Aging-US

BUFFALO, NY- November 7, 2023 – A new #researchpaper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 20, entitled, “Deciphering reproductive aging in women using a NOD/SCID mouse model for distinct physiological ovarian phenotypes.”

Female fertility is negatively correlated with age, with noticeable declines in oocyte quantity and quality until menopause. To understand this physiological process and evaluate human approaches for treating age-related infertility, preclinical studies in appropriate animal models are needed. In this new study, researchers María Marchante, Noelia Ramirez-Martin, Anna Buigues, Jessica Martinez, Nuria Pellicer, Antonio Pellicer, and Sonia Herraiz from IVIRMA, University of Valencia and Instituto Investigación Sanitaria La Fe aimed to characterize an immunodeficient physiological aging mouse model displaying ovarian characteristics of different stages during women's reproductive life.

“The main purpose of our study was to establish a physiological ovarian aging mouse model that could be employed to evaluate potential therapeutic interventions derived from human origin.”

NOD/SCID mice of different ages (8-, 28-, and 36–40-week-old) were employed to mimic ovarian phenotypes of young, Advanced Maternal Age (AMA), and old women (~18–20-, ~36–38-, and >45-years-old, respectively). Mice were stimulated, mated, and sacrificed to recover oocytes and embryos. Then, ovarian reserve, follicular growth, ovarian stroma, mitochondrial dysfunction, and proteomic profiles were assessed. Age-matched C57BL/6 mice were employed to cross-validate the reproductive outcomes.

The quantity and quality of oocytes were decreased in AMA and Old mice. These age-related effects associated spindle and chromosome abnormalities, along with decreased developmental competence to blastocyst stage. Old mice had less follicles, impaired follicle activation and growth, an ovarian stroma inconducive to growth, and increased mitochondrial dysfunctions. Proteomic analysis corroborated these histological findings. Based on that, NOD/SCID mice can be used to model different ovarian aging phenotypes and potentially test human anti-aging treatments.

“In summary, in this study we characterized the quality of the ovarian microenvironment and reproductive outcomes of an immunodeficient murine model of physiological ovarian aging by evaluating fertility outcomes, ovarian reserve and stroma, mitochondrial dysfunctions, and the ovarian proteome at different stages. This model adequately mimicked the characteristics of the reproductive stages in women, without external agents compromising folliculogenesis, or disrupting molecular mechanisms and ovarian function, which could mask the processes of physiological aging.”

DOI - https://doi.org/10.18632/aging.205086

Corresponding author - Sonia Herraiz - [email protected]

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- November 1, 2023 – A new research perspective was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 20, entitled, “Cholinergic centro-cingulate network in Parkinson disease and normal aging.”

In their new perspective, researchers Nicolaas I. Bohnen, Sygrid van der Zee and Roger Albin from University of Michigan, Veterans Administration Ann Arbor Healthcare System, University of Groningen, and the University Medical Center Groningen discussed Parkinson disease (PD). Decreased cholinergic binding within the recently identified centro-cingulate brain network has been shown to robustly correlate with the severity of cognitive impairment in PD. This network with key hubs within the cingulum, operculum and peri-central cortical regions also correlates with elements of parkinsonian motor impairments, including postural instability and gait difficulties, such as falls or freezing.

“We recently reported novel data-driving findings suggesting that cholinergic innervation deficits in centro-cingulate brain regions may be an important contributor to cognitive impairments in PD [1].”

MRI neuroimaging studies have shown that the anterior midcingulate cortex is a key node for cognitive aspects of movement generation, i.e., intentional motor control. Recent evidence also suggests a novel aspect of organization of primary motor cortex, describing “effector” regions for fine movement control intercalated with interlinked “inter-effector” regions devoted to whole-body control.

A distinguishing feature of inter-effector regions is tight linkage to the cingular and opercular regions. Such inter-effector regions have been proposed to be part of a greater somato-cognitive action network necessary for integration of goals and movement. Recent evidence also points to vulnerabilities of cholinergic nerve terminals in the centro-cingulate network in older non-PD adults. These features of normal aging underscore that cortical cholinergic terminal losses in age-associated neurodegenerative disorders are likely not exclusively the result of disease-specific etiologies but also related to otherwise normal aging.

“Practical implications of this overlap are that addressing disease-specific and general aging etiologies involved in neurodegeneration, may be of benefit in age-associated neurodegenerative disorders where significant cholinergic systems degeneration is present.”

