinal homeostasis. RPE is a specialised, fully differentiated tissue that is mitotically inactive, with no regenerative potential. Unsurprisingly, given all its characteristics, functions and metabolic demands, the RPE is particularly susceptible to aging, sustaining significant morphologic and physiologic changes. 

“Aging is recognised as the highest risk factor for age-related macular degeneration (AMD), the leading cause of adult visual impairment and blindness in the Northern Hemisphere, which is directly linked to specific pathological changes of the RPE located in the macula, i.e., the central part of retina; these changes, therefore, affect central vision required for reading, driving, and discerning details of pictures, faces, shapes and colors.”

DOI - https://doi.org/10.18632/aging.205914

Corresponding author - Luminita Paraoan - Luminita.Paraoan@edgehill.ac.uk

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Keywords - aging, RPE, vision, omics

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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.

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Aging Retinal Pigmented Epithelium: Omics-based Insights Into Vision Decline

BUFFALO, NY- July 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 12, entitled, “Aging exacerbates oxidative stress and liver fibrosis in an animal model of Down Syndrome.”

Down Syndrome (DS) is a common genetic disorder characterized by an extra copy of chromosome 21, leading to dysregulation of various metabolic pathways. Oxidative stress in DS is associated with neurodevelopmental defects, neuronal dysfunction, and a dementia onset resembling Alzheimer's disease. Additionally, chronic oxidative stress contributes to cardiovascular diseases and certain cancers prevalent in DS individuals.

In this new study, researchers Sebastiano Giallongo, Jessica Ferrigno, Rosario Caltabiano, Giuseppe Broggi, Amer M. Alanazi, Alfio Distefano, Emanuela Tropea, Antonella Tramutola, Marzia Perluigi, Giovanni Li Volti, Eugenio Barone, and Ignazio Alberto Barbagallo from the University of Catania, King Saud University, and Sapienza University of Rome investigated the impact of aging on oxidative stress and liver fibrosis using a DS murine model (Ts2Cje mice). 

“Our results show that DS mice show increased liver oxidative stress and impaired antioxidant defenses, as evidenced by reduced glutathione levels and increased lipid peroxidation.” 

DS liver exhibited an altered inflammatory response and mitochondrial fitness as the researchers showed by assaying the expression of HMOX1, CLPP, and the heat shock proteins Hsp90 and Hsp60. DS liver also displayed dysregulated lipid metabolism, indicated by altered expression of PPARα, PPARγ, FATP5, and CTP2. Consistently, these changes might contribute to non-alcoholic fatty liver disease development, a condition characterized by liver fat accumulation. Consistently, histological analysis of DS liver revealed increased fibrosis and steatosis, as showed by Col1a1 increased expression, indicative of potential progression to liver cirrhosis. Therefore, their findings suggest an increased risk of liver pathologies in DS individuals, particularly when combined with the higher prevalence of obesity and metabolic dysfunctions in DS patients.

“These results shed a light on the liver's role in DS-associated pathologies and suggest potential therapeutic strategies targeting oxidative stress and lipid metabolism to prevent or mitigate liver-related complications in DS individuals.”

DOI - https://doi.org/10.18632/aging.205970

Corresponding author - Giovanni Li Volti - livolti@unict.it

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Keywords - aging, Down Syndrome, oxidative stress, liver

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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.)

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Aging Exacerbates Oxidative Stress and Liver Fibrosis in an Animal Model of Down Syndrome

BUFFALO, NY- July 15, 2024 – A new #research paper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 13, entitled, “Roles of pigment epithelium-derived factor in exercise-induced suppression of senescence and its impact on lung pathology in mice.”

Senescent cells contribute to tissue aging and underlie the pathology of chronic diseases. The benefits of eliminating senescent cells have been demonstrated in several disease models, and the efficacy of senolytic drugs is currently being tested in humans. Exercise training has been shown to reduce cellular senescence in several tissues; however, the mechanisms responsible remain unclear.

In this new study, researchers Hiromichi Tsushima, Hirobumi Tada, Azusa Asai, Mikako Hirose, Tohru Hosoyama, Atsushi Watanabe, Taro Murakami, and Masataka Sugimoto from Tokyo Metropolitan Institute for Geriatrics and Gerontology, Shigakkan University, and National Center for Geriatrics and Gerontology investigated myocyte-secreted factors with the potential to suppress cellular senescence, aiming to explore their protective effects against lung disease. 

