We sit down with José Cordeiro, author of The Death of Death, to uncover the timeline scientists believe could end aging — and even achieve immortality. From the promise of longevity escape velocity by 2030 to Ray Kurzweil’s bold prediction of immortality by 2045, José reveals the breakthroughs, roadblocks, and revolutionary ideas shaping the future of human life.
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Aging is a primary risk factor for multi-morbidity and declining quality of life. The geroscience hypothesis states that targeting biological aging mechanisms may prevent or delay morbidity; however, translating theory into practice remains challenging. Unknown long-term risks and a lack of well-validated, responsive, and practical surrogate endpoints especially hinder the field’s preventive aspirations. This review addresses these obstacles by introducing the regeneration model of aging—a novel framework that integrates biological aging processes and distills the complexity of aging into a series of fundamental steps. The model provides insights into potential trade-offs of anti-aging interventions and can guide strategies to slow aging across diverse populations.
Hematopoietic aging extends far beyond the confines of the bone marrow, functioning as a central regulator of systemic decline through its influence on inflammation, immune dysregulation, and inter-organ communication. Moreover, reciprocal signaling from peripheral organs, such as the brain and gut, further shapes hematopoietic aging, highlighting the bidirectional nature of these interactions (Figure 3).
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At SciCon 2024, John Cumbers, founder and CEO of SynBioBeta, explores the groundbreaking and controversial potential of synthetic biology and AI in brain and body replacement. He delves into stem cell research and AI’s role in regenerating brain function, while also addressing the provocative idea of gradually replacing parts of the brain and body. Cumbers discusses how these advancements could one day lead to life extension, challenging traditional views on aging, and raising ethical questions about the future of human biology.
SciCon (2024) is ResearchHub’s annual conference, which unites truth-seekers and innovators to push the boundaries of open science.
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In a nonrandomized phase 2 trial of adults with advanced dMMR/MSI-H noncolorectal cancers, combined nivolumab/ipilimumab showed an objective response rate of 63% and 6-month progression-free survival rate of 71%.
Main Outcomes and Measures The co-primary end points were objective response rate (ORR) and 6-month progression-free survival (6-PFS) as assessed by Response Evaluation Criteria in Solid Tumors (RECIST) version 1.1, with the secondary end points being median overall survival (mOS), progression-free survival (PFS), and treatment-related toxic effects.
Results Overall, 52 participants were included. The median (range) age of participants was 62 (29−84) years; 41 (79%) were female individuals and 11 (21%) were male individuals. Overall, 52 patients representing 17 tumor types were enrolled, with the most common tumor type being endometrial cancer (26 [50%]). Twenty-seven patients (52%) were pretreated for metastatic disease. ORR was 63% (95% CI, 50% to 75%) with the median duration of response not being reached and 79% of responses being ongoing. The median PFS and OS have not been reached and the 6-month PFS was 71% (95% CI, 57%-81%). Overall, 12 patients (23%) experienced a grade 3/4 immune-related adverse event.
Conclusions and Relevance This nonrandomized clinical trial found that combined anti–PD-1/CTLA-4 blockade was associated with a high rate of durable responses in dMMR/MSI-H noncolorectal cancers, comparing favorably to published trials using anti–PD-1/programmed cell death ligand 1 monotherapy. Anti–PD-1/CTLA-4 blockade using nivolumab and ipilimumab may represent an alternative treatment option to monotherapy in this patient population.
A landmark international study that pooled brain scans and memory tests from thousands of adults has shed new light on how structural brain changes are tied to memory decline as people age.
The findings — based on more than 10,000 MRI scans and over 13,000 memory assessments from 3,700 cognitively healthy adults across 13 studies — show that the connection between shrinking brain tissue and declining memory is nonlinear, stronger in older adults, and not solely driven by known Alzheimer’s-associated genes like APOE ε4. This suggests that brain aging is more complex than previously thought, and that memory vulnerability reflects broad structural changes across multiple regions, not just isolated pathology.
Published in Nature Communications, the study, “Vulnerability to memory decline in aging revealed by a mega-analysis of structural brain change,” found that structural brain change associated with memory decline is widespread, rather than confined to a single region. While the hippocampus showed the strongest association between volume loss and declining memory performance, many other cortical and subcortical regions also demonstrated significant relationships. This suggests that cognitive decline in aging reflects a distributed macrostructural brain vulnerability, rather than deterioration in a few specific brain regions. The pattern across regions formed a gradient, with the hippocampus at the high end and progressively smaller but still meaningful effects across large portions of the brain.
https://www.nature.com/articles/s41467-025-66354-y
Genetic risk for Alzheimer’s and widespread brain shrinkage linked to greater memory loss — even in otherwise healthy adults.
Proteostasis in the lifespan of hematopoietic stem cells.
The hematopoietic system represents an excellent model to study how proteostasis (protein homeostasis) influences different cell types within the same tissue. This review focuses on mechanisms of proteostasis that preserve the lifespan of rare hematopoietic stem cells (HSCs).
Although most proteostasis network components are expressed in all cells, their activation and utilization are cell type-specific. HSCs maintain low translation rates and a preference for autophagy over proteasomal degradation to minimize protein stress.
To protect the integrity of the stem cell pool, HSCs are thought to respond to damage by clearing defective organelles and proteins or by eliminating compromised cells through differentiation or apoptosis.
A stressed proteome accelerates HSC aging, and the immune system derived from aged HSCs is suspected to contribute to the decline of other tissues. This highlights the importance of maintaining healthy HSCs to preserve organismal wellbeing.
Several experimental treatments in mouse models have been shown to boost HSC activity in older organisms by enhancing proteostasis.
This promising research opens up new possibilities for interventions that could improve aging through regenerative medicine. sciencenewshighlights ScienceMission https://sciencemission.com/longevity-from-blood-stem-cells
Cell Communication and Signaling — The exponential growth of immunometabolism-related studies in the last 10 years has made it very clear that metabolism is a key player in the effector functions of immune cells. Such is the case in cells with lymphoid origin, as CD4 + and CD8 + T cells undergo a series of metabolic reprogramming steps during their differentiation process, which is associated with a change in their effector characteristics. Only recently have factors such as biological aging and cellular senescence been examined in relation to memory T-cell generation and the metabolic reprogramming that accompanies their differentiation. In this review, we examine the emerging roles of cellular senescence and biological aging in shaping T-cell metabolism and immune function, and how these changes in the T-cell landscape contribute to disease onset. We then discuss recent studies on T-cell metabolic reprogramming to highlight how understanding the impact of senescence on T-cell metabolism may reveal new therapeutic opportunities.
