Aging-US Aging (Aging-US) Podcast

BUFFALO, NY- June 5, 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 10, entitled, “Serine racemase expression profile in the prefrontal cortex and hippocampal subregions during aging in male and female rats.”

Aging is associated with a decrease in N-methyl-D-aspartate (NMDA) receptor function, which is critical for maintaining synaptic plasticity, learning, and memory. Activation of the NMDA receptor requires binding of the neurotransmitter glutamate and also the presence of co-agonist D-serine at the glycine site. The enzymatic conversion of L-serine to D-serine is facilitated by the enzyme serine racemase (SR).

Subsequently, SR plays a pivotal role in regulating NMDA receptor activity, thereby impacting synaptic plasticity and memory processes in the central nervous system. As such, age-related changes in the expression of SR could contribute to decreased NMDA receptor function. However, age-associated changes in SR expression levels in the medial and lateral prefrontal cortex (mPFC, lPFC), and in the dorsal hippocampal subfields, CA1, CA3, and dentate gyrus (DG), have not been thoroughly elucidated.

In this new study, researchers Linda Bean, Prodip K. Bose, Asha Rani, and Ashok Kumar from Indiana University School of Medicine, North Florida/South Georgia Veterans Health System, and the University of Florida aimed to determine the SR expression profile, including protein levels and mRNA, for these regions in aged and young male and female Fischer-344 rats. Their results demonstrate a significant reduction in SR expression levels in the mPFC and all hippocampal subfields of aged rats compared to young rats. No sex differences were observed in the expression of SR.

“These findings suggest that the decrease in SR levels may play a role in the age-associated reduction of NMDA receptor function in brain regions crucial for cognitive function and synaptic plasticity.”

DOI - https://doi.org/10.18632/aging.205841

Corresponding author - Ashok Kumar - kash@ufl.edu

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Keywords - aging, serine racemase, hippocampus, medial prefrontal cortex (mPFC), NMDA receptor

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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BUFFALO, NY- June 3, 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 10, entitled, “Integrated liver and serum proteomics uncover sexual dimorphism and alteration of several immune response proteins in an aging Werner syndrome mouse model.”

Werner syndrome (WS) is a progeroid disorder caused by mutations in a protein containing both a DNA exonuclease and DNA helicase domains. Previous studies indicated that males lacking the helicase domain of the Wrn protein orthologue exhibited hepatic transcriptomic and metabolic alterations.

In this new study, researchers Lucie Aumailley, Marie Julie Dubois, André Marette, and Michel Lebel from Université Laval used a label-free liquid chromatography-tandem mass spectrometry approach to uncover proteins abundance associated with specific biological processes that differed depending on the age (four or ten months) and/or the genotype (wild type or Wrn mutant) in the serum and liver of mice. Principal component analysis of the proteomic data from both serum and hepatic tissue revealed a sexual dimorphism regardless of the age and the genotype of the mice.

“Moreover, although all Wrn mutant mice exhibited fatty liver by the age of ten months, a significant age and genotype dependent enrichment of proteins involved in lipid and fatty acid metabolic processes were uncovered only in males.”

Also, a genotype dependent increase in serum oxidant detoxification processes was observed in the serum of Wrn mutant males. Despite these sexual differences, several aspects of the immune system were affected in both females and males. Finally, an increase of specific immunoglobulin molecules was common in the liver and serum of both older Wrn mutant females and males.

“Such results suggest that specific immunoglobulin variants maybe associated with fatty liver progression in WS.”

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

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

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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.)

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BUFFALO, NY- May 22, 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 9, entitled, “Cell type-dependent modulation of senescence features using Weo electrolyzed water.”

Electrolyzed-reduced water has powerful antioxidant properties with constituents that scavenge reactive oxygen species (ROS), which are known to be produced by several intrinsic and extrinsic processes. When there is an imbalance between ROS production and antioxidant defenses, oxidative stress occurs. Persistent oxidative stress leads to cellular senescence, an important hallmark of aging, and is involved in several age-related conditions and illnesses.

In this new study, researchers Brenda L. Court-Vazquez, Shirley A. Arroyo-Vizcarrondo, Jonathan A. Poli, Lara Nyman, Kelly Halderman, Anthony Ginter, and Pierre-Yves Desprez from Weo LLC and California Pacific Medical Center investigated whether Weo electrolyzed water (WEW) could modulate the phenotype of senescent cells.

“The focus of this study was to utilize two different cell types, human normal fibroblasts and human breast cancer cells, to investigate the impact of Weo electrolyzed water (WEW) on markers of cellular senescence, inflammation, and stress response genes.”

The researchers compared normal human lung fibroblasts (BJ) and breast cancer cells (T47D) treated with hydrogen peroxide (H2O2) to induce senescence. They assessed the molecular impact of WEW on markers of cellular senescence, senescence-associated secretory phenotype (SASP) factors, and stress response genes. Treatment with WEW modulated markers of cellular senescence, such as the senescence-associated β-galactosidase (SA-β-gal) activity, EdU incorporation and p21 expression, similarly in both cell types.