“We found that myocyte-derived factors significantly extended the replicative lifespan of fibroblasts, suggesting that myokines mediate the anti-senescence effects of exercise.”

A number of proteins within myocyte-derived factors were identified by mass spectrometry. Among these, pigment epithelium-derived factor (PEDF) exerted inhibitory effects on cellular senescence. Eight weeks of voluntary running increased PEDF levels in skeletal muscles and suppressed senescence markers in the lungs. The administration of PEDF reduced senescence markers in multiple tissues and attenuated the decline in respiratory function in the pulmonary emphysema mouse model. The researchers also showed that blood levels of PEDF inversely correlated with the severity of COPD in patients. 

“Collectively, these results strongly suggest that PEDF contributes to the beneficial effects of exercise, potentially suppressing cellular senescence and its associated pathologies.”

DOI - https://doi.org/10.18632/aging.205976

Corresponding authors - Masataka Sugimoto - msugimot@tmig.or.jp

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Keywords - aging, senescence, exercise, PEDF, myokine, COPD

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Roles of PEDF in Exercise-induced Suppression of Senescence and its Impact on Lung Pathology in Mice

BUFFALO, NY- July 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 13, entitled, “Modulating in vitro lung fibroblast activation via senolysis of senescent human alveolar epithelial cells.”

Idiopathic pulmonary fibrosis (IPF) is an age-related disease with poor prognosis and limited therapeutic options. Activation of lung fibroblasts and differentiation to myofibroblasts are the principal effectors of disease pathology, but damage and senescence of alveolar epithelial cells, specifically type II (ATII) cells, has recently been identified as a potential trigger event for the progressive disease cycle. Targeting ATII senescence and the senescence-associated secretory phenotype (SASP) is an attractive therapeutic strategy; however, translatable primary human cell models that enable mechanistic studies and drug development are lacking.

In this new study, researchers Joseph S. Spina, Tracy L. Carr, Lucy A. Phillips, Heather L. Knight, Nancy E. Crosbie, Sarah M. Lloyd, Manisha A. Jhala, Tony J. Lam, Jozsef Karman, Meghan E. Clements, Tovah A. Day, Justin D. Crane, and William J. Housley from AbbVie Bioresearch Center and Northeastern University describe a novel system of conditioned medium (CM) transfer from bleomycin-induced senescent primary alveolar epithelial cells (AEC) onto normal human lung fibroblasts (NHLF) that demonstrates an enhanced fibrotic transcriptional and secretory phenotype compared to non-senescent AEC CM treatment or direct bleomycin damage of the NHLFs. 

“In the current study, we confirm the presence of senescent cell populations within the human IPF lung, as well as assess primary cell reagents for sensitivity to senescent cell targeting therapies.”

In this system, the bleomycin-treated AECs exhibited classical hallmarks of cellular senescence, including SASP and a gene expression profile that resembles aberrant epithelial cells of the IPF lung. Fibroblast activation by CM transfer was attenuated by pre-treatment of senescent AECs with the senolytic Navitoclax and AD80, but not with the standard of care agent Nintedanib or senomorphic JAK-targeting drugs (e.g., ABT-317, ruxolitinib). This model provided a relevant human system for profiling novel senescence-targeting therapeutics for IPF drug development.

“Taken together, the model described herein provides a physiologically relevant, primary human cell system to study the effects of alveolar epithelial cell senescence on lung fibroblasts in the context of chronic fibrotic lung disease.”

DOI - https://doi.org/10.18632/aging.205994

Corresponding author - Tovah A. Day - t.day@northeastern.edu

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Modulating Lung Fibroblast Activation via Senolysis of Senescent Human Alveolar Epithelial Cells

Over the human lifespan, our cells encounter numerous stressors that can trigger an intrinsic defense mechanism called cellular senescence. Cellular senescence is characterized by irreversible growth arrest and can act as a safeguard against cancer. However, when senescent cells accumulate in various tissues as we age, it can contribute to tissue degeneration and chronic diseases. 

The senescence-associated secretory phenotype (SASP), a hallmark of senescent cells, plays a critical role by secreting inflammatory factors, proteases, and growth factors, disrupting tissue balance and fueling pathological conditions. Consequently, selectively eliminating senescent cells has emerged as a promising therapeutic strategy, potentially restoring tissue function and mitigating age-related disorders.

