BUFFALO, NY- December 11, 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 21 on November 14, 2024, entitled, “Adolescents and young adults with sickle cell disease exhibit accelerated aging with elevated T-cell p16INK4a expression.”

Researchers Samuel R. Wilson, Natalia Mitin, Vanessa L. Ayer Miller, Andrew B. Smitherman, and Marcus A. Carden, from the University of North Carolina at Chapel Hill,  Sapere Bio, Campbell University, and Cogent Biosciences have discovered that young people with sickle cell disease (SCD) exhibit signs of accelerated biological aging compared to those without the disease. By measuring levels of p16INK4a, a key marker of cellular aging, the team found significantly higher levels in individuals with SCD. Remarkably, some participants showed biological aging equivalent to an additional 43 years. These findings suggest that SCD may drive faster aging in the body, offering new insights into the disease's long-term impact.

Sickle cell disease (SCD) is a genetic condition primarily affecting individuals of African or Mediterranean descent. While treatments have advanced, people with SCD often face significant health challenges, including complications that mimic the effects of aging.

Cellular aging, or senescence, occurs when cells stop dividing yet continue to send harmful signals that damage surrounding tissues. Researchers believe this process happens at an accelerated rate in people with SCD, underscoring the importance of finding ways to slow it down and mitigate its impact.

The study compared p16INK4a levels in 18 adolescents and young adults with SCD to 27 healthy people of the same age. The results showed that even the youngest participant with SCD had higher levels of this aging marker than anyone in the non-SCD group. 

“Our youngest participant, a 15-year-old with SCD, had a higher p16 expression than all the comparators, underscoring the early rise of p16 expression in this population.”

The researchers believe this faster aging could be caused by the chronic inflammation, lack of oxygen, and stress on the body associated with SCD. Along with managing the symptoms of the disease, SCD patients also face a higher risk of aging-related problems like organ damage and physical decline much earlier in life.

The findings suggest that measuring p16INK4a levels could help clinicians identify patients at risk for these problems earlier and offer targeted care. The study also opens the door to new treatments, such as drugs that aim to remove old, damaged cells. These therapies could potentially slow down the aging process.

Further research is essential to confirm these findings and to gain a deeper understanding of how to support SCD patients effectively. Larger, long-term studies could investigate whether therapies targeting cell aging can help prevent complications and improve the quality of life for individuals with SCD.

In conclusion, this study marks an important step in understanding how SCD accelerates aging and offers new ways to improve the lives of those living with the condition.

DOI - https://doi.org/10.18632/aging.206152

Corresponding author - Samuel R. Wilson - samuel.wilson@med.unc.edu

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

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​​.

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Aging (Aging-US)

Accelerated Aging in Young Sickle Cell Patients Linked to Elevated T-cell p16INK4a

BUFFALO, NY — November 18, 2025 — A new #research paper was #published in Volume 17, Issue 10 of Aging-US on October 3, 2025, titled “Growth hormone excess drives liver aging via increased glycation stress.”

In this study, led by first author Parminder Singh alongside with corresponding authors Pankaj Kapahi from the Buck Institute for Research on Aging and Andrzej Bartke from Southern Illinois University School of Medicine, researchers investigated how elevated growth hormone (GH) levels contribute to liver aging and dysfunction. They found that excess GH disrupts liver metabolism in ways that resemble aging-related liver damage. The study suggests that managing glycation stress may help prevent or treat liver diseases linked to abnormal hormone levels.

Excess GH is known to cause different disorders, but its long-term impact on internal organs like the liver has remained unclear. To address this, researchers used a mouse model engineered to overproduce bovine GH and examined how chronic hormone exposure affects liver function over time.

“Pathological conditions such as acromegaly or pituitary tumors result in elevated circulating GH levels, which have been implicated in a spectrum of metabolic disorders, potentially by regulating liver metabolism.”

The team found that young mice with GH overexpression showed molecular and cellular patterns similar to those in naturally aged livers. In both groups, genes involved in metabolism were suppressed, while those linked to immune and inflammatory responses were activated. On one hand, the metabolic changes were associated with the buildup of advanced glycation end products, harmful compounds formed when sugars attach to proteins or fats without proper regulation. On the other hand, the immune and inflammatory changes reflected a process known as “inflammaging,” a form of chronic, low-grade inflammation commonly associated with aging. By revealing the overlap between hormone-driven and age-related liver dysfunction, the study provides new insight into how GH may accelerate aging processes.

