BUFFALO, NY — July 8, 2025 — As populations worldwide continue to age, understanding the mechanisms and manifestations of cognitive aging is increasingly urgent for science, medicine, and society. Age-related cognitive decline ranges from mild memory lapses to the onset of dementia, and is shaped by a complex interplay of molecular, cellular, systemic, and social determinants.

In this special collection, Aging (Aging-US) seeks to bring together cutting-edge research that spans the cellular and molecular underpinnings of cognitive aging with insights into the psychosocial, behavioral, and environmental factors that modulate its course. By integrating basic biology with translational and societal dimensions, this collection aims to foster a holistic understanding of how and why cognitive function changes with age—and what can be done to preserve it.

We welcome original research articles, reviews, and perspectives across model systems and human studies, particularly those that promote interdisciplinary insights and translational potential.

POTENTIAL TOPICS

Molecular and Cellular Mechanisms

-Senescence, inflammation, and neurodegeneration in cognitive decline
-Mitochondrial dysfunction and oxidative stress in aging neurons
-Neurovascular aging and blood-brain barrier integrity
-Single-cell and spatial transcriptomics of the aging brain
-mTOR, autophagy, and proteostasis in age-related cognitive impairment
-The role of glial cells (microglia, astrocytes) in brain aging

 Genetics and Biomarkers

-Genetic risk factors and epigenetic modifications associated with cognitive aging
-Biomarkers of cognitive resilience and vulnerability
-Neuroimaging and fluid-based biomarkers in aging populations

Interventions and Lifestyle Factors

-Cognitive benefits of caloric restriction, exercise, or senolytic therapies
-Preclinical and clinical trials targeting aging pathways to prevent cognitive decline
-Impact of sleep, nutrition, and metabolic health on cognition in older adults
-Use of cognitive strategies and compensatory techniques to maintain or enhance function in aging

Environmental and Social Contexts

-Impact of social isolation, education, and socioeconomic status on cognitive trajectories
-Lifelong cognitive reserve and its determinants
-Cross-cultural and demographic studies on aging and cognition
-Digital health tools for monitoring or enhancing cognitive function in the elderly

SUBMISSION DETAILS:

-Submission Deadline: March 31, 2026
-Manuscript Format: Please follow the journal’s submission guidelines
-Peer Review: All submissions will undergo a rigorous peer-review process
-Submission Link: https://aging.msubmit.net/cgi-bin/main.plex

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Aging (Aging-US)

Now Accepting Submissions: Special Collection on Cognitive Aging

Treading Angels

BUFFALO, NY – July 9, 2025 – A new #review was #published in Volume 16 of Oncotarget on June 25, 2025, titled “Challenges and resistance mechanisms to EGFR targeted therapies in head and neck cancers and breast cancer: Insights into RTK dependent and independent mechanisms.”

Researchers from the University of Cincinnati and Cincinnati Veterans Affairs Medical Center reviewed current research on why Epidermal Growth Factor Receptor (EGFR)-targeted therapies often fail in breast and head and neck cancers. The article by Shreya Shyamsunder, Zhixin Lu, Vinita Takiar, and Susan E. Waltz explores how cancer cells evade these treatments by activating alternative survival pathways. This review offers an in-depth look at the molecular barriers to EGFR inhibition and provides insights that could inform the development of more effective and durable treatments.

EGFR is a critical protein that regulates cell growth and survival, and it is frequently overexpressed in breast and head and neck cancers. Although therapies targeting EGFR showed early promise, resistance has become a significant challenge. In breast cancer, resistance mechanisms include the movement of EGFR from the cell surface into the nucleus, where it promotes DNA repair, as well as ligand-dependent activation that helps tumor growth despite therapy. In head and neck cancers, resistance often arises from inflammatory signaling through the TLR4-MyD88 pathway and the loss of tumor suppressor genes like PTEN, which allow cancer cells to bypass EGFR inhibition. The review also describes how tumor cells in both cancers commonly activate other receptor tyrosine kinases (RTKs), such as MET, AXL, and RON, to continue growing even when EGFR is blocked.