Full blog - https://aging-us.org/2024/07/links-between-exercise-senescence-and-lung-health/

Research Paper DOI - https://doi.org/10.18632/aging.205976

Corresponding author - Masataka Sugimoto - msugimot@tmig.or.jp

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Keywords - aging, senescence, exercise, PEDF, myokine, COPD

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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.

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Links Between Exercise, Senescence, and Lung Health

BUFFALO, NY- July 23, 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 13, entitled, “Co-analysis of methylation platforms for signatures of biological aging in the domestic dog reveals previously unexplored confounding factors.”

Chronological age reveals the number of years an individual has lived since birth. By contrast, biological age varies between individuals of the same chronological age at a rate reflective of physiological decline. Differing rates of physiological decline are related to longevity and result from genetics, environment, behavior, and disease. The creation of methylation biological age predictors is a long-standing challenge in aging research due to the lack of individual pre-mortem longevity data. 

In this new study, researchers Aitor Serres Armero, Reuben M. Buckley, Lajoyce Mboning, Gabriella J. Spatola, Steve Horvath, Matteo Pellegrini, and Elaine A. Ostrander from the National Human Genome Research Institute, the University of California Los Angeles, and Altos Labs ask whether dogs experience changes in their epigenetic age at a rate predicted by breed longevity.

“The consistent differences in longevity between domestic dog breeds enable the construction of biological age estimators which can, in turn, be contrasted with methylation measurements to elucidate mechanisms of biological aging.”

The researchers drew on three flagship methylation studies using distinct measurement platforms and tissues to assess the feasibility of creating biological age methylation clocks in the dog. They expanded epigenetic clock building strategies to accommodate phylogenetic relationships between individuals, thus controlling for the use of breed standard metrics. The team observed that biological age methylation clocks are affected by population stratification and require heavy parameterization to achieve effective predictions. 

“Finally, we observe that methylation-related markers reflecting biological age signals are rare and do not colocalize between datasets.”

DOI - https://doi.org/10.18632/aging.206012

Corresponding author - Elaine A. Ostrander - eostrand@mail.nih.gov

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Keywords - aging, biological age, methylation, dog, lifespan, penalized regression

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.)

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Co-analysis of Methylation Platforms for Signatures of Biological Aging in the Domestic Dog

BUFFALO, NY- August 5, 2024 – A new #research paper was #published on the #cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 14, entitled, “Association between osteoporosis and the rate of telomere shortening.”

A shorter leukocyte telomere length (LTL) is reported to be associated with age-related diseases, including osteoporosis. Many studies have tried identifying the association between LTL and osteoporosis, although it remains controversial. 

In this current study, researchers Myung-Hoon Han , Hyuk Sung Kwon, Mina Hwang, Hyun-Hee Park, Jee Hyang Jeong, Kyung Won Park, Eun-Joo Kim, Soo Jin Yoon, Bora Yoon, Jae-Won Jang, Jin Yong Hong, Seong Hye Choi, and Seong-Ho Koh from Hanyang University Guri Hospital, Hanyang University Graduate School of Biomedical Science and Engineering, Ewha Womans University College of Medicine, Dong-A University College of Medicine, Pusan National University Hospital, Eulji University Hospital, Eulji University School of Medicine, Konyang University College of Medicine, Kangwon National University School of Medicine, Yonsei University Wonju College of Medicine, and Inha University College of Medicine, aimed to determine whether osteoporosis is independently associated with LTL shortening in a prospective longitudinal cohort.

“We compared the LTL values for each participant at baseline and over a 2-year follow-up period.” 

Multivariable linear regression was conducted to identify whether osteoporosis is independently associated with the rate of telomere shortening. A total of 233 subjects (from 55 to 88 years) from the KBASE cohort were finally enrolled in the study. 

Multivariable linear regression analysis indicated that only osteoporosis was independently associated with rapid LTL shortening over 2 years (B, -8.08; p = 0.038).

“We sought to identify an association between osteoporosis and LTL shortening in an independent prospective cohort.”

DOI - https://doi.org/10.18632/aging.206034

Corresponding authors - Seong Hye Choi - seonghye@inha.ac.kr, and Seong-Ho Koh - ksh213@hanyang.ac.kr

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Keywords - aging, leukocyte telomere length, osteoporosis, interleukin-6, prospective cohort

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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.