Importantly, the team showed that reducing glycation stress can reverse many of these negative effects. Mice treated with a compound that lowers glycation levels demonstrated improved liver health, reduced insulin resistance, and enhanced physical function. This intervention also corrected several abnormal genetic patterns caused by excess GH. The findings point to a potential therapeutic strategy for liver diseases associated with aging and hormonal imbalances.

Overall, this research identifies glycation and its byproducts as key contributors to liver damage caused by excess GH. It suggests that targeting glycation could offer broad therapeutic benefits, not only for hormone-related conditions but also for supporting liver health during aging.

DOI - https://doi.org/10.18632/aging.206327

Corresponding authors - Andrzej Bartke - abartke@siumed.edu and Pankaj Kapahi - pkapahi@buckinstitute.org

Abstract video - https://www.youtube.com/watch?v=6v8xi5muLwA

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Keywords - aging, growth hormone, glycation stress, Gly-Low

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Aging-US

How Growth Hormone Excess Accelerates Liver Aging via Glycation Stress

BUFFALO, NY – November 18, 2025 – A new #review was #published in Oncotarget (Volume 16) on November 14, 2025, titled “Mechanism of anticancer action of bifidobacterium: Insights from gut microbiota.”

This review, led by first author Hoang Do and correspondent author Ashakumary Lakshmikuttyamma from Thomas Jefferson University, explores how bifidobacterium, a common probiotic found in the gut, may contribute to cancer prevention and therapy. By analyzing existing studies, the authors highlight the growing importance of gut health in cancer treatment and shed light on how bifidobacterium could complement standard cancer therapies.

Bifidobacterium is widely known for promoting digestive health and is often included in fermented foods and dietary supplements. However, emerging evidence suggests it may also play a broader role in immune regulation and cancer defense. The review explains how certain strains of bifidobacterium may enhance the effectiveness of chemotherapy, radiation, and immunotherapy in cancers such as breast, lung, colorectal, and gastric cancers.

According to the review, bifidobacterium influences cancer outcomes through several biological mechanisms. It helps regulate immune function by reducing inflammation and supporting the activity of immune cells that target tumors. For instance, strains like B. longum and B. breve have been shown to lower levels of harmful inflammatory markers and boost anti-inflammatory responses. These changes can make cancer treatments more effective while also reducing side effects.

“Presence of Bifidobacterium breve in gut microbiota extended the median progression-free survival of NSCLC patients.”

The review also discusses how bifidobacterium helps detoxify the body by breaking down cancer-causing compounds and limiting their ability to damage cells. In preclinical studies, the probiotic reduced the activity of enzymes that produce carcinogens and helped in converting food-based substances into cancer-fighting agents. Some strains were even found to suppress genes that promote tumor growth and increase molecules that trigger cancer cell death.

The authors emphasize that diet plays a critical role in supporting the growth of bifidobacterium. Foods rich in dietary fiber, especially those containing inulin and oligosaccharides like garlic, onions, or leeks, can help increase its levels in the gut. This suggests that simple dietary changes could not only improve gut health but also support cancer prevention and treatment strategies.

Although the review presents compelling evidence, the authors stress the need for more clinical trials to determine how different strains of bifidobacterium affect specific types of cancer. Personalized approaches may be necessary to match the right probiotic strains with individual treatment plans.

As research continues to uncover the link between gut microbes and cancer, bifidobacterium stands out as a promising natural ally that could enhance the body’s defenses and improve cancer treatment outcomes.

DOI - https://doi.org/10.18632/oncotarget.28779

Correspondence to - Ashakumary Lakshmikuttyamma - axl025@jefferson.edu

Abstract video - https://www.youtube.com/watch?v=KTWJDAN15lY
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Oncotarget

Probiotic Bifidobacterium May Boost Cancer Treatment and Suppress Tumors

Cancer is a disease caused by the uncontrolled growth of cells that escape the body’s natural defenses. One way cancer protects itself is by taking advantage of certain immune cells called regulatory T cells, or Tregs. Normally, Tregs help prevent autoimmune diseases by controlling the immune system. But inside tumors, they behave differently. Instead of defending the body, they suppress the immune cells that could attack the cancer.