DOI - https://doi.org/10.18632/aging.205209

Corresponding author - Nicolaas I. Bohnen - [email protected]

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Keywords - aging, centro-cingulate network, cholinergic, cognition, motor, Parkinson disease

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- October 31, 2023 – A new priority 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 15, Issue 20, entitled, “Proteomic quantification of native and ECM-enriched mouse ovaries reveals an age-dependent fibro-inflammatory signature.”

The ovarian microenvironment becomes fibrotic and stiff with age, in part due to increased collagen and decreased hyaluronan. However, the extracellular matrix (ECM) is a complex network of hundreds of proteins, glycoproteins, and glycans which are highly tissue specific and undergo pronounced changes with age. In this new study, researchers Shweta S. Dipali, Christina D. King, Jacob P. Rose, Joanna E. Burdette, Judith Campisi, Birgit Schilling, and Francesca E. Duncan from Northwestern University’s Feinberg School of Medicine, the Buck Institute for Research on Aging and the University of Illinois at Chicago used label-free quantitative proteomic methods to define comprehensive, age-dependent changes in the murine ovarian proteome and ECM in an unbiased manner.

“To obtain an unbiased and comprehensive profile of age-associated alterations to the murine ovarian proteome and ECM, we used a label-free quantitative proteomic methodology.”

The researchers validated conditions to enrich for the ECM prior to proteomic analysis. Following analysis by data-independent acquisition (DIA) and quantitative data processing, they observed that both native and ECM-enriched ovaries clustered separately based on age, indicating distinct age-dependent proteomic signatures. The team identified a total of 4,721 proteins from both native and ECM-enriched ovaries, of which 383 proteins were significantly altered with advanced age, including 58 ECM proteins.

Several ECM proteins upregulated with age have been associated with fibrosis in other organs, but to date their roles in ovarian fibrosis are unknown. Pathways regulating DNA metabolism and translation were downregulated with age, whereas pathways involved in ECM remodeling and immune response were upregulated. Interestingly, immune-related pathways were upregulated with age even in ECM-enriched ovaries, suggesting a novel interplay between the ECM and the immune system.

Moreover, the researchers identified putative markers of unique immune cell populations present in the ovary with age. These findings provide evidence from a proteomic perspective that the aging ovary provides a fibroinflammatory milieu, and their study suggests target proteins which may drive these age-associated phenotypes for future investigation.”

“To our knowledge, this is the first study to utilize unbiased proteomic approaches to investigate the effect of reproductive aging on the murine ovarian proteome and matrisome.

DOI - https://doi.org/10.18632/aging.205190

Corresponding authors - Francesca E. Duncan - [email protected], and Birgit Schilling - [email protected]

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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Between 1904 and 2008, researchers found that approximately 75% of patients with Werner syndrome (WS) worldwide were of Japanese descent. WS is a rare genetic disorder that causes premature aging and increases the risk of various age-related diseases, such as diabetes, cardiovascular disease and cancer. One of the hallmarks of WS is the loss of subcutaneous fat, which is the layer of fat under the skin that helps regulate body temperature and store energy. Subcutaneous fat loss leads to severe insulin resistance, which means that the body cannot use glucose effectively and has high blood sugar levels. But what causes subcutaneous fat loss in WS? And how does it affect the metabolism and health of WS patients?

In a new study, researchers Daisuke Sawada, Hisaya Kato, Hiyori Kaneko, Daisuke Kinoshita, Shinichiro Funayama, Takuya Minamizuka, Atsushi Takasaki, Katsushi Igarashi, Masaya Koshizaka, Aki Takada-Watanabe, Rito Nakamura, Kazuto Aono, Ayano Yamaguchi, Naoya Teramoto, Yukari Maeda, Tomohiro Ohno, Aiko Hayashi, Kana Ide, Shintaro Ide, Mayumi Shoji, Takumi Kitamoto, Yusuke Endo, Hideyuki Ogata, Yoshitaka Kubota, Nobuyuki Mitsukawa, Atsushi Iwama, Yasuo Ouchi, Naoya Takayama, Koji Eto, Katsunori Fujii, Tomozumi Takatani, Tadashi Shiohama, Hiromichi Hamada, Yoshiro Maezawa, and Koutaro Yokote from Chiba University Graduate School of Medicine, Chiba University Hospital, Kazusa DNA Research Institute, The University of Tokyo, Kyoto University, and International University of Welfare and Health School of Medicine aimed to shed light on these questions by investigating the molecular mechanisms of subcutaneous fat dysfunction in WS. On October 3, 2023, their research paper was published in Aging’s Volume 15, Issue 19, entitled, “Senescence-associated inflammation and inhibition of adipogenesis in subcutaneous fat in Werner syndrome.”

“[...] research on WS is important as it can provide insights into the pathogenesis and development of treatments not only for WS but also for general age-related diseases."

