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.

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Aging

Aging-US published this trending research paper on September 9, 2021, entitled, “Hyperbaric oxygen therapy alleviates vascular dysfunction and amyloid burden in an Alzheimer’s disease mouse model and in elderly patients” by researchers from the School of Neurobiology, Biochemistry and Biophysics, The George S. Wise Faculty of Life Sciences, Tel Aviv University, Tel-Aviv, Israel; Sagol School of Neuroscience, Tel Aviv University, Tel-Aviv, Israel; Sackler School of Medicine, Tel Aviv University, Tel-Aviv, Israel; Sagol Center for Hyperbaric Medicine and Research, Assaf Harofeh Medical Center, Be’er Ya’akov, Israel.

Abstract
Vascular dysfunction is entwined with aging and in the pathogenesis of Alzheimer’s disease (AD) and contributes to reduced cerebral blood flow (CBF) and consequently, hypoxia. Hyperbaric oxygen therapy (HBOT) is in clinical use for a wide range of medical conditions. In the current study, we exposed 5XFAD mice, a well-studied AD model that presents impaired cognitive abilities, to HBOT and then investigated the therapeutical effects using two-photon live animal imaging, behavioral tasks, and biochemical and histological analysis. HBOT increased arteriolar luminal diameter and elevated CBF, thus contributing to reduced hypoxia. Furthermore, HBOT reduced amyloid burden by reducing the volume of pre-existing plaques and attenuating the formation of new ones. This was associated with changes in amyloid precursor protein processing, elevated degradation and clearance of Aß protein and improved behavior of 5XFAD mice. Hence, our findings are consistent with the effects of HBOT being mediated partially through a persistent structural change in blood vessels that reduces brain hypoxia. Motivated by these findings, we exposed elderly patients with significant memory loss at baseline to HBOT and observed an increase in CBF and improvement in cognitive performances. This study demonstrates HBOT efficacy in hypoxia-related neurological conditions, particularly in AD and aging.

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DOI - https://doi.org/10.18632/aging.203485

Full text - https://www.aging-us.com/article/203485/text

Correspondence to: Uri Ashery email: uria@tauex.tau.ac.il

Keywords: Alzheimer's disease, hyperbaric oxygen therapy, vascular dysfunction, cerebral blood flow, amyloid burden, aging

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 http://www.Aging-US.com​​ or connect with us on:

Twitter - https://twitter.com/AgingJrnl
Facebook - https://www.facebook.com/AgingUS/
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YouTube - https://www.youtube.com/agingus​
LinkedIn -  https://www.linkedin.com/company/aging​

Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls

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Trending with Impact: Hyperbaric Oxygen Therapy Alleviates Vascular Dysfunction and Amyloid Burden

Aging-US published this high-scoring research paper on August 15, 2019, entitled, “Rejuvenation of brain, liver and muscle by simultaneous pharmacological modulation of two signaling determinants, that change in opposite directions with age,” by researchers from the Department of Bioengineering and QB3 Institute, University of California, Berkeley, Berkeley, CA; Department of Molecular, Cell and Developmental Biology, University of California, Santa Cruz, Santa Cruz, CA.

Abstract:
We hypothesize that altered intensities of a few morphogenic pathways account for most/all the phenotypes of aging. Investigating this has revealed a novel approach to rejuvenate multiple mammalian tissues by defined pharmacology. Specifically, we pursued the simultaneous youthful in vivo calibration of two determinants: TGF-beta which activates ALK5/pSmad 2,3 and goes up with age, and oxytocin (OT) which activates MAPK and diminishes with age. The dose of Alk5 inhibitor (Alk5i) was reduced by 10-fold and the duration of treatment was shortened (to minimize overt skewing of cell-signaling pathways), yet the positive outcomes were broadened, as compared with our previous studies. Alk5i plus OT quickly and robustly enhanced neurogenesis, reduced neuro-inflammation, improved cognitive performance, and rejuvenated livers and muscle in old mice. Interestingly, the combination also diminished the numbers of cells that express the CDK inhibitor and marker of senescence p16 in vivo. Summarily, simultaneously re-normalizing two pathways that change with age in opposite ways (up vs. down) synergistically reverses multiple symptoms of aging.

