Synucleinopathies are a group of age-related neurological disorders, including Parkinson’s disease, dementia with Lewy bodies, and multiple system atrophy. Most individuals are not diagnosed until these diseases have significantly progressed, as early symptoms, such as a reduced sense of smell, subtle cognitive or motor changes are too vague to serve as reliable indicators. 

To uncover specific biological signs that appear earlier and clearly point to the disease process, researchers from Saarland University developed a study titled “Brain region-specific and systemic transcriptomic alterations in a human alpha-synuclein overexpressing rat model,” featured as the cover Aging-US, Volume 17, Issue 10.

Full blog - https://aging-us.org/2025/11/alpha-synuclein-overexpression-in-rats-reveals-early-clues-to-synucleinopathies/

Paper DOI - https://doi.org/10.18632/aging.206331

Corresponding author - Thomas Hentrich - thomas.hentrich@uni-saarland.de

Abstract video - https://www.youtube.com/watch?v=Yl6AfVchkb0

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Keywords - aging, alpha-synuclein, transgenic rat model, different brain regions, transcriptome analysis

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Aging-US

Alpha-Synuclein Overexpression in Rats Reveals Early Clues to Synucleinopathies

BUFFALO, NY - November 12, 2025 – A new #research paper was #published in Oncotarget (Volume 16) on November 6, 2025, titled “LRIG1-3 in gliomas: LRIG1 protein expression decreased in higher grade gliomas.”

In this study by Marlene Happe, Saskia Kuhl, Lukas Görtz, Roland Goldbrunner and Marco Timmer, from the University of Cologne, researchers found that the LRIG1 protein, which may help suppress tumors, is present at lower levels in more aggressive gliomas, a type of brain tumor. The findings suggest that LRIG1 could serve as a useful marker for tumor severity and potentially as a target for future therapies.

Gliomas are the most common malignant brain tumors in adults and carry a poor prognosis, particularly in their most severe form, glioblastoma. This study investigated three related proteins: LRIG1, LRIG2, and LRIG3, which are involved in regulating cell growth signals. While LRIG1 and LRIG3 have shown tumor-suppressing effects in previous studies, LRIG2 is thought to support tumor growth. The researchers analyzed tumor samples from patients to understand how these proteins behave across different glioma grades and how they respond to chemotherapy.

The results showed that LRIG1 protein levels decline significantly as tumor grade increases. Low-grade gliomas displayed much higher LRIG1 expression than high-grade tumors. Among high-grade tumors, primary glioblastomas had the lowest levels of LRIG1. Interestingly, secondary glioblastomas, which typically develop from lower-grade tumors, had higher levels of LRIG1 than primary glioblastomas. This difference may contribute to their relatively better clinical outcomes. These results highlight LRIG1’s potential role in slowing tumor progression.

In contrast, LRIG2 showed a more complex pattern. While its gene expression was higher in lower-grade tumors, the actual protein levels were slightly elevated in higher-grade ones, which are more aggressive. This mismatch suggests that processes occurring after gene transcription may influence how much LRIG2 protein is produced. 

“However, our data on LRIG2 indicate that its role in glioma may be more complex than previously thought, warranting further investigation.”

Concerning LRIG3, it was found in higher amounts in glioma tissue compared to surrounding healthy tissue. Its expression was particularly high in low-grade tumors. However, chemotherapy did not consistently affect LRIG3 levels, and results varied depending on tumor type and treatment status.

Overall, the study suggests that members of the LRIG protein family, especially LRIG1, could serve as important biomarkers to distinguish between glioma types and grades. Although chemotherapy did not significantly change their expression in most cases, these proteins have high potential as diagnostic tools or therapeutic targets. Further research is needed to better understand their roles in glioma development and treatment response.

DOI - https://doi.org/10.18632/oncotarget.28775

Correspondence to - Marco Timmer - marco.timmer@uk-koeln.de

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

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Keywords - cancer, oncology, glioma, glioblastoma, LRIG1, LRIG2, LRIG3

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Oncotarget

Lower LRIG1 Expression Linked to Aggressive Gliomas

Aging-US proudly sponsored the Future of Aging Research (FAR) Mixer 2025, hosted by the Aging Initiative on November 7 in Cambridge, MA, uniting students, researchers, and biotechnology leaders to advance aging research and shape a healthier, longer-lived future.

Highlights from the FAR Mixer 2025

The 2025 FAR Mixer featured keynote speaker Dr. Kristen Fortney, Co-Founder and CEO of BioAge Labs, who shared insights into how translational research and clinical pipelines have evolved over the past decade. 

Dr. Fortney highlighted how obesity-targeting drugs are opening new avenues for metabolic and aging research. She explained that while obesity and osteoporosis are currently major therapeutic priorities, the next wave of reimbursable diseases will likely focus on muscle loss and chronic inflammation, reflecting their growing recognition as key factors in healthy aging. 

She also emphasized the importance of human databases in target discovery, cross-sector partnerships between pharma and biotech, and the increasing focus on small-molecule interventions to address age-related diseases.

Focus talks showcased the diversity and depth of modern aging research.

Full recap - https://aging-us.org/2025/11/aging-us-supports-the-future-of-aging-research-mixer-2025/

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Aging-US Supports the Future of Aging Research Mixer 2025

BUFFALO, NY — November 13, 2025 — A new #research paper was #published in Volume 17, Issue 10 of Aging-US on October 3, 2025, titled “The role of phenylalanine and tyrosine in longevity: a cohort and Mendelian randomization study.”

In this study led by Jie V. Zhao, Yitang Sun, Junmeng Zhang, and Kaixiong Ye from the University of Hong Kong and the University of Georgia, researchers investigated whether two amino acids, phenylalanine and tyrosine, affect  how long people live (lifespan). The results suggest that higher levels of tyrosine are linked to shorter life expectancy in men, pointing to potential sex-specific approaches to promoting longevity.