Full blog - https://aging-us.org/2023/10/rapamycins-therapeutic-potential-in-treating-werner-syndrome/

Paper DOI - https://doi.org/10.18632/aging.205078

Corresponding authors - Hisaya Kato - [email protected], Yoshiro Maezawa - [email protected], and Koutaro Yokote - [email protected]

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Keywords - aging, Werner syndrome, premature aging, lipodystrophy, stromal vascular fraction, SASP

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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Dr. Dechao Feng from the Department of Urology, Institute of Urology, West China Hospital, Sichuan University, discusses a research paper he co-authored that was published by Aging (Aging-US) in Volume 15, Issue 18, entitled, “Identification of senescence-related lncRNA prognostic index correlating with prognosis and radiosensitivity in prostate cancer patients.”

DOI - https://doi.org/10.18632/aging.204888

Corresponding authors - Dechao Feng - [email protected], and Ping Han - [email protected]

Video interview - https://www.youtube.com/watch?v=zHiWwd5RlJw

Transcription - https://aging-us.net/2023/10/26/behind-the-study-senescence-related-lncrna-prognostic-index-in-prostate-cancer/

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Keywords - aging, prostate cancer, senescence-related lncRNA prognostic index, biochemical recurrence, radiosensitivity, androgen 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.

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Dr. Frank Pun, Diana Zagirova, Dr. Anatoly Urban, and Geoffrey Leung from Insilico Medicine Hong Kong Ltd., discuss a research paper they co-authored that was published by Aging (Aging-US) in Volume 15, Issue 18, entitled, “Biomedical generative pre-trained based transformer language model for age-related disease target discovery.”

DOI - https://doi.org/10.18632/aging.205055

Corresponding author - Alex Zhavoronkov - [email protected]

Video interview - https://www.youtube.com/watch?v=kIJvrY7n3n0

Interview transcription - https://aging-us.net/2023/10/25/behind-the-study-biomedical-transformer-language-model-for-age-related-disease-discovery/

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Keywords - aging, transformers, deep learning, therapeutic target discovery, aging biomarkers, human 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.

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BUFFALO, NY- October 25, 2023 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 19, entitled, “Live while the DNA lasts. The role of autophagy in DNA loss and survival of diploid yeast cells during chronological aging.”

Aging is inevitable and affects all cell types. Thus, yeast cells are often used as a model in aging studies. There are two approaches to studying aging in yeast: replicative aging, which describes the proliferative potential of cells, and chronological aging, which is used for studying post-mitotic cells. In this new study, while analyzing the chronological lifespan (CLS) of diploid Saccharomyces cerevisiae cells, researchers Tuguldur Enkhbaatar, Marek Skoneczny, Karolina Stępień, Mateusz Mołoń, and Adrianna Skoneczna from the Polish Academy of Sciences and Rzeszów University discovered a remarkable phenomenon: ploidy reduction during aging progression.

“To uncover the mechanism behind this unusual process we used yeast strains undergoing a CLS assay, looking for various aging parameters.”

Cell mortality, regrowth ability, autophagy induction and cellular DNA content measurements indicated that during the CLS assay, dying cells lost their DNA, and only diploids survived. The researchers demonstrated that autophagy was responsible for the gradual loss of DNA. The nucleophagy marker activation at the start of the CLS experiment correlated with the significant drop in cell viability. The activation of piecemeal microautophagy of nucleus (PMN) markers appeared to accompany the chronological aging process until the end.

“Our findings emphasize the significance of maintaining at least one intact copy of the genome for the survival of post-mitotic diploid cells.”

During chronological aging, cellular components, including DNA, are exposed to increasing stress, leading to DNA damage and fragmentation in aging cells. The researchers propose that PMN-dependent clearance of damaged DNA from the nucleus helps prevent genome rearrangements. However, as long as one copy of the genome can be rebuilt, cells can still survive.

“The observations we made in aging research using yeast as the eukaryotic cell model may help to understand the mechanisms that prevent aneuploidy during aging or cancerogenesis in cells where chromothripsis has occurred.”

DOI - https://doi.org/10.18632/aging.205102

Corresponding author - Adrianna Skoneczna - [email protected]

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Keywords - aging, genome instability, lifespan, autophagy, double-strand breaks

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- October 24, 2023 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 19, entitled, “Metabolic switch in the aging astrocyte supported via integrative approach comprising network and transcriptome analyses.”

