Avsnitt
-
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 - [email protected]
Sign up for free Altmetric alerts about this article -
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205609
Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts
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.
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 Contact
18009220957
[email protected] -
BUFFALO, NY- March 20, 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 5, entitled, “FoxO6-mediated ApoC3 upregulation promotes hepatic steatosis and hyperlipidemia in aged rats fed a high-fat diet.”
FoxO6, an identified factor, induces hyperlipidemia and hepatic steatosis during aging by activating hepatic lipoprotein secretion and lipogenesis leading to increased ApoC3 concentrations in the bloodstream. However, the intricate mechanisms underlying hepatic steatosis induced by elevated FoxO6 under hyperglycemic conditions remain intricate and require further elucidation.
In this new study, researchers Dae Hyun Kim, Seulah Lee, Sang Gyun Noh, Jaewon Lee, and Hae Young Chung from Pusan National University aimed to delineate the regulatory pathway involving ApoC3 controlled by FoxO6 and its resultant functional impacts.
“[...] we employed a spectrum of models including liver cell cultures, aged rats subjected to HFD, transgenic mice overexpressing FoxO6 (FoxO6-Tg), and FoxO6 knockout mice (FoxO6-KO).”
Their findings indicate that FoxO6 triggered ApoC3-driven lipid accumulation in the livers of aged rats on an HFD and in FoxO6-Tg, consequently leading to hepatic steatosis and hyperglycemia. Conversely, the absence of FoxO6 attenuated the expression of genes involved in lipogenesis, resulting in diminished hepatic lipid accumulation and mitigated hyperlipidemia in murine models. Additionally, the upregulation of FoxO6 due to elevated glucose levels led to increased ApoC3 expression, consequently instigating cellular triglyceride mediated lipid accumulation. The transcriptional activation of FoxO6 induced by both the HFD and high glucose levels resulted in hepatic steatosis by upregulating ApoC3 and genes associated with gluconeogenesis in aged rats and liver cell cultures.
“Our conclusions indicate that the upregulation of ApoC3 by FoxO6 promotes the development of hyperlipidemia, hyperglycemia, and hepatic steatosis in vivo, and in vitro. Taken together, our findings underscore the significance of FoxO6 in driving hyperlipidemia and hepatic steatosis specifically under hyperglycemic states by enhancing the expression of ApoC3 in aged rats.”
DOI - https://doi.org/10.18632/aging.205610
Corresponding author - Hae Young Chung - [email protected]
Sign up for free Altmetric alerts about this article -
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205610
Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts
Keywords - aging, HFD-feeding aging, forkhead transcription factor O6, ApoC3, lipid accumulation, hepatic steatosis
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.
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
[email protected] -
Saknas det avsnitt?
-
BUFFALO, NY- March 19, 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 5, entitled, “PR55α-controlled protein phosphatase 2A inhibits p16 expression and blocks cellular senescence induction by γ-irradiation.”
Cellular senescence is a permanent cell cycle arrest that can be triggered by both internal and external genotoxic stressors, such as telomere dysfunction and DNA damage. The execution of senescence is mainly by two pathways, p16/RB and p53/p21, which lead to CDK4/6 inhibition and RB activation to block cell cycle progression. While the regulation of p53/p21 signaling in response to DNA damage and other insults is well-defined, the regulation of the p16/RB pathway in response to various stressors remains poorly understood.
In this new study, researchers Chitra Palanivel, Lepakshe S. V. Madduri, Ashley L. Hein, Christopher B. Jenkins, Brendan T. Graff, Alison L. Camero, Sumin Zhou, Charles A. Enke, Michel M. Ouellette, and Ying Yan from the University of Nebraska Medical Center report a novel function of PR55α, a regulatory subunit of PP2A Ser/Thr phosphatase, as a potent inhibitor of p16 expression and senescence induction by ionizing radiation (IR), such as γ-rays.
“During natural aging, there is a gradual accumulation of p16-expressing senescent cells in tissues [76]. To investigate the significance of PR55α in this up-regulation of p16, we compared levels of the p16 and PR55α proteins in a panel of normal tissue specimens derived from young (≤43 y/o) and old (≥68 y/o) donors.”