By analyzing these resistance mechanisms, the authors highlight combination therapies from current research that target EGFR and other key molecular pathways. Strategies such as dual inhibition of EGFR and MET or blocking inflammation-driven survival signals may enhance treatment outcomes. Several clinical trials are evaluating these approaches in patients. For example, in breast cancer, combinations of EGFR inhibitors with chemotherapy and immune checkpoint inhibitors are being tested to improve responses, particularly in triple-negative breast cancer. In head and neck cancers, trials are investigating EGFR-blocking antibodies like cetuximab combined with immunotherapies such as pembrolizumab and nivolumab. These efforts aim to overcome resistance and provide more effective treatment options for patients with EGFR-driven tumors. The review also emphasizes the necessity of identifying biomarkers to predict which patients are most likely to benefit from EGFR-based therapies.

“A recent phase 1 study has shown that patients with recurrent or metastatic head and neck cancer who received BCA101, a bifunctional dual targeting drug that targets EGFR and TGF-β in combination with pembrolizumab, were able to achieve an overall response rate of 65%.”

This work brings together current knowledge about EGFR resistance and illustrates the difficulties involved in treating breast and head and neck cancers. By mapping the many ways tumors overcome EGFR inhibition, the review highlights opportunities for more tailored and effective treatments in the future.

DOI - https://doi.org/10.18632/oncotarget.28747

Correspondence to - Susan E. Waltz - susan.waltz@uc.edu, and Vinita Takiar - takiarva@ucmail.uc.edu

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Oncotarget

EGFR-Targeted Therapy Resistance in Breast and Head & Neck Cancers

BUFFALO, NY — July 10, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 6, on June 7, 2025, titled “Spermidine supplementation and protein restriction protect from organismal and brain aging independently.”

In this study, led by YongTian Liang and Stephan J. Sigrist from Freie Universität Berlin, Charité Universitätmediz Berlin, and the  Leibniz-German Center for Neurodegenerative Diseases (DZNE), researchers investigated how spermidine, a natural substance in the body, and protein intake levels influence aging in fruit flies. They found that spermidine supplementation and changes in protein intake influenced brain health and aging in distinct ways. These insights could guide the development of new strategies to slow age-related decline in humans.

“In this study, we combined low- and high-protein diets (2% versus 12% yeast in food) with spermidine supplementation in aging Drosophila fruit flies.”

Aging of the brain and body contributes to cognitive decline and diseases in older populations. Scientists have long explored dietary restriction and fasting as ways to slow these processes. This study reveals that spermidine supplementation supports brain health by enhancing mitochondrial function and memory, while protein restriction independently promotes longevity and protects against movement decline.

The researchers discovered that spermidine improved memory and preserved physical activity in aging flies regardless of protein intake. In contrast, reducing protein alone boosted mitochondrial activity and extended lifespan without directly enhancing memory. Importantly, the combined approach of protein restriction and spermidine supplementation provided additive benefits, suggesting potential for synergistic effects.

This work highlights that spermidine acts through a pathway involving hypusination, a vital process where cells modify proteins to support energy production and repair, while protein restriction works via nutrient-sensing pathways that promote longevity. These independent mechanisms may explain why combining the two interventions offers greater protection against aging effects.

Although conducted in flies, the study underscores the possibility of designing dietary and supplement-based interventions to combat human age-related decline. As spermidine levels naturally decline with age, supplementation combined with moderated protein intake could offer a safe way to promote brain health and longevity in humans.

The authors point out that it takes further studies in mammals and humans to validate these results. If confirmed, such strategies could lead the way for accessible approaches to promote healthy aging and reduce the burden of cognitive disorders in older populations.