Many cancer treatments aim to activate the immune system to fight tumors more effectively. However, the presence of Tregs within the tumor makes this difficult. These cells act like bodyguards for the cancer, blocking the immune response that might otherwise slow or stop tumor growth.

Researchers have tried to eliminate Tregs by targeting a protein called CD25, found on their surface. However, earlier efforts often failed because these treatments also interfere with interleukin-2 (IL-2), a molecule that is essential for other immune cells to function. Blocking IL-2 weakens the entire immune response, limiting the treatment’s effectiveness.

To overcome this challenge, scientists recently developed a new antibody called 2B010. This study, titled “A novel anti-human CD25 mAb with preferential reactivity to activated T regulatory cells depletes them from the tumor microenvironment,” was published in Oncotarget (Volume 16).

Full blog - https://www.oncotarget.org/2025/11/19/new-antibody-removes-tregs-to-boost-immune-response-against-cancer/

Paper DOI - https://doi.org/10.18632/oncotarget.28752

Correspondence to - Ethan M. Shevach - eshevach@Niaid.NIH.gov

Abstract video - https://www.youtube.com/watch?v=2NJcGsI7WXA

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Keywords - cancer, Treg, CD25, TME, mAb, GVHD

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New Antibody Removes Tregs to Boost Immune Response Against Cancer

BUFFALO, NY — November 20, 2025 — A new #research paper was #published in Volume 17, Issue 10 of Aging-US on October 10, 2025, titled “Developmental arrest rate of an embryo cohort correlates with advancing reproductive age, but not with the aneuploidy rate of the resulting blastocysts in good prognosis patients: a study of 25,974 embryos.”

In this large-scale study, Andres Reig of the IVIRMA Global Research Alliance and Robert Wood Johnson Medical School, along with Emre Seli of the IVIRMA Global Research Alliance and  Yale School of Medicine, investigated how female age and chromosomal abnormalities affect embryo development in patients undergoing in vitro fertilization (IVF). They found that embryo developmental arrest (EDA) becomes more common as women age. However, this arrest is not directly associated with the presence of chromosomal errors in the embryos that continue to develop. These findings could help improve fertility counseling and treatment strategies.

The researchers analyzed 25,974 embryos from 1,928 IVF cycles, all from patients with a good chance of success. The study showed that the percentage of embryos that stopped developing before reaching the blastocyst stage increased with age: from 33% in women under 35 to 44% in those over 42. Despite this rise, the rate of chromosomal abnormalities, known as aneuploidy, in the embryos that did reach the blastocyst stage did not show a strong connection with the rate of arrest after adjusting for age.

This distinction  is important  because both developmental arrest and aneuploidy reduce the number of embryos suitable for transfer. But this study suggests they are caused by different biological processes. In other words, an embryo may stop developing even if it has the correct number of chromosomes, and some embryos with chromosomal abnormalities may still grow to the blastocyst stage.

“A very weak positive correlation was identified between EDA rate and the rate of aneuploidy (r: 0.07, 95% CI 0.03–0.11; R2: 0.00, p < 0.01) when evaluating all cohorts.”

The authors suggest that other factors, such as the health of the egg’s mitochondria or mutations in maternal-effect genes, may explain why some embryos stop developing. These insights could help researchers identify new ways to improve embryo quality, especially for older women undergoing IVF.

Importantly, the study focused on embryos that developed far enough to be tested, which helped avoid technical problems that come with analyzing arrested embryos directly. This approach allowed for more reliable comparisons across age groups and embryo quality.

Overall, the study highlights the importance of maternal age as a key factor in embryo development, independent of chromosomal results. It also opens new directions for research, aiming to better understand why embryos fail to develop and how this knowledge might lead to improved fertility treatments in the future.