The results show that ectopic PR55α expression in normal pancreatic cells inhibits p16 transcription, increases RB phosphorylation, and blocks IR-induced senescence. Conversely, PR55α-knockdown by shRNA in pancreatic cancer cells elevates p16 transcription, reduces RB phosphorylation, and triggers senescence induction after IR. Furthermore, this PR55α function in the regulation of p16 and senescence is p53-independent because it was unaffected by the mutational status of p53. Moreover, PR55α only affects p16 expression but not p14 (ARF) expression, which is also transcribed from the same CDKN2A locus but from an alternative promoter. In normal human tissues, levels of p16 and PR55α proteins were inversely correlated and mutually exclusive.
“Collectively, these results describe a novel function of PR55α/PP2A in blocking p16/RB signaling and IR-induced cellular senescence.”
DOI - https://doi.org/10.18632/aging.205619
Corresponding authors - Michel M. Ouellette - [email protected], and Ying Yan - [email protected]
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).
Please visit our website at https://www.Aging-US.com.
[email protected] -
BUFFALO, NY- March 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 5, entitled, “Genome-wide transcriptome profiling and development of age prediction models in the human brain.”
Aging-related transcriptome changes in various regions of the healthy human brain have been explored in previous works, however, a study to develop prediction models for age based on the expression levels of specific panels of transcripts is lacking. Moreover, studies that have assessed sexually dimorphic gene activities in the aging brain have reported discrepant results, suggesting that additional studies would be advantageous. The prefrontal cortex (PFC) region was previously shown to have a particularly large number of significant transcriptome alterations during healthy aging in a study that compared different regions in the human brain.
In this new study, researchers Joseph A. Zarrella and Amy Tsurumi from the Harvard T.H. Chan School of Public Health, Massachusetts General Hospital, Harvard Medical School, and Shriner's Hospitals for Children-Boston aimed to profile PFC transcriptome changes during healthy human aging overall and comparing potential differences between female and male samples, as well as developing chronological age prediction models by various methods.
“We harmonized neuropathologically normal PFC transcriptome datasets obtained from the Gene Expression Omnibus (GEO) repository, ranging in age from 21 to 105 years, and found a large number of differentially regulated transcripts in the old and elderly, compared to young samples overall, and compared female and male-specific expression alterations.”
The team assessed the genes that were associated with age by employing ontology, pathway, and network analyses. Furthermore, they applied various established (least absolute shrinkage and selection operator (Lasso) and Elastic Net (EN)) and recent (eXtreme Gradient Boosting (XGBoost) and Light Gradient Boosting Machine (LightGBM)) machine learning algorithms to develop accurate prediction models for chronological age and validated them. Studies to further validate these models in other large populations and molecular studies to elucidate the potential mechanisms by which the transcripts identified may be related to aging phenotypes would be advantageous.
“Our results support the notions that specific gene expression changes in the PFC are highly correlated with age, that some transcripts show female and male-specific differences, and that machine learning algorithms are useful tools for developing prediction models for age based on transcriptome information.”
DOI - https://doi.org/10.18632/aging.205609
Corresponding author - Amy Tsurumi - [email protected]
Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts
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:
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
[email protected] -
Dr. Azra Frkatović-Hodžić from Genos Glycoscience Research Laboratory in Zagreb, Croatia, discusses a #research paper she co-authored that was #published by Aging (Aging-US) in Volume 15, Issue 24, entitled, “Mapping of the gene network that regulates glycan clock of ageing.”
DOI - https://doi.org/10.18632/aging.205106
Corresponding authors - Azra Frkatović-Hodžić - [email protected], and Gordan Lauc - [email protected]
Video - https://www.youtube.com/watch?v=5ExLCMDhpdE
Video transcription - https://aging-us.net/2024/03/13/behind-the-study-mapping-of-gene-network-that-regulates-glycan-clock-of-aging/
Abstract
Glycans are an essential structural component of immunoglobulin G (IgG) that modulate its structure and function. However, regulatory mechanisms behind this complex posttranslational modification are not well known. Previous genome-wide association studies (GWAS) identified 29 genomic regions involved in regulation of IgG glycosylation, but only a few were functionally validated. One of the key functional features of IgG glycosylation is the addition of galactose (galactosylation), a trait which was shown to be associated with ageing. We performed GWAS of IgG galactosylation (N=13,705) and identified 16 significantly associated loci, indicating that IgG galactosylation is regulated by a complex network of genes that extends beyond the galactosyltransferase enzyme that adds galactose to IgG glycans. Gene prioritization identified 37 candidate genes. Using a recently developed CRISPR/dCas9 system we manipulated gene expression of candidate genes in the in vitro IgG expression system. Upregulation of three genes, EEF1A1, MANBA and TNFRSF13B, changed the IgG glycome composition, which confirmed that these three genes are involved in IgG galactosylation in this in vitro expression system.