DOI - https://doi.org/10.18632/aging.206267

Corresponding authors - YongTian Liang - yongtian.tim.liang@gmail.com, and Stephan J. Sigrist - stephan.sigrist@fu-berlin.de

Video short - https://www.youtube.com/watch?v=QfxpK9tka7U

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Keywords - aging, brain aging, spermidine, protein restriction, mitochondria

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Spermidine and Protein Restriction Independently Protect Brain and Body from Aging in Flies

Dr. Amparo Santamaria describes a #research paper she co-authored that was #published in Volume 17, Issue 6 of Aging (Aging-US), titled “Enhancing oocyte activation in women with ovarian failure: clinical outcomes of the Stem Cell Regenera study using G-CSF mobilization of peripheral blood stem cells and intraovarian injection of stem cell factor-enriched platelet rich plasma in real-world-practice.”

DOI - https://doi.org/10.18632/aging.206274

Corresponding author -Amparo Santamaria - Amparo.santamaria@ivirma.com

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

Abstract

The study assesses the effectiveness and safety of the Stem Cell Regenera Treatment for oocyte activation in women with ovarian failure, including conditions such as Poor Ovarian Response (POR), Diminished Ovarian Reserve (DOR), and Premature Ovarian Insufficiency (POI). This retrospective observational study was conducted from January 2023 to December 2024 at the IVIRMA Alicante Clinics in Spain.

Women diagnosed with ovarian failure participated in the study, which involved mobilizing Hematopoietic Stem Cells from bone marrow into peripheral blood using granulocyte colony- stimulating factor (G-CSF). This was followed by an intraovarian injection of Stem Cell Factor- enriched Platelet Rich Plasma (SCFE-PRP).

The primary outcome measures were the rate of oocyte activation, leukocytes and stem cell count, and pregnancy rates. Oocyte activation was defined as an increase in total Antral Follicle Count of three or more follicles after treatment and/or at least a 20% rise in Anti-Müllerian Hormone levels. Safety was assessed based on adverse effects. Pregnancy rates were evaluated for both spontaneous gestation and following in vitro fertilization (IVF) treatment.

A total of 145 women participated: the overall activation rate was 68.28%, with 7.07% achieving spontaneous gestation and 14.14% achieving pregnancy following IVF. Mobilization of CD34+ cells was successful in all participants, with an average collection of 32.96 CD34+ cells/μl. No severe adverse effects were observed. The study concluded that the Stem Cell Regenera Treatment is effective and safe for oocyte activation in women with ovarian failure in real-world practice.

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Keywords - aging, Stem Cell Regenera, oocyte activation, ovarian regeneration, G-CSF, SCFE-PRP, ovarian failure

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Behind the Study: Enhancing Oocyte Activation in Women with Ovarian Failure

BUFFALO, NY – July 14, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on June 25, 2025, titled “Hypoxia induced lipid droplet accumulation promotes resistance to ferroptosis in prostate cancer.”

In this study, researchers led by Shailender S. Chauhan and Noel A. Warfel from the University of Arizona discovered that prostate cancer cells survive treatment by storing fats in tiny cellular compartments when oxygen levels are low. This process makes the cancer cells less vulnerable to a type of cell death known as ferroptosis. The findings provide new insight into why prostate tumors often resist therapies and suggest potential strategies to improve treatment outcomes.

This study focused on ferroptosis, a form of programmed cell death that relies on iron and lipid oxidation to destroy cancer cells. Researchers tested prostate cancer cells under normal and low oxygen conditions and found that hypoxia, or reduced oxygen levels, allowed cancer cells to build up lipid droplets (LD). These structures act as storage units for fats, shielding cancer cells from oxidative damage and preventing ferroptosis from occurring.

The researchers found that this adaptation of prostate cancer cells made them less sensitive to ferroptosis-inducing drugs like Erastin and RSL3, even when these drugs were combined for a stronger effect. The team also reported that hypoxia caused significant changes in lipid metabolism, decreasing the availability of specific fatty acids that normally promote ferroptosis. 