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DOI - https://doi.org/10.18632/aging.102148

Full text - https://www.aging-us.com/article/102148/text

Correspondence to: Irina M. Conboy email: iconboy@berkeley.edu

Keywords: muscle repair, TGF-beta, oxytocin, neurogenesis, neuro-inflammation, cognition, liver health

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 http://www.Aging-US.com​​ or connect with us on:

Twitter - https://twitter.com/AgingJrnl​
Facebook - https://www.facebook.com/AgingUS/​
SoundCloud - https://soundcloud.com/aging-us​
YouTube - https://www.youtube.com/agingus​
LinkedIn -  https://www.linkedin.com/company/aging​

Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls

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MEDIA@IMPACTJOURNALS.COM

Top-Performer: TGF-beta and Oxytocin Reversed to Reverse Aging

Aging-US published this trending research paper - selected as the cover for Volume 13, Issue 17 - on September 7, 2021, entitled, “Reduced uremic metabolites are prominent feature of sarcopenia, distinct from antioxidative markers for frailty” by researchers from the Geriatric Unit, Graduate School of Medicine, Kyoto University, Kyoto, Japan; G0 Cell Unit, Okinawa Institute of Science and Technology Graduate University (OIST), Okinawa, Japan.

Abstract
Due to global aging, frailty and sarcopenia are increasing. Sarcopenia is defined as loss of volume and strength of skeletal muscle in elderlies, while frailty involves multiple domains of aging-related dysfunction, impaired cognition, hypomobility, and decreased social activity. However, little is known about the metabolic basis of sarcopenia, either shared with or discrete from frailty. Here we analyzed comprehensive metabolomic data of human blood in relation to sarcopenia, previously collected from 19 elderly participants in our frailty study. Among 131 metabolites, we identified 22 sarcopenia markers, distinct from 15 frailty markers, mainly including antioxidants, although sarcopenia overlaps clinically with physical frailty. Notably, 21 metabolites that decline in sarcopenia or low SMI are uremic compounds that increase in kidney dysfunction. These comprise TCA cycle, urea cycle, nitrogen, and methylated metabolites. Sarcopenia markers imply a close link between muscle and kidney function, while frailty markers define a state vulnerable to oxidative stress.

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DOI - https://doi.org/10.18632/aging.203498

Full text - https://www.aging-us.com/article/203498/text

Correspondence to: Mitsuhiro Yanagida email: myanagid@gmail.com

Keywords: sarcopenia, muscle mass, metabolomics, frailty, uremic metabolites, aging

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 http://www.Aging-US.com​​ or connect with us on:

Twitter - https://twitter.com/AgingJrnl
Facebook - https://www.facebook.com/AgingUS/
SoundCloud - https://soundcloud.com/aging-us​
YouTube - https://www.youtube.com/agingus​
LinkedIn -  https://www.linkedin.com/company/aging​

Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls

Media Contact
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MEDIA@IMPACTJOURNALS.COM

Trending with Impact: DNA Markers Distinguish Sarcopenia from Frailty

Aging-US published this trending research paper on August 10, 2021, entitled, “Senescence-associated hyper-activation to inflammatory stimuli in vitro” by researchers from the College of Medicine, University of Florida, Gainesville, FL, and the College of Pharmacy, University of Florida, Gainesville, FL.

Abstract
Aging is associated with an increased susceptibility to adverse inflammatory conditions such as sepsis and cytokine storm. We hypothesized that senescent cells (SnCs) play a central role in this age-associated pathology in part due to their expression of the senescence-associated secretory phenotype (SASP), which may prime SnCs to inflammatory stimulation. To test this hypothesis, we examined the expression of various inflammatory cytokines and chemokines at the levels of gene transcription and protein production in various SnCs in vitro in response to lipopolysaccharide (LPS), interleukin-1β (IL1β), and tumor necrosis factor α (TNFα) stimulation. We found that SnCs not only expressed higher basal levels of various inflammatory cytokines and chemokines as a manifestation of the SASP, but more importantly exhibited hyper-activation of the induction of a variety of inflammatory mediators in response to LPS, IL1β and TNFα stimulation as compared with non-SnCs. This senescence-associated hyper-activation is likely mediated in part via the p38MAPK (p38) and NFκB pathways because LPS stimulation elicited significantly higher levels of p38 phosphorylation and NFκB p65 nuclear translation in SnCs when compared to their non-senescent counterparts and inhibition of these pathways with losmapimod (a p38 specific inhibitor) and BMS-345541 (a selective NFκB inhibitor) attenuated LPS-induced expression of IL6, TNFα, CCL5, and IL1β mRNA in SnCs. These findings suggest that SnCs may play an important role in the age-related increases in the susceptibility to developing an exacerbated inflammatory response and highlight the potential to use senotherapeutics to ameliorate the severity of various devastating inflammatory conditions in the elderly.