Dysregulated central-energy metabolism is a hallmark of brain aging. Supplying enough energy for neurotransmission relies on the neuron-astrocyte metabolic network. In their new study, researchers Alejandro Acevedo, Felipe Torres, Miguel Kiwi, Felipe Baeza-Lehnert, L. Felipe Barros, Dasfne Lee-Liu, and Christian González-Billault from Universidad de Chile, Cedenna, University of California, San Diego, Centro de Estudios Científicos (CECs), Geroscience Center for Brain Health and Metabolism (GERO), Universidad San Sebastián, and the Buck Institute for Research on Aging aimed to identify genes contributing to age-associated brain functional decline.

“[...] we formulated an approach to analyze the metabolic network by integrating flux, network structure and transcriptomic databases of neurotransmission and aging.”

Their findings support that during brain aging: (1) The astrocyte undergoes a metabolic switch from aerobic glycolysis to oxidative phosphorylation, decreasing lactate supply to the neuron, while the neuron suffers intrinsic energetic deficit by downregulation of Krebs cycle genes, including mdh1 and mdh2 (Malate-Aspartate Shuttle); (2) Branched-chain amino acid degradation genes were downregulated, identifying dld as a central regulator; (3) Ketone body synthesis increases in the neuron, while the astrocyte increases their utilization, in line with neuronal energy deficit in favor of astrocytes.

“The genes identified here are valuable candidates for future studies to understand the molecular mechanisms of healthy brain aging and prevent brain age-associated failure using energy metabolism as a target.”

DOI - https://doi.org/10.18632/aging.204663

Corresponding authors - Christian González-Billault - [email protected], and Dasfne Lee-Liu - [email protected]

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Keywords - aging, astrocyte, neuron, brain aging, flux balance analysis, network centrality

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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Dr. Wenbo Yu, Stanley from the Centre for Cancer Biology, SA Pathology and University of South Australia details a #research perspective he co-authored that was #published by Aging (Aging-US) in Volume 15, Issue 17, entitled, “A Poisson distribution-based general model of cancer rates and a cancer risk-dependent theory of aging.”

#author #authorinterview #interview #aging #cancer #entropy #poisson #perspective #openaccess #openscience #peerreview #journal #publication #meded #agingshort #video

DOI - https://doi.org/10.18632/aging.205016

Corresponding author - Wenbo Yu - [email protected]

Video interview - https://www.youtube.com/watch?v=1n7puuJrido

Transcription - https://aging-us.net/2023/10/23/behind-the-study-poisson-distribution-based-model-of-cancer-rates-cancer-risk-dependent-theory-of-aging/

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Keywords - aging, cancer incidence model, poisson distribution, entropy

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- October 18, 2023 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 15, Issue 19, entitled, “Reduction of double-strand DNA break repair exacerbates vascular aging.”

Advanced age is the greatest risk factor for cardiovascular disease (CVD), the leading cause of death. Arterial function is impaired in advanced age which contributes to the development of CVD. One underexplored hypothesis is that DNA damage within arteries leads to this dysfunction, yet evidence demonstrating the incidence and physiological consequences of DNA damage in arteries, and in particular, in the microvasculature, in advanced age is limited.

In their new study, researchers Samuel I. Bloom, Jordan R. Tucker, Daniel R. Machin, Hossein Abdeahad, AdeLola O. Adeyemo, Tyler G. Thomas, R. Colton Bramwell, Lisa A. Lesniewski, and Anthony J. Donato from The University of Utah, Florida State University and the Veterans Affairs Medical Center-Salt Lake City began by assessing the abundance of DNA damage in human and mouse lung microvascular endothelial cells and found that aging increases the percentage of cells with DNA damage.

“To explore the physiological consequences of increases in arterial DNA damage, we evaluated measures of endothelial function, microvascular and glycocalyx properties, and arterial stiffness in mice that were lacking or heterozygous for the double-strand DNA break repair protein ATM kinase.”

Surprisingly, in young mice, vascular function remained unchanged which led the researchers to rationalize that perhaps aging is required to accumulate DNA damage. Indeed, in comparison to wild type littermate controls, mice heterozygous for ATM that were aged to ~18 mo (Old ATM +/−) displayed an accelerated vascular aging phenotype characterized by increases in arterial DNA damage, senescence signaling, and impairments in endothelium-dependent dilation due to elevated oxidative stress. Furthermore, old ATM +/− mice had reduced microvascular density and glycocalyx thickness as well as increased arterial stiffness.

“Collectively, these data demonstrate that DNA damage that accumulates in arteries in advanced age contributes to arterial dysfunction that is known to drive CVD.”

DOI - https://doi.org/10.18632/aging.205066

Corresponding author - Anthony J. Donato - [email protected]

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Keywords - aging, DNA damage, vascular function, endothelial cell, senescence, oxidative stress, arterial stiffness

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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