Sign up for free Altmetric alerts about this article -
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205106
Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts
Keywords - aging, genome-wide association study, glycosylation, glycan clock, immunoglobulin G, CRISPR/dCas9
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/
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/
Media Contact
18009220957
[email protected] -
BUFFALO, NY- March 13, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 4, entitled, “Single-Cell RNA-seq reveals transcriptomic modulation of Alzheimer’s disease by activated protein C.”
Single-Cell RNA sequencing reveals changes in cell population in Alzheimer’s disease (AD) model 5xFAD (5x Familial AD mutation) versus wild type (WT) mice. In this new study, researchers Mohammad Kasim Fatmi, Hao Wang, Lily Slotabec, Changhong Wen, Blaise Seale, Bi Zhao, and Ji Li from the University of South Florida, University of Mississippi Medical Center and the G.V. (Sonny) Montgomery VA Medical Center used single-cell RNA sequencing and bioinformatic analysis to analyze the effects of APC [Activated Protein C] treatment on AD transgenic mice.
“In our investigation, we utilized transgenic mice that contain expression for five major amyloid pathologies that allow for rapid progression of AD and Aβ deposition known as 5xFAD mice.”
The returned sequencing data was processed through the 10x Genomics CellRanger platform to perform alignment and form corresponding matrix to perform bioinformatic analysis. Alterations in glial cells occurred in 5xFAD versus WT, especially increases in microglia proliferation were profound in 5xFAD. Differential expression testing of glial cells in 5xFAD versus WT revealed gene regulation. Globally, the critical genes implicated in AD progression are upregulated such as Apoe, Ctsb, Trem2, and Tyrobp.
Using this differential expression data, GO term enrichment was completed to observe possible biological processes impacted by AD progression. Utilizing anti-inflammatory and cyto-protective recombinant Activated Protein C (APC), the researchers uncovered inflammatory processes to be downregulated by APC treatment in addition to recuperation of nervous system processes. Moreover, animal studies demonstrated that administration of recombinant APC significantly attenuated Aβ burden and improved cognitive function of 5xFAD mice.
“The downregulation of highly expressed AD biomarkers in 5xFAD could provide insight into the mechanisms by which APC administration benefits AD.”
DOI - https://doi.org/10.18632/aging.205624
Corresponding authors - Bi Zhao - [email protected], and Ji Li - [email protected]
Sign up for free Altmetric alerts about this article -
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205624
Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts
Keywords - aging, APC, Alzheimer’s disease, inflammation
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:
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 Contact
18009220957
[email protected] -
BUFFALO, NY- March 12, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 4, entitled, “Associations of prenatal one-carbon metabolism nutrients and metals with epigenetic aging biomarkers at birth and in childhood in a US cohort.”
Epigenetic gestational age acceleration (EGAA) at birth and epigenetic age acceleration (EAA) in childhood may be biomarkers of the intrauterine environment. In this new study, researchers Anne K. Bozack, Sheryl L. Rifas-Shiman, Andrea A. Baccarelli, Robert O. Wright, Diane R. Gold, Emily Oken, Marie-France Hivert, and Andres Cardenas from Stanford University School of Medicine, Harvard Medical School, Harvard T.H. Chan School of Public Health, Columbia University, and Icahn School of Medicine at Mount Sinai investigated the extent to which first-trimester folate, B12, 5 essential and 7 non-essential metals in maternal circulation are associated with EGAA and EAA in early life.
“[...] we hypothesized that OCM [one-carbon metabolism] nutrients and essential metals would be positively associated with EGAA and non-essential metals would be negatively associated with EGAA. We also investigated nonlinear associations and associations with mixtures of micronutrients and metals.”
Bohlin EGAA and Horvath pan-tissue and skin and blood EAA were calculated using DNA methylation measured in cord blood (N=351) and mid-childhood blood (N=326; median age = 7.7 years) in the Project Viva pre-birth cohort. A one standard deviation increase in individual essential metals (copper, manganese, and zinc) was associated with 0.94-1.2 weeks lower Horvath EAA at birth, and patterns of exposures identified by exploratory factor analysis suggested that a common source of essential metals was associated with Horvath EAA. The researchers also observed evidence of nonlinear associations of zinc with Bohlin EGAA, magnesium and lead with Horvath EAA, and cesium with skin and blood EAA at birth. Overall, associations at birth did not persist in mid-childhood; however, arsenic was associated with greater EAA at birth and in childhood.