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DOI - https://doi.org/10.18632/aging.203396

Full text - https://www.aging-us.com/article/203396/text

Correspondence to: Daohong Zhou email: zhoudaohong@cop.ufl.edu

Keywords: cellular senescence, inflammation, SASP, aging

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 http://www.Aging-US.com​​ or connect with us on:

Twitter - https://twitter.com/AgingJrnl
Facebook - https://www.facebook.com/AgingUS/
SoundCloud - https://soundcloud.com/aging-us​
YouTube - https://www.youtube.com/agingus​
LinkedIn -  https://www.linkedin.com/company/aging​

Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls

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MEDIA@IMPACTJOURNALS.COM

Top-Performer: Senescent Cells and Inflamm-Aging

Aging-US published this trending review on August 12, 2021, entitled, “Cellular senescence in lymphoid organs and immunosenescence,” by researchers from the Genetics and Genomics Graduate Program, Genetics Institute, College of Medicine, University of Florida, Gainesville, FL; Department of Neuroscience, McKnight Brain Institute, College of Medicine, University of Florida, Gainesville, FL; Department of Pharmacodynamics, College of Pharmacy, University of Florida, Gainesville, FL.


Abstract:
Immunosenescence is a multi-faceted phenomenon at the root of age-associated immune dysfunction. It can lead to an array of pathological conditions, including but not limited to a decreased capability to surveil and clear senescent cells (SnCs) and cancerous cells, an increased autoimmune responses leading to tissue damage, a reduced ability to tackle pathogens, and a decreased competence to illicit a robust response to vaccination. Cellular senescence is a phenomenon by which oncogene-activated, stressed or damaged cells undergo a stable cell cycle arrest. Failure to efficiently clear SnCs results in their accumulation in an organism as it ages. SnCs actively secrete a myriad of molecules, collectively called senescence-associated secretory phenotype (SASP), which are factors that cause dysfunction in the neighboring tissue. Though both cellular senescence and immunosenescence have been studied extensively and implicated in various pathologies, their relationship has not been greatly explored. In the wake of an ongoing pandemic (COVID-19) that disproportionately affects the elderly, immunosenescence as a function of age has become a topic of great importance. The goal of this review is to explore the role of cellular senescence in age-associated lymphoid organ dysfunction and immunosenescence, and provide a framework to explore therapies to rejuvenate the aged immune system.

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DOI - https://doi.org/10.18632/aging.203405

Full text - https://www.aging-us.com/article/203405/text

Correspondence to: Daohong Zhou email: zhoudaohong@cop.ufl.edu

Keywords: cellular senescence, immunosenescence, immune senescence, senescence associated secretory phenotype (SASP), thymus

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 http://www.Aging-US.com​​ or connect with us on:

Twitter - https://twitter.com/AgingJrnl​
Facebook - https://www.facebook.com/AgingUS/​
SoundCloud - https://soundcloud.com/aging-us​
YouTube - https://www.youtube.com/agingus​
LinkedIn -  https://www.linkedin.com/company/aging​

Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls

Media Contact
18009220957
MEDIA@IMPACTJOURNALS.COM

Top-Performer: Cellular Senescence in Lymphoid Organs and Immunosenescence

Aging-US published this trending research paper on August 18, 2021, entitled, “COVID-19 mortality rate in children is U-shaped” by researchers from Buckingham Browne and Nichols School, Cambridge, MA; Division of Genetics, Department of Medicine, Brigham and Women’s Hospital and Harvard Medical School, Boston, MA; Biotein, Wellesley, MA.

Abstract
Children are known to be better protected from COVID-19 than adults, but their susceptibility patterns and the risk relative to other diseases are insufficiently defined. Here, we found that the COVID-19 mortality rate is U-shaped in childhood: it initially decreases, reaching the minimum at the ages 3-10 years, and then increases throughout life. All-cause mortality and mortality from other diseases, such as pneumonia and influenza, show a similar pattern; however, childhood mortality rates from COVID-19 are considerably lower than from other diseases, with the best relative protection achieved at the youngest ages. Consistent with this, the fraction of COVID-19 deaths among all deaths increases as a function of age throughout childhood and the entire life. We discuss implications of the elevated postnatal COVID-19 risk and lower childhood COVID-19 mortality compared to other diseases.

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DOI - https://doi.org/10.18632/aging.203442

Full text - https://www.aging-us.com/article/203442/text

Correspondence to: Vadim N. Gladyshev email: vgladyshev@rics.bwh.harvard.edu

Keywords: mortality, COVID-19, SARS-CoV-2, pediatrics, aging

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 http://www.Aging-US.com​​ or connect with us on:

Twitter - https://twitter.com/AgingJrnl
Facebook - https://www.facebook.com/AgingUS/
SoundCloud - https://soundcloud.com/aging-us​
YouTube - https://www.youtube.com/agingus​
LinkedIn -  https://www.linkedin.com/company/aging​

Aging-US is published by Impact Journals, LLC please visit http://www.ImpactJournals.com​​ or connect with @ImpactJrnls

Media Contact
18009220957
MEDIA@IMPACTJOURNALS.COM

Aging

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