“Transcriptomic analysis revealed that hypoxia significantly reduced the expression of genes related to incorporating polyunsaturated fatty acids into phospholipids (ACSL4, LPCAT3), and parallel lipidomic analysis demonstrated that hypoxia significantly decreased the levels of the ferroptosis-prone lipid class, phosphatidylethanolamine (PE) and increased production of neutral lipid species, cholesteryl ester (ChE (22:5)) and triglycerides (TG(48:1), TG:(50:4), and TG(58:4)).”

This research highlights the importance of the tumor microenvironment, particularly oxygen levels, in shaping how cancer cells respond to therapy. By altering their metabolism and storing lipids, prostate tumors may evade treatments designed to trigger ferroptosis. These findings underscore the need to develop new strategies targeting LD dynamics or lipid metabolism to overcome this resistance.

Understanding how prostate cancer (Pca) adapts to survive in hypoxic conditions offers a potential avenue for improving therapies. For example, preventing lipid accumulation in cancer cells or releasing stored fats may restore their sensitivity to ferroptosis and improve the effectiveness of current therapies. This approach could have broader implications for treating other solid tumors that share similar metabolic features.

DOI - https://doi.org/10.18632/oncotarget.28750

Correspondence to - Noel A. Warfel - warfelna@arizona.edu, and Shailender S. Chauhan - shailenderc@arizona.edu

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Keywords - cancer, hypoxia, lipid droplets, ferroptosis, resistance, prostate

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Prostate Cancer Cells Survive Treatment by Storing Fat in Low Oxygen Conditions

Scientists have uncovered a promising new strategy to weaken cancer cells’ natural defense mechanisms, potentially making chemotherapy more effective. In a study published in Volume 16 of Oncotarget, researchers identified the protein PRDX1 as a key player in helping tumors resist treatment. By targeting this protein, they propose a novel way to combat aggressive, treatment-resistant cancers.

Understanding Why Some Cancers Resist Treatment

Chemotherapy works by damaging the DNA of cancer cells, forcing them to self-destruct. However, many cancers develop robust repair systems that fix this damage, allowing the tumor to survive and grow. A central component of this repair machinery is a protein called ATM, which acts like a first responder in the cell, detecting DNA damage and coordinating its repair.

In ovarian cancer and other aggressive tumors, high levels of ATM have been associated with poor survival rates and resistance to chemotherapy.

The Study: How PRDX1 Protects Cancer Cells

The study, titled “PRDX1 protects ATM from arsenite-induced proteotoxicity and maintains its stability during DNA damage signaling,” was led by first author Reem Ali and corresponding author Dindial Ramotar from Hamad Bin Khalifa University in Qatar, in collaboration with researchers from the University of Nottingham in the UK. 

Full blog - https://www.oncotarget.org/2025/07/14/prdx1-identified-as-key-to-chemotherapy-resistance-in-cancer-cells/

Paper DOI - https://doi.org/10.18632/oncotarget.28720

Correspondence to - Dindial Ramotar - dramotar@hbku.edu.qa

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Keywords - cancer, redox signaling, homologous recombination, protein interaction, cell cycle, protein modification

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PRDX1 Identified as Key to Chemotherapy Resistance in Cancer Cells

BUFFALO, NY — July 15, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 6, on June 5, 2025, titled “Senescence caused by telomerase inactivation in myeloid, mesenchymal, and endothelial cells has distinct effects on cancer progression.”

In this study, first author Joseph Rupert, along with corresponding author Mikhail G. Kolonin and colleagues from The Brown Foundation Institute of Molecular Medicine for the Prevention of Human Diseases, McGovern Medical School, at The University of Texas Health Sciences Center at Houston, investigated how aging-related changes in different cell types affect cancer progression. By turning off telomerase in specific cell populations in mice, the researchers discovered that cell aging, or senescence, can slow primary tumor growth but also trigger unexpected effects. This work sheds light on the complex relationship between aging cells and cancer and may help guide future anti-cancer strategies.