“Prenatal metals, including essential metals and arsenic, are associated with epigenetic aging in early life, which might be associated with future health.”
DOI - https://doi.org/10.18632/aging.205602
Corresponding author - Andres Cardenas - [email protected]
Sign up for free Altmetric alerts about this article -
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205602
Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts
Keywords - aging, epigenetic age acceleration, metals, folate, B12, prenatal exposures
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.
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
[email protected] -
BUFFALO, NY- March 11, 2024 – Impact Journals #publishes scholarly #journals in the #biomedical sciences with a focus on all areas of cancer and aging research. Aging is one of the most prominent journals published by Impact Journals.
Impact Journals will be participating as an exhibitor at the American Association for Cancer Research (AACR) Annual Meeting 2024 from April 5-10 at the San Diego Convention Center in San Diego, California. This year, the AACR meeting theme is “Inspiring Science • Fueling Progress • Revolutionizing Care.”
Visit booth number 4159 at the AACR Annual Meeting 2024 to connect with members of the Aging team.
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).
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 Contact
18009220957
[email protected] -
Dr. Jiajian Wang from Sun Yat-Sen University, The Chinese University of Hong Kong, the Chinese Academy of Sciences, and the Shenzhen Key Laboratory of Metabolic Health, describes a #research paper he co-authored and #published in Aging’s Volume 16, Issue 3, entitled, “Generating detailed intercellular communication patterns in psoriasis at the single-cell level using social networking, pattern recognition, and manifold learning methods to optimize treatment strategies.”
Here is an audio version of a written Q&A that was submitted by Dr. Jiajian Wang on this research.
Full Q&A - https://aging-us.net/2024/03/11/behind-the-study-analyzing-psoriasis-communication-patterns-for-treatment-optimization/
Paper DOI - https://doi.org/10.18632/aging.205478
Corresponding Authors - Jiajian Wang - [email protected], and Bo Wu - [email protected]
Sign up for free Altmetric alerts about this article - https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205478
Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts
Keywords - communication patterns, single cell transcriptome, cell type-specific regulons (CTSRs), proteomic sequencing, social networking
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:
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 Contact
18009220957
[email protected] -
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 - [email protected]
Sign up for free Altmetric alerts about this article -
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205552
Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts
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.
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 Contact
18009220957
[email protected] -
BUFFALO, NY- March 6, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 4, entitled, “Exploring the effects of Dasatinib, Quercetin, and Fisetin on DNA methylation clocks: a longitudinal study on senolytic interventions.”
Senolytics, small molecules targeting cellular senescence, have emerged as potential therapeutics to enhance health span. However, their impact on epigenetic age remains unstudied. In this new study, researchers Edwin Lee, Natàlia Carreras-Gallo, Leilani Lopez, Logan Turner, Aaron Lin, Tavis L. Mendez, Hannah Went, Alan Tomusiak, Eric Verdin, Michael Corley, Lishomwa Ndhlovu, Ryan Smith, and Varun B. Dwaraka from the Institute For Hormonal Balance, TruDiagnostic, Buck Institute for Research on Aging, and Cornell University aimed to assess the effects of senolytic treatments on DNA methylation (DNAm), epigenetic age, and immune cell subsets.
“[...] this study aims to comprehensively assess the impact of senolytic drugs on epigenetic aging through two longitudinal studies to address our research objective. The initial investigation focuses on a combination treatment of Dasatinib and Quercetin, while the subsequent phase incorporates Fisetin into the treatment regimen.”
In a Phase I pilot study, 19 participants received Dasatinib and Quercetin (DQ) for 6 months, with DNAm measured at baseline, 3 months, and 6 months. Significant increases in epigenetic age acceleration were observed in first-generation epigenetic clocks and mitotic clocks at 3 and 6 months, along with a notable decrease in telomere length. However, no significant differences were observed in second and third-generation clocks.
Building upon these findings, a subsequent investigation evaluated the combination of DQ with Fisetin (DQF), a well-known antioxidant and antiaging senolytic molecule. After one year, 19 participants (including 10 from the initial study) received DQF for 6 months, with DNAm assessed at baseline and 6 months. Remarkably, the addition of Fisetin to the treatment resulted in non-significant increases in epigenetic age acceleration, suggesting a potential mitigating effect of Fisetin on the impact of DQ on epigenetic aging.
“Furthermore, our analyses unveiled notable differences in immune cell proportions between the DQ and DQF treatment groups, providing a biological basis for the divergent patterns observed in the evolution of epigenetic clocks. These findings warrant further research to validate and comprehensively understand the implications of these combined interventions.”