DOI - https://doi.org/10.18632/aging.206328

Corresponding author - Emre Seli - emre.seli@yale.edu

Abstract video - https://www.youtube.com/watch?v=g0oS3HBNmuQ

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Keywords - aging, ovarian aging, reproductive aging, embryonic arrest, embryonic aneuploidy, developmental arrest

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Embryo Arrest in IVF Linked to Maternal Age, Not Chromosomal Abnormalities

BUFFALO, NY — November 25, 2025 — A new #research paper was #published in Volume 17, Issue 10 of Aging-US on October 13, 2025, titled “Hospitalization with infections and risk of Dementia: a systematic review and meta-analysis.”

This large-scale meta-analysis, led by first author Wei Yu Chua from the National University of Singapore and corresponding author Eng-King Tan from the National Neuroscience Institute and Duke-NUS Medical School in Singapore, shows that adults hospitalized with infections have a significantly higher risk of developing dementia. The findings are especially important as global populations grow older and hospitalizations for infections increase, highlighting a potential new approach for dementia prevention.

“Out of 1900 studies that were screened initially, 16 studies comprising 4,266,276 patients were included for analysis.” 

The researchers analyzed data from over 4 million individuals across 16 studies, making this study the most comprehensive review to date on the association between infection-related hospital stays and long-term brain health. The results showed that being hospitalized for an infection raised the risk of all-cause dementia by 83%. Among the types of infections studied, sepsis carried the highest risk, followed by pneumonia, urinary tract infections, and skin or soft tissue infections. The risk of developing vascular dementia was notably higher than that of Alzheimer’s disease.

One possible explanation for the association between infections and dementia is that infections trigger systemic inflammation that may reach the brain. Inflammatory molecules can cross the blood-brain barrier, potentially leading to the buildup of damaging proteins and the death of brain cells. This process may be more severe in older adults, whose immune systems are often slower to respond and recover. The study also suggests that even a single infection-related hospitalization can speed up cognitive decline, especially in individuals already at higher risk.

Importantly, the risk of dementia was greatest within the first year following an infection but remained elevated for many years afterward. In fact, studies with follow-ups longer than a decade showed even stronger associations. These results suggest the need for early cognitive monitoring after hospital discharge, particularly in older adults recovering from infections.

These findings have important implications for healthcare systems, particularly those serving aging populations, and underscore the lasting impact that infections can have on the brain. This research highlights the importance of looking beyond genetics and lifestyle for prevention strategies. With over 50 million people affected by dementia worldwide and annual care costs in the U.S. exceeding $300 billion, identifying new and preventable risk factors is critical. Reducing infections, improving hospital care, and monitoring brain health after illness may offer promising ways to protect cognitive function in aging populations.

DOI - https://doi.org/10.18632/aging.206329

Corresponding author - Eng-King Tan - tan.eng.king@singhealth.com.sg

Abstract video - https://www.youtube.com/watch?v=uyv5VHHHIA4

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Hospital Infections Associated with Higher Risk of Dementia

Interest in healthier, longer lives is rising, supported by recent scientific advances in aging research. But turning those discoveries into everyday healthcare solutions remains a work in progress. In this landscape, longevity clinics have attracted attention as personalized alternatives to traditional medicine.

What Are Longevity Clinics?

Longevity clinics are private centers offering tailored programs designed to improve long-term health and slow biological aging. Using advanced diagnostics such as genetic sequencing, full-body imaging, and blood tests, they develop personalized plans that may include exercise, nutrition, hormone therapy, or experimental treatments. Frequently found in countries like the United States, Switzerland, and the United Arab Emirates, these clinics reflect a growing global interest in preventive healthcare, though their high costs and scientific credibility remain subjects of debate.

The Editorial

“Longevity clinics: between promise and peril,” an editorial by Marco Demaria, Editor-in-Chief of Aging-US, from the European Research Institute for the Biology of Ageing (ERIBA), University Medical Center Groningen (UMCG), University of Groningen (RUG), was published in Aging-US (Volume 17, Issue 10). 