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Association Between Osteoporosis and Telomere Shortening

BUFFALO, NY- August 6, 2024 – On July 28, 2024, Mikhail V. Blagosklonny M.D., Ph.D., from Roswell Park Comprehensive Cancer Center #published a new #editorial in Volume 16, Issue 14 of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), entitled, “Targeted cancer therapy: the initial high concentration may slow down the selection for resistance.”

“Unfortunately, any targeted therapy is, always, started with low levels of the drug in the organism, selecting for drug resistance. One should propose that initial drug levels must be maximized, and durations may be minimized, ideally, as portions of preemptive combination of targeted drugs.”

Read the full paper: DOI: https://doi.org/10.18632/aging.206046

Corresponding Author: Mikhail V. Blagosklonny - Blagosklonny@oncotarget.com, Blagosklonny@rapalogs.com

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Keywords - aging, lung cancer, resistance, brain metastases, METex14, capmatinib, rapamycin

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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.

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Targeted Cancer Therapy: Initial High Concentration May Slow Down Selection for Resistance

BUFFALO, NY- August 7, 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 14 on July 26, 2024, entitled, “mTORC1 activation in presumed classical monocytes: observed correlation with human size variation and neuropsychiatric disease.”

In this new study, researchers Karl Berner, Naci Oz, Alaattin Kaya, Animesh Acharjee, and Jon Berner from Woodinville Psychiatric Associates, Virginia Commonwealth University, University of Birmingham, University Hospitals Birmingham, and MRC Health Data Research UK, aimed to measure phosphorylated p70S6K, a marker for mTORC1 activity, in individuals with psychiatric disease to determine whether phosphorylated p70S6K could predict medication response.

Their results showed that mTORC1 activity correlated highly with classical biometrics (height, macrocephaly, pupil distance) and specific neuropsychiatric disease profiles (anxiety and autism).

“Our data suggest that human variability of mTORC1 gain of function observed during the differentiation of stem-like monocytes into vascular tissue-resident macrophages correlates with physical size, subsets of neuropsychiatric disease, and clinical ketamine or rapamycin response.”

DOI - https://doi.org/10.18632/aging.206033

Corresponding author - Jon Berner - jonbernermd@gmail.com

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Keywords - aging, ketamine, lithium, monocyte, mTORC1, rapamycin

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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.

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mTORC1 in Classical Monocytes: Links to Human Size Variation & Neuropsychiatric Disease

BUFFALO, NY- August 13, 2024 – 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 14 on July 19, 2024, entitled, “Lipid accumulation drives cellular senescence in dopaminergic neurons.”

As highlighted in the Abstract of this perspective, Parkinson’s disease (PD) is an age-related movement disorder caused by the loss of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNpc) of the midbrain. However, the underlying causes of this DA neuron loss in PD are unknown, and there are currently no effective treatments to prevent or slow neuronal loss or the progression of related symptoms. 

In their perspective, researchers Taylor Russo and Markus Riessland from Stony Brook University found that artificially inducing GluCer accumulation leads to cellular senescence of DA neurons. This suggests that lipid aggregation plays a crucial role in the pathology of PD by driving senescence in these vulnerable neurons.

“Here, we discuss the relevance of the age-related aggregation of lipids as well as the direct functional link between general lipid aggregation, cellular senescence, and inflammaging of DA neurons.”

Additionally, they propose that the expression of a cellular senescence phenotype in the most vulnerable neurons in PD can be triggered by lysosomal impairment and lipid aggregation. 

“Importantly, we highlight additional data that perilipin (PLIN2) is significantly upregulated in senescent DA neurons, suggesting an overall enrichment of lipid droplets (LDs) in these cells.”

DOI - https://doi.org/10.18632/aging.206030

Corresponding author - Markus Riessland - markus.riessland@stonybrook.edu

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Keywords - aging, lipids, cellular senescence, Parkinson’s disease, glucosylceramides, lysosomes, neuroinflammation

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.)

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Lipid Accumulation Drives Cellular Senescence in Dopaminergic Neurons

BUFFALO, NY- August 14, 2024 – A new #editorial was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 14 on July 17, 2024, entitled, “Recalibrate concepts of epigenetic aging clocks in human health.”

As detailed in the opening of this editorial, DNA methylation-based epigenetic clocks are used as biomarkers of biological age in human health. Multiple epigenetic clocks have rapidly emerged in the past decade by modeling DNA methylation changes with age in large cohorts, primarily using peripheral blood samples. Despite efforts to understand the functional implications of features used to estimate biological age, the underlying mechanisms of these clocks remain poorly understood, leading to potential misinterpretations of their associations with health outcomes.