DOI - https://doi.org/10.18632/aging.205581
Corresponding authors - Varun B. Dwaraka - [email protected]
Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts
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:
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
[email protected] -
BUFFALO, NY- March 5, 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 4, entitled, “On standardization of controls in lifespan studies.”
In this new paper, researchers Olga Spiridonova, Dmitrii Kriukov, Nikolai Nemirovich-Danchenko, and Leonid Peshkin from Harvard Medical School's Department of Systems Biology discuss the burgeoning field of the search for interventions to slow down, and even reverse, aging. Currently available literature cites hundreds of supposedly beneficial pharmacological and genetic interventions in model organisms: mice, rats, flies, and worms, where research into physiology is routinely accompanied by lifespan data. However, when experimental animals from one article live as long as controls from another article, comparing the results of interventions across studies can yield misleading outcomes.
“Theoretically, all lifespan data are ripe for re-analysis: we could contrast the molecular targets and pathways across studies and help focus the further search for interventions.”
Alas, the results of most longevity studies are difficult to compare. This is in part because there are no clear, universally accepted standards for conducting such experiments or even for reporting such data. The situation is worsened by the fact that the authors often do not describe experimental conditions completely. As a result, works on longevity make up a set of precedents, each of which might be interesting in its own right, yet incoherent and incomparable at least for the reason that in a general context, it may indicate, for example, not prolonging the life of an average organism, but compensating for any genetic abnormalities of a particular sample or inappropriate living conditions.
“Here we point out specific issues and propose solutions for quality control by checking both inter- and intra-study consistency of lifespan data.”
DOI - https://doi.org/10.18632/aging.205604
Corresponding author - Leonid Peshkin - [email protected]
Sign up for free Altmetric alerts about this article -
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205604
Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts
Keywords - aging, animal disease models, survival modeling, data standardization
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:
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 Contact
18009220957
[email protected] -
BUFFALO, NY- February 29, 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 4, entitled, “Mapping the core senescence phenotype of primary human colon fibroblasts.”
Advanced age is the largest risk factor for many diseases and several types of cancer, including colorectal cancer (CRC). Senescent cells are known to accumulate with age in various tissues, where they can modulate the surrounding tissue microenvironment through their senescence associated secretory phenotype (SASP). Recently, researchers showed that there is an increased number of senescent cells in the colons of CRC patients and demonstrated that senescent fibroblasts and their SASP create microniches in the colon that are conducive to CRC onset and progression. However, the composition of the SASP is heterogenous and cell-specific, and the precise senescence profile of colon fibroblasts has not been well-defined.
In this new study, to generate a SASP atlas of human colon fibroblasts, researchers Namita Ganesh Hattangady, Kelly Carter, Brett Maroni-Rana, Ting Wang, Jessica Lee Ayers, Ming Yu, and William M. Grady from Fred Hutchinson Cancer Center and the University of Washington School of Medicine induced senescence in primary human colon fibroblasts using various in vitro methods and assessed the resulting transcriptome.
“[...] we utilized various relevant stressors to induce senescence in primary cultures of colon fibroblasts and perform RNA sequencing (RNASeq) to define an atlas of stressor-specific senescent profiles and a core senescent profile that is commonly regulated by all senescence inducers.”
Using RNA Sequencing and further validation by quantitative RT-PCR and Luminex assays, the team define and validate a ‘core senescent profile’ that might play a significant role in shaping the colon microenvironment. They also performed KEGG analysis and GO analyses to identify key pathways and biological processes that are differentially regulated in colon fibroblast senescence. These studies provide insights into potential driver proteins involved in senescence-associated diseases, like CRC, which may lead to therapies to improve overall health in the elderly and to prevent CRC.
“Further studies will be needed to address the limitations of our study and to translate our understanding of the SASP and disease into clinical care.”
DOI - https://doi.org/10.18632/aging.205577
Corresponding authors - William M. Grady - [email protected], and Ming Yu - [email protected]
Sign up for free Altmetric alerts about this article -
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205577
Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts
Keywords - aging, senescence, senescence associated secretory phenotype, SASP, colorectal cancer, cancer
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:
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 Contact
18009220957
[email protected] -
BUFFALO, NY- February 28, 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 3, entitled, “Prognostic model development and molecular subtypes identification in bladder urothelial cancer by oxidative stress signatures.”
