Researchers from the Chinese Academy of Sciences and Capital Medical University utilized gene editing to create senescence-resistant human mesenchymal progenitor cells (SRCs). In a 44-week trial on aged macaques, biweekly intravenous SRC injections induced no adverse effects and spurred multi-system rejuvenation in 10 major physiological systems and 61 tissue types. Treated macaques displayed enhanced cognitive function and diminished age-related degeneration. The SRCs work by releasing exosomes that curb cellular senescence and inflammation. This study presents the first primate-level proof of cell therapy’s safety and efficacy in reversing aging, presenting a potential multi-system approach for human anti-aging research.
Caffeine has long been associated with health benefits, including a reduced risk of age-related diseases. However, the specifics of how caffeine interacts with cellular mechanisms and nutrient and stress-responsive gene networks have remained elusive — until now.
In this pioneering research, published in the journal Microbial Cell, scientists used fission yeast, a single-celled organism with surprising similarities to human cells, to delve deeper into caffeine’s impact.
The researchers discovered that caffeine influences aging by engaging an ancient cellular energy system.
A few years ago, the same team found that caffeine prolongs cell life by acting on a growth regulator known as TOR (Target of Rapamycin). TOR is a molecular switch that regulates cell growth based on available food and energy and has been part of the evolutionary landscape for over 500 million years.
However, their latest study unveiled a surprising new finding: caffeine does not directly act on the TOR switch. Instead, it activates AMPK, a cellular fuel gauge that is conserved through evolution in both yeast and humans.
“When your cells are low on energy, AMPK kicks in to help them cope,” senior author Charalampos (Babis) Rallis, a reader in genetics, genomics and fundamental cell biology at Queen Mary University of London, said in a news release. “And our results show that caffeine helps flip that switch.”
Intriguingly, AMPK is also the target of metformin, a common diabetes medication currently under scrutiny for its potential to extend human lifespan when used alongside rapamycin.
An MRI scan revealed a brain tumor located in a difficult area, and performing a biopsy would carry significant risks for the patient, who had initially sought medical help due to double vision. Cases like this, discussed by a multidisciplinary team of cancer specialists, led researchers at Charité – Universitätsmedizin Berlin, along with their collaborators, to search for alternative diagnostic methods.
Their solution is an AI model that analyzes specific features in the genetic material of tumors, particularly their epigenetic fingerprint, which can be obtained from sources such as cerebrospinal fluid. As reported in the journal Nature Cancer, the model classifies tumors both rapidly and with high accuracy.
Researchers led by John T. Wilson, Vanderbilt University associate professor of chemical and biomolecular engineering and biomedical engineering, have developed a new approach using a molecularly designed nanobody platform that seeks to make immunotherapy more effective in the treatment of cancer.
The research, “Potentiating Cancer Immunotherapies with Modular Albumin-Hitchhiking Nanobody-STING Agonist Conjugates,” is published in Nature Biomedical Engineering.
Immunotherapy is revolutionizing cancer treatment, but few patients benefit from the treatment, according to researchers. However, Wilson and his Immunoengineering Lab at Vanderbilt, along with collaborators at Vanderbilt University Medical Center, SOMBS, and the College of Arts and Sciences, aim to solve this problem.
A new study has revealed compelling evidence that brain criticality—a dynamic balance between neural excitation and inhibition—has a strong genetic foundation and is associated with cognitive performance. The research was published on June 23 in the Proceedings of the National Academy of Sciences.
Led by Prof. Liu Ning from the Institute of Biophysics of the Chinese Academy of Sciences (CAS) and Prof. Yu Shan from the Institute of Automation of CAS, the team analyzed resting-state functional MRI (rs-fMRI) data from the Human Connectome Project S1200 release. The dataset included 250 monozygotic twins, 142 dizygotic twins, and 437 unrelated individuals, providing a robust framework for examining the heritability of critical brain dynamics.
The results showed that brain criticality is significantly influenced by genetic factors, with stronger genetic effects observed in primary sensory cortices compared to higher-order association regions. These findings suggest that the capacity of the brain to maintain near-critical dynamics—previously associated with optimal information processing and cognitive flexibility—is, to a substantial degree, inherited.
And an increased all-cause mortality risk…
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Researchers from Osaka Metropolitan University have identified a gene that, when activated by metabolic stress, damages pancreatic β-cells—the cells responsible for insulin production and blood sugar control—pushing them toward dysfunction. The findings highlight a promising new target for early intervention in type 2 diabetes. The study is published in the Journal of Biological Chemistry.
While many factors can contribute to type 2 diabetes, lifestyle, especially diet, plays a major role in its onset. Genetics matter, but poor eating habits can greatly increase the risk of developing what is now often called a “silent epidemic.”
“Type 2 diabetes occurs when pancreatic β-cells, which secrete insulin to regulate blood glucose, become impaired due to prolonged stress caused by poor dietary habits, a condition known as oxidative stress,” said Naoki Harada, an associate professor at Osaka Metropolitan University’s Graduate School of Agriculture and lead author of this study.