Researchers Ze Zhang, Brock C. Christensen, and Lucas A. Salas from the Divisions of Population Sciences and Medical Oncology, Dana-Farber Cancer Institute, Harvard Medical School, the Department of Epidemiology, Geisel School of Medicine, Dartmouth College, Dartmouth Cancer Center, Dartmouth-Hitchcock Medical Center, and the Department of Molecular and Systems Biology, Geisel School of Medicine, Dartmouth College explored the association of 12 immune cell types with epigenetic age acceleration (EAA) in both healthy and diseased populations. 

Their work sheds light on the complex interplay between immune cell composition and epigenetic aging, utilizing high-resolution methylation cytometry in blood samples.

“In this editorial, we aim to address the key implications of our study on epigenetic aging clocks in human health from a broader perspective. While epigenetic clocks are widely hyped as aging biomarkers today, it's essential to recalibrate some fundamental concepts in this field.”

DOI - https://doi.org/10.18632/aging.206027

Corresponding author - Lucas A. Salas - lucas.a.salas@dartmouth.edu

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Keywords - aging, epigenetics, DNA methylation, epigenetic clock, epigenetic age acceleration, methylation cytometry

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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.)

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Recalibrating Principles of Epigenetic Aging Clocks in Human Health

BUFFALO, NY- August 16, 2024 – A new #review was #published as the #cover paper of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 15, entitled, “Types of cell death and their relations to host immunological pathways”.

Various immune pathways in the host, such as TH1, TH2, TH3, TH9, TH17, TH22, TH1-like, and THαβ, have been identified. While TH2 and TH9 responses primarily target multicellular parasites, host immune pathways against viruses, intracellular microorganisms (like bacteria, protozoa, and fungi), and extracellular microorganisms utilize programmed cell death mechanisms to initiate immune responses and effectively eliminate pathogens.

In their review, researchers Kuo-Cheng Lu, Kuo-Wang Tsai, Yu-Kuen Wang, and Wan-Chung Hu from Taipei Tzu Chi Hospital, Fu Jen Catholic University, Taoyuan Armed Forces General Hospital, Tri-Service General Hospital and Ming Chuan University, reviewed these cell death pathways associated with the host immunological pathways.

"These relationships can help us understand the host defense mechanisms against invading pathogens and provide new insights for developing better therapeutic strategies against infections or autoimmune disorders.”

DOI - https://doi.org/10.18632/aging.206035

Corresponding authors - Wan-Chung Hu - Wanchung.Hu09@tzuchi.com.tw

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Keywords - aging, apoptosis, autophagy, ferroptosis, necroptosis, NETosis, pyroptosis

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.

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Cell Death Types and Their Relations to Host Immune Pathways

BUFFALO, NY- August 20, 2024 – A new #editorial was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 15 on July 19, 2024, entitled, “Physical fitness and lifestyles associated with biological aging”.

Given the growing aging population worldwide, it is crucial to develop interventional strategies that target aging itself, rather than focusing solely on organ- or disease-based medicine. The geroscience hypothesis, which suggests that delaying aging can prevent the onset of diseases, is gaining traction due to advancements in aging biomarkers, driven by improvements in both measurement techniques (e.g., omics) and analytical technologies (e.g., bioinformatics).

In their editorial, researchers Takuji Kawamura, Radak Zsolt, Mitsuru Higuchi, and Kumpei Tanisawa from the Faculty of Sport Sciences at Waseda University and the Research Center for Molecular Exercise Science at Hungarian University of Sports Science, emphasize the importance of investigating the relationship between cardiorespiratory fitness (CRF) and the DNA methylation (DNAm) aging clock. Their goal is to establish fitness reference values that could help delay aging. They also discuss their recent report on the "Associations between cardiorespiratory fitness and lifestyle-related factors with DNA methylation-based aging clocks in older men: WASEDA’S Health Study."

"Our study reinforces the geroscience concept that active lifestyle choices may impact quantifiable molecular biomarkers that capture biological aging.”

DOI - https://doi.org/10.18632/aging.206031

Corresponding author - Takuji Kawamura - takuji3@aoni.waseda.jp

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Keywords - aging, DNA methylation, epigenetic clock, physical fitness, anthropometry, blood biochemical parameters, nutritional intake

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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.