Mounting studies indicate that oxidative stress (OS) significantly contributes to tumor progression. In this new study, researchers Ying Dong, Xiaoqing Wu, Chaojie Xu, Yasir Hameed, Mostafa A. Abdel-Maksoud, Taghreed N. Almanaa, Mohamed H. Kotob, Wahidah H. Al-Qahtani, Ayman M. Mahmoud, William C. Cho, and Chen Li from Shenzhen Second People’s Hospital, China Academy of Chinese Medical Sciences, Peking University, The Islamia University of Bahawalpur, King Saud University, University of Vienna, Manchester Metropolitan University, Queen Elizabeth Hospital, and Free University of Berlin focused on bladder urothelial cancer (BLCA), an escalating malignancy worldwide that is growing rapidly.
“Our objective was to verify the predictive precision of genes associated with overall survival (OS) by constructing a model that forecasts outcomes for bladder cancer and evaluates the prognostic importance of these genetic markers.”
Full press release - https://www.aging-us.com/news-room/Prognostic-Model-Development-and-Molecular-Subtypes-Identification-in-Bladder-Urothelial-Cancer
DOI - https://doi.org/10.18632/aging.205499
Corresponding authors - Yasir Hameed - [email protected], William C. Cho - [email protected], and Chen Li - [email protected]
Sign up for free Altmetric alerts about this article -
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205499
Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts
Keywords - aging, oxidative stress, bladder urothelial cancer, tumor microenvironment, immunotherapy
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:
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 Contact
18009220957
[email protected] -
BUFFALO, NY- February 27, 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 3, entitled, “The anti-aging effect of vitamin D and vitamin D receptor in Drosophila midgut.”
Adult stem cells are pivotal for maintaining tissue homeostasis, and their functional decline is linked to aging and its associated diseases, influenced by the niche cells’ environment. Age- and cancer-related reduction of vitamin D and its receptor levels are well documented in human clinical studies. However, the mechanisms through which the vitamin D/vitamin D receptor (VitD/VDR) pathway contributes to anti-aging and extends life expectancy are not well understood. In this new study, researchers Joung-Sun Park, Hyun-Jin Na and Yung-Jin Kim from Pusan National University and Korea Food Research Institute aimed to determine the protective role of the vitamin D/vitamin D receptor pathway in differentiated enterocytes (ECs) during intestinal stem cell (ISC) aging.
“This study aimed to determine the protective role of VitD/VDR in differentiated ECs during ISC aging using the adult Drosophila intestine model.”
By utilizing a well-established Drosophila midgut model for stem cell aging biology, the researchers revealed that vitamin D receptor knockdown in ECs induced ISC proliferation, EC death, ISC aging, and enteroendocrine cell differentiation. Additionally, age- and oxidative stress-induced increases in ISC proliferation and centrosome amplification were reduced by vitamin D treatment. In conclusion, this study provides direct evidence of the anti-aging role of the VitD/VDR pathway, involving protecting ECs during aging, and provides valuable insights for exploring the molecular mechanisms underlying enhanced healthy aging in Drosophila.
“Our findings suggest a direct evidence of the anti-aging role of the vitamin D/vitamin D receptor pathway and provides insights into the molecular mechanisms underlying healthy aging in Drosophila.”
DOI - https://doi.org/10.18632/aging.205518
Corresponding author - Joung-Sun Park - [email protected]
Sign up for free Altmetric alerts about this article -
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205518
Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts
Keywords - aging, Drosophila, vitamin D, vitamin D receptor, anti-aging, intestinal stem cell
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:
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 Contact
18009220957
[email protected] -
BUFFALO, NY- February 21, 2024 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 3, entitled, “Disruption of mitochondrial unfolded protein response results in telomere shortening in mouse oocytes and somatic cells.”
Caseinolytic peptidase P (CLPP) plays a central role in mitochondrial unfolded protein response (mtUPR) by promoting the breakdown of misfolded proteins and setting in motion a cascade of reactions to re-establish protein homeostasis. Global germline deletion of Clpp in mice results in female infertility and accelerated follicular depletion. Telomeres are tandem repeats of 5’-TTAGGG-3’ sequences found at the ends of the chromosomes. Telomeres are essential for maintaining chromosome stability during somatic cell division and their shortening is associated with cellular senescence and aging.
In this new study, researchers Mauro Cozzolino, Yagmur Ergun, Emma Ristori, Akanksha Garg, Gizem Imamoglu, and Emre Seli from Yale School of Medicine, IVIRMA Global Research Alliance and Imperial College London asked whether the infertility and ovarian aging phenotype caused by global germline deletion of Clpp is associated with somatic aging, and tested telomere length in tissues of young and aging mice.