Full blog - https://aging-us.org/2025/11/longevity-clinics-balancing-innovation-with-regulation/

Paper DOI - https://doi.org/10.18632/aging.206330

Corresponding author - Marco Demaria — m.demaria@umcg.nl

Abstract video - https://www.youtube.com/watch?v=Bt84xBdii0s

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Keywords - aging, longevity clinics, biomarkers, frailty, senescence

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Longevity Clinics: Balancing Innovation with Regulation

BUFFALO, NY — December 1, 2025 — A new #research paper featured on the #cover of Volume 17, Issue 11 of Aging-US was #published on October 30, 2025, titled “SAMP-Score: a morphology-based machine learning classification method for screening pro-senescence compounds in p16 positive cancer cells.”

In this study led by first author Ryan Wallis along with corresponding author Cleo L. Bishop, from Queen Mary University of London, researchers developed a machine learning tool to identify compounds that induce cancer cells into senescence. The tool, called SAMP-Score, offers a new strategy for drug discovery in cancers with poor treatment options like basal-like breast cancer.

Senescence is a process where damaged or aged cells stop dividing. In cancer therapy, inducing senescence is an approach to control tumor growth. However, it is difficult to detect true senescence in cancer cells that already appear aged. These cancers, often called Sen-Mark+ cancers, include basal-like breast cancer and typically lack reliable markers to confirm senescence. SAMP-Score was designed to address this problem.

Instead of relying on traditional markers, the researchers built a machine learning model trained to recognize patterns based on senescent cells’ shape and structure under a microscope. These visual patterns, known as senescence-associated morphological profiles (SAMPs), allowed the model to distinguish real signs of aging from other effects such as toxicity or normal variation. By analyzing thousands of cell images, the model learned to classify whether a cell had truly entered senescence.

“To demonstrate the potential application of SAMP-Score in p16 positive cancer therapeutic discovery, we assessed a diversity screen of 10,000 novel chemical entities in MB-468 cells (p16 positive BLBC).”

The team used SAMP-Score to screen more than 10,000 experimental compounds. One compound, QM5928, consistently triggered senescence in several cancer cell types without killing them, making it a promising candidate for further study. Importantly, it worked in cancers resistant to known drugs like palbociclib, which are often ineffective in cancers with high p16 expression like basal-like breast cancer. 

Further analysis revealed that QM5928 caused the p16 protein to move into the nucleus of cancer cells, a possible sign that the protein is helping stop cell division. This subtle effect was only detectable using the detailed imaging and analysis made possible by SAMP-Score, highlighting the tool’s ability to distinguish true senescence from toxic responses and making it a powerful resource in cancer drug discovery.

By combining machine learning with high-resolution imaging, this study introduces a new way to find and evaluate cancer therapies. SAMP-Score could accelerate efforts to develop treatments that exploit the body’s natural aging processes to fight cancer, especially for patients with resistant tumors. The tool is openly available at GitHub, making it accessible for other researchers exploring senescence-based cancer therapies.

DOI - https://doi.org/10.18632/aging.206333

Corresponding author - Cleo L. Bishop - c.l.bishop@qmul.ac.uk

Abstract video - https://www.youtube.com/watch?v=qXI_KI3EgHE

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Machine Learning Identifies Senescence-Inducing Compound for p16-Positive Cancer Cells

BUFFALO, NY — December 3, 2025 — A new #essay was #published in Volume 17, Issue 11 of Aging-US on November 19, 2025, titled “On the intergenerational transfer of ideas in aging and cancer research: from the hypothalamus according to V.M. Dilman to the mTOR protein complex according to M.V. Blagosklonny.”

In this work, Aleksei G. Golubev from the N.N. Petrov National Medical Research Center of Oncology reflects on the legacy of two influential Russian scientists, Vladimir M. Dilman and his son Mikhail V. Blagosklonny, who each introduced groundbreaking ideas about aging and cancer. Drawing from his own experience working in Dilman’s lab, Golubev explores how their ideas remain deeply relevant to today’s scientific understanding.

The essay connects Dilman’s “elevation theory” with Blagosklonny’s “hyperfunction theory,” two frameworks that challenge the conventional view of aging as a process of decline. Instead, both propose that aging results from continued biological processes that once supported growth but eventually become harmful when left unchecked.