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How Physical Fitness and Lifestyle Impact Biological Aging

BUFFALO, NY- August 21, 2024 – A new #editorial was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 15 on August 8, 2024, entitled, “The benefits of exercise on aging: focus on muscle biomarkers.”

The focus on maintaining health and vitality (e.g., good healthspan) in later life has become increasingly important as the world’s population ages. Over the past few decades, groundbreaking research in the field of aging has deepened our understanding of the molecular basis of this process. In the last decade, advances in aging research have identified biomarkers such as DNA methylation (DNAm) and gene expression, offering insights into both chronological and biological aging.

Researchers Robin Grolaux, Bernadette Jones-Freeman, Macsue Jacques, and Nir Eynon from the Australian Regenerative Medicine Institute at Monash University in Melbourne, explore the impact of exercise on these biomarkers in human skeletal muscle—a critical tissue for metabolism, thermogenesis, and movement—revealing its potential to foster healthier aging.

This study represents the first quantitative and qualitative analysis of the effects of exercise on age-related biomarkers in human skeletal tissues. Future research could explore the global effects of exercise on various molecular pathways and differentiate between exercise types to develop more effective personalized therapies.

“We have the opportunity to uncover functional therapies that effectively impact aging.”

DOI - https://doi.org/10.18632/aging.206064

Corresponding Author - Nir Eynon - nir.eynon@monash.edu

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Keywords - aging, skeletal muscle, exercise, epigenetics, OMICs, biomarkers

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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.

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Impact of Exercise on Aging: Highlighting Muscle Biomarkers

In this #review, #researchers explore the intricate relationship between various cell death pathways and host immunological responses.

Kuo-Cheng Lu, Kuo-Wang Tsai, Yu-Kuen Wang, and Wan-Chung Hu
from Taipei Tzu Chi Hospital, Fu Jen Catholic University, Taoyuan Armed Forces General Hospital, Tri-Service General Hospital and Ming Chuan University, have delved into the literature surrounding cell death pathways and their connections to host immunological pathways. 

Their review was published as the cover paper of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science), Volume 16, Issue 15, entitled, “Types of Cell Death and Their Relations to Host Immunological Pathways.”

Full blog - https://aging-us.org/2024/08/exploring-links-between-cell-death-pathways-and-immune-responses/

Paper DOI - https://doi.org/10.18632/aging.206035

Corresponding author - Wan-Chung Hu - Wanchung.Hu09@tzuchi.com.tw

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Keywords - aging, apoptosis, autophagy, ferroptosis, necroptosis, NETosis, pyroptosis

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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.

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Exploring Links Between Cell Death Pathways and Immune Responses

BUFFALO, NY- August 27, 2024 – 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 15 on July 25, 2024, entitled, “Trioxidized cysteine and aging: a molecular binomial that extends far beyond classical proteinopathic paradigms.”

Oxidative stress (OS) - characterized by an imbalance between oxidants and antioxidants - leads to the formation of oxidative posttranslational modifications (PTMs), including those involving cysteine (Cys) residues in aging proteomes. Specifically, the formation of trioxidized Cys (t-Cys) results in permanent protein damage. Recent findings in rodents have revealed that irregular regulation of t-Cys residues in the aging proteome disrupts homeostatic phosphorylation signaling, leading to alterations in proteins similar to those caused by phosphorylated serine (p-Ser) residues.

In this perspective, researchers José Antonio Sánchez Milán, María Mulet, Aida Serra and Xavier Gallart-Palau from University Hospital Arnau de Vilanova (HUAV) and University of Lleida (UdL), present novel data, validating the increase of specific t-Cys sites associated with aging in a blood-related circulating human proteome.

"The scope and findings included here support the hypothesis that t-Cys residues may serve as important mechanistic and biological markers, warranting further exploration in the context of unhealthy aging and age-related major diseases.”

DOI - https://doi.org/10.18632/aging.206036

Corresponding authors - Aida Serra - aida.serra@udl.cat, and Xavier Gallart-Palau - xgallart@irblleida.cat

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Keywords - aging, oxidative stress, unhealthy aging, t-Cys, aging diseases, aging proteome

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

Trioxidized Cysteine and Aging: Beyond Proteinopathic Paradigms

Cancer and aging are two sides of age-related tumorigenesis.

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.)

Read about the Aging (Aging-US) Scientific Integrity Process: https://aging-us.com/scientific-integrity

Aging (Aging-US) Podcast

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