“In this study, we asked whether the infertility and ovarian aging phenotype caused by global germline deletion of Clpp is associated with somatic aging, and tested telomere length in young and aging mice gametes, gonads and somatic tissues.”
The team found that impaired mtUPR caused by the lack of CLPP is associated with accelerated telomere shortening in both oocytes and somatic cells of aging mice. In addition, expression of several genes that maintain telomere integrity was decreased, and double-strand DNA breaks were increased in telomeric regions. Their results highlight how impaired mtUPR can affect telomere integrity and demonstrate a link between loss of mitochondrial protein hemostasis, infertility, and somatic aging.
“Our findings demonstrate how loss of mitochondrial protein homeostasis may accelerate telomere shortening in oocytes and somatic cells, and provide a link between reproductive and somatic aging.”
DOI - https://doi.org/10.18632/aging.205543
Corresponding author - Emre Seli - [email protected]
Sign up for free Altmetric alerts about this article -
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205543
Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts
Keywords - aging, telomere length, Clpp, mitochondrial dysfunction, unfolded protein response
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:
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 Contact
18009220957
[email protected] -
BUFFALO, NY- February 20, 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 3, entitled, “Defining the progeria phenome.”
Progeroid disorders are a heterogenous group of rare and complex hereditary syndromes presenting with pleiotropic phenotypes associated with normal aging. Due to the large variation in clinical presentation the diseases pose a diagnostic challenge for clinicians which consequently restricts medical research. In this new study, researchers Cecilie Worm, Maya Elena Ramirez Schambye, Garik V. Mkrtchyan, Alexander Veviorskiy, Anastasia Shneyderman, Ivan V. Ozerov, Alex Zhavoronkov, Daniela Bakula, and Morten Scheibye-Knudsen from the University of Copenhagen and Insilico Medicine aimed to accommodate this challenge by compiling a list of known progeroid syndromes and calculating the mean prevalence of their associated phenotypes, defining what they term the ‘progeria phenome’.
“In this study, we have utilized phenome explorations to define the phenotypes associated with progerias and to develop tools to diagnose patients and identify new progeroid syndromes.”
The data were used to train a support vector machine that is available at https://www.mitodb.com and able to classify progerias based on phenotypes. Furthermore, this allowed the researchers to investigate the correlation of progeroid syndromes and syndromes with various pathogenesis using hierarchical clustering algorithms and disease networks. They detected that ataxia-telangiectasia like disorder 2, spastic paraplegia 49 and Meier-Gorlin syndrome display strong association to progeroid syndromes, thereby implying that the syndromes are previously unrecognized progerias.
“In conclusion, our study has provided tools to evaluate the likelihood of a syndrome or patient being progeroid. This is a considerable step forward in our understanding of what constitutes a premature aging disorder and how to diagnose them.”
DOI - https://doi.org/10.18632/aging.205537
Corresponding author - Morten Scheibye-Knudsen - [email protected]
Sign up for free Altmetric alerts about this article -
https://aging.altmetric.com/details/email_updates?id=10.18632%2Faging.205537
Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts
Keywords - aging, progeria, premature aging, phenome, clinical phenotype
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:
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 Contact
18009220957
[email protected] -
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 [email protected]. -
BUFFALO, NY- February 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 3, entitled, “GV1001 reduces neurodegeneration and prolongs lifespan in 3xTg-AD mouse model through anti-aging effects.”
GV1001, which mimics the activity of human telomerase reverse transcriptase, protects neural cells from amyloid beta (Aβ) toxicity and other stressors through extra-telomeric function, as noted in our prior in vitro studies. As per a recent phase II clinical trial, it improves cognitive function in patients with moderate to severe dementia. However, the underlying protective mechanisms remain unclear.
In this new study, researchers Hyun-Hee Park, Hyuk Sung Kwon, Kyu-Yong Lee, Ye Eun Kim, Jeong-Woo Son, Na-Young Choi, Myung-Hoon Han, Dong Woo Park, Sangjae Kim, and Seong-Ho Koh from Hanyang University Guri Hospital, Hanyang University Graduate School of Biomedical Science and Engineering and Teloid Inc. aimed to investigate the effects of GV1001 on neurodegeneration, senescence, and survival in triple transgenic Alzheimer’s disease (AD) (3xTg-AD) mice.