The team used genetically modified mice to deactivate telomerase, the enzyme that maintains chromosome ends, specifically in immune, connective tissue, and blood vessel cells. This caused these cells to enter a state of senescence, where they stop dividing and release inflammatory signals. The researchers then implanted breast, prostate, and pancreatic cancer cells into the mice and tracked how tumors developed. They found that when telomerase was inactivated in immune cells or connective tissue cells, tumors grew more slowly. However, these tumors showed signs of increased tissue damage and potential aggressiveness.

Interestingly, when telomerase was turned off in endothelial cells, which cover blood vessels, tumors shrank and became poorly supplied with blood, leading to oxygen deprivation. In the case of pancreatic cancer cells, this low-oxygen environment made them more likely to spread to the liver, highlighting a potential risk of targeting these cells.

“[…] this study shows that senescence and metabolic dysfunction resulting from telomerase inactivation in distinct cells in the tumor microenvironment have different effects on tumor growth and metastasizing of carcinomas.”

This research provides important insights into how aging cells within the tumor microenvironment (TME) influence cancer behavior. While senescence in certain cell types can help suppress tumor growth, it may also create conditions that favor cancer metastasis. These findings highlight the need to consider cell type-specific effects when developing therapies that target senescent cells. By mapping how different cell populations contribute to cancer progression in aging tissues, this study opens the door for more precise approaches to prevent both tumor growth and spread.

DOI - https://doi.org/10.18632/aging.206268

Corresponding author - Mikhail G. Kolonin - mikhail.g.kolonin@uth.tmc.edu

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Keywords - aging, senescence, telomerase, myeloid, mesenchymal, endothelial

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How Telomerase Inactivation in Aging Cells Influences Cancer Growth and Metastasis

BUFFALO, NY - July 16, 2025 – A new #research paper was #published in Volume 16 of Oncotarget on July 9, 2025, titled “A novel anti-human CD25 mAb with preferential reactivity to activated T regulatory cells depletes them from the tumor microenvironment.”

In this study, researchers from the National Institute of Allergy and Infectious Diseases, led by first author Maja Buszko and corresponding author Ethan M. Shevach, discovered a new monoclonal antibody that selectively targets a subset of immune cells called regulatory T cells (Tregs). These cells, while normally important for preventing autoimmunity, also can block the body’s ability to fight cancer by suppressing anti-tumor immune responses. This discovery could lead to novel cancer therapies that strengthen the immune system’s capacity to attack tumors.

The researchers identified an anti-CD25 monoclonal antibody with several atypical properties and named it 2B010.  To evaluate its effects, they used humanized mice, laboratory mice that are engineered to carry human immune cells, to closely mimic how human immune systems respond to cancer. The treatment of these mouse models with 2B010 significantly decreased the number of Tregs in tumors and boosted the activity of CD8+ T cells, which are essential for killing cancer cells. Importantly, 2B010 worked without disrupting other key immune functions. Unlike traditional Anti-CD25 antibodies, it did not interfere with interleukin-2 (IL-2) signaling, which is essential for the growth and activity of effector T cells that fight cancer. 

“2B010 also had no effect on IL-2 induced STAT5 phosphorylation or CD4+ T cell proliferation in vitro while both were blocked by Clone D1 further supporting the view that 2B010 does not recognize the IL-2 binding site.”

This finding is especially significant because high levels of Tregs in tumors are associated with poor outcomes in many cancers. By specifically removing these cells, 2B010 may help overcome one of the main barriers to current immunotherapy approaches. Its ability to preserve IL-2 signaling could also make it safer and more effective when used alone or in combination with existing therapies such as immune checkpoint inhibitors.

While the 2B010 antibody showed strong effects in reducing Tregs and boosting immune cell activity, the study did not observe changes in tumor size in these models. Researchers suggest this may be due to limitations in the preclinical systems used, such as the lack of tumor-specific T cells in humanized mice. Nevertheless, these findings demonstrate that 2B010 has a unique mechanism of action that could complement other cancer immunotherapies in future clinical trials.