However, WEW modulated the expression of SASP factors and stress response genes in a cell type-dependent and opposite fashion, significantly decreasing them in BJ cells, while stimulating their expression in T47D cells. Reduction in the expression of SASP factors and stress-related genes in BJ cells suggests that WEW acts as a protective factor, thereby reducing oxidative stress in normal cells, while making cancer cells more sensitive to the effects of cellular stress, thus increasing their elimination and consequently reducing their deleterious effects.

“In conclusion, we have shown here that the new technology developed by Weo, WEW, could attenuate the overall process of cellular senescence in both normal BJ fibroblasts and cancer T47D cells.”

DOI - https://doi.org/10.18632/aging.205789

Corresponding authors - Brenda L. Court-Vazquez - bco@we-o.com, and Pierre-Yves Desprez - pydesprez@cpmcri.org

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Keywords - aging, cellular senescence, senescence-associated secretory phenotype, oxidative stress, lung fibroblasts, breast cancer cells, senomorphic

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.

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Dr. Leonid Peshkin from the Department of Systems Biology at Harvard Medical School details a research perspective he co-authored that was published by Aging (Aging-US) in Volume 16, Issue 4, entitled, “On standardization of controls in lifespan studies.”
#aging #author #interview #researcher#data #standardization #lifespan #longevity #study #perspective #openaccess #openscience #peerreview #journal #publication #publishing #meded #spotlight #agingshort #video

DOI - https://doi.org/10.18632/aging.205604

Corresponding author - Leonid Peshkin - pesha@hms.harvard.edu

Video interview - https://www.youtube.com/watch?v=N_tL2aTN2Jw

Interview transcript - https://aging-us.net/2024/05/22/behind-the-study-on-standardization-of-controls-in-lifespan-studies/

Abstract

The search for interventions to slow down and even reverse aging is a burgeoning field. The 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.

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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.

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BUFFALO, NY- May 21, 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 9, entitled, “Germicidal lamps using UV-C radiation may pose health safety issues: a biomolecular analysis of their effects on apoptosis and senescence.”

The battle against the COVID-19 pandemic has spurred a heightened state of vigilance in global healthcare, leading to the proliferation of diverse sanitization methods. Among these approaches, germicidal lamps utilizing ultraviolet (UV) rays, particularly UV-C (wavelength ranging from 280 to 100 nm), have gained prominence for domestic use.

These light-emitting diode (LED) lamps are designed to sanitize the air, objects, and surfaces. However, the prevailing concern is that these UV lamps are often introduced into the market without adequate accompanying information to ensure their safe utilization. Importantly, exposure to absorbed UV light can potentially trigger adverse biological responses, encompassing cell death and senescence.

In this new study, researchers Nicola Alessio, Alessia Ambrosino, Andrea Boggi, Domenico Aprile, Iole Pinto, Giovanni Galano, Umberto Galderisi, and Giovanni Di Bernardo from the University of Campania Luigi Vanvitelli, Regional Public Health Laboratory in Siena, Italy, ASL Napoli 1 Centro P.S.I. Napoli Est-Barra, and Temple University performed a series of investigations aimed at comprehending the biological repercussions of UV-C radiation exposure from readily available domestic lamps.

“Our focus centered on epithelial retinal cells, keratinocytes, and fibroblasts, components of the skin and ocular targets frequently exposed to UV irradiation.”

Their findings underscore the potential harm associated with even brief exposure to UV, leading to irreversible and detrimental alterations in both skin cells and retinal cells of the eye. Notably, epithelial retinal cells exhibited heightened sensitivity, marked by substantial apoptosis. In contrast, keratinocytes demonstrated resilience to apoptosis even at elevated UV doses, though they were prone to senescence. Meanwhile, fibroblasts displayed a gradual amplification of both senescence and apoptosis as radiation doses escalated.

“In summary, despite the potential benefits offered by UV-C in deactivating pathogens like SARS-CoV-2, it remains evident that the concurrent risks posed by UV-C to human health cannot be ignored.”

DOI - https://doi.org/10.18632/aging.205787

Corresponding authors - Umberto Galderisi - umberto.galderisi@unicampania.it, and Giovanni Di Bernardo - gianni.dibernardo@unicampania.it

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Keywords - aging, senescence, apoptosis, UV light, public health

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.

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BUFFALO, NY- May 20, 2024 – Aging is a contributor at the 2024 Systems Aging Gordon Research Conference (GRC) on “Systems Modeling, Aging Biomarkers, and Longevity Interventions” — taking place from June 2–7, 2024, in Castelldefels, Barcelona, Spain.

“The conference will present recent advances in systemic rejuvenation, multi-omics approaches, applications of machine learning/artificial intelligence, and approaches for enhancing the chance of successfully translating basic research results to the clinic.” – GRC.org

Additionally, many Aging authors have been invited to speak and lead discussions at the 2024 Systems Aging GRC. Among them are distinguished members of Aging’s Editorial Board, including Steve Horvath, David Sinclair, Vera Gorbunova, Vadim Gladyshev, Guido Kroemer, and Anne Brunet.

“The program will include speakers from diverse fields who are united in their pursuit of pioneering longevity and rejuvenating interventions. The 2024 Systems Aging GRC also aims to present advanced approaches for identifying comprehensive interventions that alleviate age-related pathology.” – GRC.org

About Aging:

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.)

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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