“ [...] we hypothesised that GV1001 might have anti-aging effects and improve neurodegeneration and senescence in vivo as a possible mechanism for its beneficial effects on AD.”
GV1001 (1 mg/kg) was subcutaneously injected into old 3xTg-AD mice thrice a week until the endpoint for sacrifice, and survival was analysed. Magnetic resonance imaging (MRI) and Prussian blue staining (PBS) were performed to evaluate entry of GV1001 entrance into the brain. Diverse molecular studies were performed to investigate the effect of GV1001 on neurodegeneration and cellular senescence in AD model mice, with a particular focus on BACE, amyloid beta1-42 (Aβ1-42), phosphorylated tau, volume of dentate gyrus, β-galactosidase positive cells, telomere length, telomerase activity, and ageing-associated proteins.
GV1001 crossed the blood-brain barrier, as confirmed by assessing the status of ferrocenecarboxylic acid-conjugated GV1001 using magnetic resonance imaging and PBS. GV1001 increased the survival of 3xTg-AD mice. It decreased BACE and Aβ1-42 levels, neurodegeneration (i.e., reduced CA1, CA3 and dentate gyrus volume, decreased levels of senescence-associated β-galactosidase positive cells, and increased telomere length and telomerase activity), and levels of ageing-associated proteins.
“We suggest that GV1001 exerts anti-ageing effects in 3xTg-AD mice by reducing neurodegeneration and senescence, which contributes to improved survival.”
DOI - https://doi.org/10.18632/aging.205489
Corresponding authors - Sangjae Kim - [email protected], and Seong-Ho Koh - [email protected]
Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts
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:
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
[email protected] -
BUFFALO, NY- February 13, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 2, entitled, “IL-17 promotes IL-18 production via the MEK/ERK/miR-4492 axis in osteoarthritis synovial fibroblasts.”
The concept of osteoarthritis (OA) as a low-grade inflammatory joint disorder has been widely accepted. Many inflammatory mediators are implicated in the pathogenesis of OA. Interleukin (IL)-18 is a pleiotropic cytokine with versatile cellular functions that are pathogenetically important in immune responses, as well as autoimmune, inflammatory, and infectious diseases. IL-17, a proinflammatory cytokine mainly secreted by Th17 cells, is upregulated in OA patients. However, the role of IL-17 in OA progression is unclear.
In this new study, researchers Kun-Tsan Lee, Chih-Yang Lin, Shan-Chi Liu, Xiu-Yuan He, Chun-Hao Tsai, Chih-Yuan Ko, Yuan-Hsin Tsai, Chia-Chia Chao, Po-Chun Chen, and Chih-Hsin Tang from National Chung-Hsing University, Taichung Veterans General Hospital, Shin-Kong Wu Ho-Su Memorial Hospital, Mackay Medical College, China Medical University, Show-Chwan Memorial Hospital, Fu-Jen Catholic University, National Taiwan Normal University, Asia University, and China Medical University Hsinchu Hospital used synovial tissues collected from healthy donors and OA patients to detect the expression level of IL-18 by immunohistochemistry stain.
“Elucidation of the molecular mechanisms and main factors involved in OA pathogenesis may help with the development of novel therapeutic targets that relieve OA pain or prevent the disease from progressing.”
The OA synovial fibroblasts (OASFs) were incubated with recombinant IL-17 and subjected to Western blot, qPCR, and ELISA to examine IL-18 expression level. The chemical inhibitors and siRNAs which targeted signal pathways were used to investigate signal pathways involved in IL-17-induced IL-18 expression. The microRNAs which participated IL-18 expression were surveyed with online databases miRWalk and miRDB, followed by validation with qPCR.
This study revealed significantly higher levels of IL-18 expression in synovial tissue from OA patients compared with healthy controls, as well as increased IL-18 expression in OASFs from rats with severe OA. In vitro findings indicated that IL-17 dose-dependently promoted IL-18 production in OASFs. Molecular investigations revealed that the MEK/ERK/miR-4492 axis stimulated IL-18 production when OASFs were treated with IL-17.
“This study provides novel insights into the role of IL-17 in the pathogenesis of OA, which may help to inform OA treatment in the future.”
DOI - https://doi.org/10.18632/aging.205462
Corresponding authors - Po-Chun Chen - [email protected], and Chih-Hsin Tang - [email protected]
Subscribe for free publication alerts from Aging - https://www.aging-us.com/subscribe-to-toc-alerts
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:
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 Contact
18009220957
[email protected] - Visa fler