Dilman believed that aging begins with reduced sensitivity in the hypothalamus, a brain region that regulates the body’s balance. This desensitization disrupts metabolism and hormone levels, setting the stage for many chronic illnesses. Decades later, Blagosklonny expanded on this idea at the molecular level. Central to his theory is the mTOR protein complex, which regulates growth and metabolism and is now a major focus in aging research.

Golubev also explores the historical and personal connections between the two scientists. Dilman, an endocrinologist trained in the Soviet Union, and Blagosklonny, a molecular biologist educated during the post-Soviet period, represent two generations shaped by a shared scientific tradition. 

“Dilman’s scientific legacy is not as well recognized as it should be, partly due to bias in citation practices.”

The essay also draws attention to a troubling trend in science: the tendency to overlook early contributions, especially from non-Western scholars. Many of Dilman’s insights, such as the connection between high blood sugar, insulin resistance, and cancer, have since been validated by modern tools, yet his work is rarely cited. Golubev points out how citation practices, language barriers, and historical isolation have contributed to this lack of recognition.

Finally, Golubev encourages the scientific community to look back and acknowledge the foundational work that shaped modern aging science. It also highlights the importance of cross-generational knowledge in moving science forward. By tracing the intellectual journey from hormonal regulation in the brain to molecular pathways in cells, this essay demonstrated the relevance of old ideas in a new biological era.

DOI - https://doi.org/10.18632/aging.206338

Corresponding author - Aleksei G. Golubev - lxglbv@rambler.ru

Abstract video - https://www.youtube.com/watch?v=LvrdghTKGws

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Keywords - aging, gerontology, history of science, hyperfunction, mTOR, hypothalamus, cancer, metabolism, immunity

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How Two Russian Scientists Changed the Way We Understand Aging and Cancer

In this episode, we meet the people behind Dementia Disco, a Stockport charity that organises discos for people affected by dementia.

You can visit alzheimers.org.uk/publications for our range of publications and factsheets designed to support and inform anyone affected by dementia.

For personalised information and advice, call our Dementia support line on 0333 150 3456, or for Welsh speakers call 03300 947 400.

‘It's an uplifting and joyful thing’ – Dementia together podcast December 2025

Colorectal cancer (CRC) remains the second leading cause of cancer-related deaths globally. While early detection significantly improves outcomes, many patients are diagnosed at advanced stages when treatment options are limited and relapse is common. To address this challenge, researchers are exploring whether existing drugs can be repurposed for cancer therapy, a strategy that could accelerate drug development while reducing associated costs and risks.

One class of drugs under investigation is statins, commonly prescribed to reduce cholesterol and prevent cardiovascular disease. Several studies have observed a potential link between elevated cholesterol and increased CRC risk. Cholesterol may support tumor growth by promoting membrane synthesis and energy metabolism in rapidly dividing cells.

Building on this connection, researchers from leading Indian institutions, including the Indian Institute of Science Education and Research and the Center of Excellence in Epigenetics at Shiv Nadar Institution of Eminence, investigated how statins influence CRC cells at the molecular level. Their goal was to determine whether these widely used drugs could have a therapeutic role in oncology.

The Study: Investigating the Molecular Impact of Statins in CRC Cells

The study, titled “Statins exhibit anti-tumor potential by modulating Wnt/β-catenin signaling in colorectal cancer,” was published in Oncotarget (Volume 16). Using a combination of lipidomics, transcriptomics, proteomics, and 3D tumor models, the researchers explored how two widely prescribed statins, atorvastatin and simvastatin, affect molecular pathways associated with CRC progression. This integrative, multi-omics strategy enabled tracing statin-induced effects across different layers of cellular function, linking lipid, transcript, and protein changes to pathway-level shifts.

Full blog - https://www.oncotarget.org/2025/12/03/repurposing-statins-exploring-anti-tumor-effects-in-colorectal-cancer/

Paper DOI - https://doi.org/10.18632/oncotarget.28755

Correspondence to - Sanjeev Galande - sanjeev.galande@snu.edu.in

Abstract video - https://www.youtube.com/watch?v=A95ICULaH3Y

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Keywords - cancer, colorectal cancer, statins, SATB1, Wnt/β-catenin signaling, tumor-suppressive phenotype

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Repurposing Statins: Exploring Anti-Tumor Effects in Colorectal Cancer

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