In conclusion, the development of 2B010 is a promising step toward selectively disrupting the immune suppressive environment in tumors. As researchers continue to refine and test this antibody, it could become a powerful tool for enhancing the effectiveness of cancer treatments and improving outcomes for patients.

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

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

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

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New Antibody Selectively Targets Immune Cells That Suppress Anti-Tumor Responses

BUFFALO, NY — July 17, 2025 — A new #research paper was #published in Aging (Aging-US) Volume 17, Issue 6, on June 9, 2025, titled “Developing a quantitative estimate of muscle age acceleration by a novel phenotypic clock: cross-sectional study in healthy, middle-aged and older adults.”

In this study, led by first authors Lucia Ventura, Antonella Cano and Marco Morrone, along with corresponding author Franca Deriu from the University of Sassari, researchers introduce a new method to predict how muscles age, offering an early warning system for sarcopenia, the condition of age-related muscle loss. The study demonstrates how a simple, low-cost approach can identify middle-aged and older adults at higher risk for declining muscle health, allowing timely preventive strategies.

The researchers developed a tool called Muscle Age Acceleration (MAA), which measures how quickly an individual’s muscles are aging compared to their actual age. By analyzing physical performance tests and body composition in 215 healthy participants aged 50 to 90 years, the researchers found that about 25% of individuals experience accelerated muscle aging. These individuals had a higher probability of developing sarcopenia, despite appearing healthy and not yet having received a diagnosis of the condition.

Sarcopenia reduces muscle strength and physical performance, being a growing concern for older adults. It contributes to frailty, falls, and an increased risk of disability. Despite greater awareness, this condition often goes undetected until significant muscle loss occurs. This new muscular clock offers an opportunity to detect subtle changes in muscle health before they progress to more severe stages.

By using common tests such as handgrip strength, walking speed, and mobility assessments, the MAA tool can classify individuals as having accelerated, normal, or decelerated muscle aging. Those with accelerated muscle aging also showed small changes in blood markers, suggesting early and hidden inflammation linked to muscle decline. This finding indicates that MAA may act as both a predictor of muscle-related aging and an indicator of overall health risks.

“According to MAA, three trajectories were identified: accelerated agers displayed higher risk for sarcopenia (19%), as compared to normal (9%; p < 0.0001) and decelerated (2%; p < 0.0001), paralleled by significant subclinical alterations of haemato-chemical markers in accelerated agers.”

If validated in future studies, this innovative approach could transform how clinicians and caregivers screen for early signs of sarcopenia. Its simplicity makes it suitable for use in clinics and community settings, helping older adults maintain independence and quality of life as they age.

In summary, these findings highlight the importance of monitoring muscle health and physical performance in older adults. By detecting early signs of muscle aging with tools like MAA, interventions such as exercise and dietary changes can be introduced earlier, potentially delaying or preventing sarcopenia and its complications.

DOI - https://doi.org/10.18632/aging.206269

Corresponding author - Franca Deriu - deriuf@uniss.it

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New Aging Clock Predicts Early Risk of Muscle Loss in Older Adults

Born Woolfinius Jackson Whürl to two itinerate circus gymnasts, Woolfin would grow tired of the performance life and would go on to seek quieter pastures as a painter and later a writer.

Oncotarget is a primarily oncology-focused, peer-reviewed, open access journal. Papers are published continuously within yearly volumes in their final and complete form and then quickly released to Pubmed.

Oncotarget is now indexed by MEDLINE, PubMed and PMC/PubMed.

Read about the Oncotarget Scientific Integrity Process: https://www.oncotarget.com/scientific_integrity/

Cancer and aging are two sides of age-related tumorigenesis.

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.)

Read about the Aging (Aging-US) Scientific Integrity Process: https://aging-us.com/scientific-integrity

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