Aging-US

BUFFALO, NY- July 23, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 13, entitled, “Co-analysis of methylation platforms for signatures of biological aging in the domestic dog reveals previously unexplored confounding factors.”

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

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

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

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

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

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

Corresponding author - Elaine A. Ostrander - [email protected]

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

About Aging-US

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

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

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

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

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

Corresponding author - Masataka Sugimoto - [email protected]

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

About Aging-US

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

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BUFFALO, NY- July 17, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 13, entitled, “Modulating in vitro lung fibroblast activation via senolysis of senescent human alveolar epithelial cells.”

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

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

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

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

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

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

Corresponding author - Tovah A. Day - [email protected]

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About Aging-US

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

Please visit our website at https://www.Aging-US.com​​ and connect with us:

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

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

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

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

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

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

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

Corresponding authors - Masataka Sugimoto - [email protected]

Video short - https://www.youtube.com/watch?v=Bzgb2PEiV9c

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

About Aging-US

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

Please visit our website at https://www.Aging-US.com​​ and connect with us:

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BUFFALO, NY- July 10, 2024 – A new #research paper was #published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 12, entitled, “Aging exacerbates oxidative stress and liver fibrosis in an animal model of Down Syndrome.”

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

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

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

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

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

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

Corresponding author - Giovanni Li Volti - [email protected]

Video short - https://www.youtube.com/watch?v=8GlAruy0xfk

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Keywords - aging, Down Syndrome, oxidative stress, liver

About Aging-US

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

Please visit our website at https://www.Aging-US.com​​ and connect with us:

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

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

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

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

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

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

Corresponding author - Luminita Paraoan - [email protected]

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Keywords - aging, RPE, vision, omics

About Aging-US

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

Please visit our website at https://www.Aging-US.com​​ and connect with us:

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

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

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

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

Corresponding authors - Bruno Bernardes de Jesus - [email protected]

Video short - https://www.youtube.com/watch?v=hbhkSu1kX5Y

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

About Aging-US

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

Please visit our website at https://www.Aging-US.com​​ and connect with us:

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

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

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

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

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

Corresponding authors - Federica Sotgia - [email protected], and Michael P. Lisanti - [email protected]

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

About Aging-US

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

Please visit our website at https://www.Aging-US.com​​ and connect with us:

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

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

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

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

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

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

Corresponding author - Ben Kirk - [email protected]

Video short - https://www.youtube.com/watch?v=NnhM3y6qi5U

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

About Aging-US

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

Please visit our website at https://www.Aging-US.com​​ and connect with us:

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BUFFALO, NY- June 25, 2024 – A new research paper was published in Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 11, entitled, “Associations of childhood, adolescence, and midlife cognitive function with DNA methylation age acceleration in midlife.”

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

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

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

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

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

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

Corresponding author - Junyu Chen - [email protected]

Video short - https://www.youtube.com/watch?v=v7xiVCqVwPw

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About Aging-US

The mission of the journal is to understand the mechanisms surrounding aging and age-related diseases, including cancer as the main cause of death in the modern aged population.

The journal aims to promote 1) treatment of age-related diseases by slowing down aging, 2) validation of anti-aging drugs by treating age-related diseases, and 3) prevention of cancer by inhibiting aging. (Cancer and COVID-19 are age-related diseases.)

Please visit our website at https://www.Aging-US.com​​ and connect with us:

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LinkedIn - https://www.linkedin.com/company/aging/

Pinterest - https://www.pinterest.com/AgingUS/

Spotify - https://open.spotify.com/show/1X4HQQgegjReaf6Mozn6Mc