Phenylalanine and tyrosine are amino acids involved in metabolism and brain function. Both are found in protein-rich foods and dietary supplements, but their long-term effects on aging are not well understood. Tyrosine, in particular, is a building block of neurotransmitters such as dopamine, which regulate mood and cognitive function, making it a molecule of interest in aging research.

The study analyzed data from more than 270,000 individuals in the UK Biobank. Using both observational and genetic methods, the researchers examined the associations between blood levels of phenylalanine and tyrosine with overall mortality and predicted lifespan. Although both amino acids were initially linked to higher mortality risk, only tyrosine showed a consistent and potentially causal association with reduced life expectancy in men. Genetic analyses estimated that elevated tyrosine levels could shorten men’s lifespan by nearly one year. No significant effect was observed in women.

These findings remained consistent even after adjusting for related factors, including the role of phenylalanine. This suggests that tyrosine may independently influence aging. The researchers also observed that men tend to have higher tyrosine levels than women, which could partly explain the gender gap in lifespan.

“Phenylalanine showed no association with lifespan in either men or women after controlling for tyrosine.”

The exact mechanisms behind this effect are still under investigation. However, tyrosine’s involvement in insulin resistance and the production of stress-related neurotransmitters may be contributing factors. Insulin resistance is associated with many age-related diseases, and hormone-related pathways influenced by tyrosine may differ between men and women, potentially explaining the sex-specific outcomes.

Although tyrosine is commonly marketed as a supplement for enhancing focus and mental performance, the study raises concerns about its long-term impact on lifespan. While the researchers did not directly study tyrosine supplementation, their findings suggest that people with high tyrosine levels may benefit from dietary adjustments. Strategies such as protein restriction could help reduce tyrosine levels and support healthier aging.

Further studies are needed to confirm these findings and explore whether diet and lifestyle changes can safely lower tyrosine levels to promote longevity.

DOI - https://doi.org/10.18632/aging.206326

Corresponding author - Jie V. Zhao - janezhao@hku.hk

Abstract video - https://www.youtube.com/watch?v=rr0G44TD36M

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High Tyrosine Levels Linked to Shorter Lifespan in Men

BUFFALO, NY – November 17, 2025 – A new #research perspective was #published in Oncotarget (Volume 16) on November 14, 2025, titled “A personal perspective of patient-centred clinical trials.”

In this perspective, led by corresponding author Jia Liu of The Kinghorn Cancer Centre, St Vincent’s Hospital, the University of New South Wales, and the Garvan Institute of Medical Research, three early-phase clinical trial participants — Trevor Tyne, Elizabeth Ivimey, and Leanne Duggan — reflect on their personal experiences with experimental cancer treatments. Their stories offer a unique perspective on the patient journey through early-phase trials and emphasize the need to design clinical research that prioritizes patients’ needs, dignity, and lived realities. The authors highlight both the life-changing opportunities that trials can provide and the systemic barriers that still prevent many patients from participating.

This perspective captures a turning point in how early-phase trials are viewed. Once considered a last resort, these trials are now increasingly offered earlier in treatment, especially with the rise of biomarker-guided therapies. In this context, the patient experience has become critical. The authors outline key benefits of participation, including access to novel therapies, ongoing medical monitoring, emotional support, and a strong sense of purpose in contributing to future medical advancements. However, they also point out significant challenges, such as restrictive eligibility criteria, high financial and logistical burdens, and communication gaps between patients and trial staff.

“While no trial guarantees success, the level of support, access to innovative therapies, and sense of contribution to medical progress can be profoundly meaningful.” 

Each narrative provides insight into the clinical trial experience. One patient explains how living with a visual impairment required tailored accessibility support throughout the trial process Another shares how genomic testing led to targeted treatment after standard options failed. Despite their different diagnoses and circumstances, all three stories reflect resilience, hope, and a shared call for trial designs that better reflect the realities of diverse patients.

To address these issues, the authors propose a number of improvements to trial design and delivery. These include expanding eligibility criteria, offering financial and logistical assistance, improving communication training for research staff, and introducing dedicated trial navigators to help guide patients through complex processes. They also focus on the importance of involving patient advocates in trial design and ensuring smoother transitions for patients moving between treatment centers.

While early-phase trials focus on safety and effectiveness, the authors argue they must also be guided by core values like ethics and patient empowerment. This perspective serves as a reminder that the future of cancer research depends not only on scientific innovation, but on an honest partnership between patients and the research community.

By sharing these real-world experiences, the article encourages a broader conversation about how to make clinical trials more responsive to the people they are designed to serve.

DOI - https://doi.org/10.18632/oncotarget.28776

Correspondence to - Jia Liu - jia.liu@svha.org.au

Abstract video - https://www.youtube.com/watch?v=2CCGN78n8ug

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Clinical Trial Participants Call for More Inclusive, Patient-Centered Cancer Research

In this episode of the Longevity & Aging Series, Dr. Amparo Santamaria from the Reproductive Hematology Unit at the IVIRMA Alicante Clinic in Spain joins Dr. Evgeniy Galimov to discuss her #research paper #published in Volume 17, Issue 6 of 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=Zlezd0x_EJQ

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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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Longevity & Aging Series (S3, E7): Amparo Santamaria

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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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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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

Aging-US is dedicated to advancing our understanding of the biological mechanisms that drive aging and the development of age-related diseases. Our mission is to serve as a platform for high-quality research that uncovers the cellular, molecular, and systemic processes underlying aging, and translates these insights into strategies to extend healthspan and delay the onset of chronic disease.

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

Aging-US Podcast

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