Through spatial multiomics, spatial stable isotope tracing and retrospective cohort analyses, this study identifies hyperglycosylation as a driver of Alzheimer’s disease and a promising therapeutic target.
Cancer remission, in which tumor cells enter a dormant state and a patient’s symptoms subside, can persist for years or decades.1 Both the cancer cells themselves and the tumor microenvironment maintain this period of inactivity.2 While inflammation has been shown to disrupt this microenvironment, leading to metastasis, the mechanisms of this process remain unclear.
Seeing a trend in increased cancer deaths in the first two years of the COVID-19 pandemic, cancer biologists Julio Aguirre-Ghiso at the Albert Einstein College of Medicine and James DeGregori at the University of Colorado suspected that viral infections could be activating dormant cancer cells. In partnership with researchers at Utrecht University, the teams showed that inflammation from viral infections activated dormant cancer cells and increased metastasis.3 The findings, published in Nature, provide important insights into cancer remission for clinicians.
“Dormant cancer cells are like the embers left in an abandoned campfire, and respiratory viruses are like a strong wind that reignites the flames,” DeGregori said in a press release about the study findings.
Though protein clumps associated with Alzheimer’s and Parkinson’s were discovered more than a century ago, researchers remain largely unable to prevent them from forming or eliminate them from the brain. And though a variety of therapies have taken aim at tau tangles, beta-amyloid plaques and Lewy bodies, among other notorious aggregates, none have been very effective at stopping disease progression.
Rockefeller’s Hermann Steller and his team in the Strang Laboratory of Apoptosis and Cancer Biology have long been focused on understanding how the cell’s protein-degrading machines, called proteasomes, are regulated. His lab discovered that a transporter protein termed PI31 shuttles proteasomes over long distances from the nerve cell body to synapses. When this system fails, synapses become depleted of degradative capacity, and proteins that should have been eliminated accumulate. As a result, synaptic communication breaks down, protein clumps form and neuronal health deteriorates.
Now a new study in Nature Communications, led by researchers from University College London and contributed to by Steller’s lab, has identified mutations in PSMF1, the gene that produces PI31, that cause the protein to malfunction. Moreover, the scientists demonstrated that these mutations cause a spectrum of severe, very early-onset neurological disorders.
People with Alzheimer’s disease who took the common supplement glucosamine were 25% more likely to die within five years than those who didn’t.
That’s the key finding of a new study that my colleagues and I published in the journal Nature Metabolism.
Glucosamine is a sugar molecule that’s sold over the counter as a remedy for joint pain and arthritis. More than 40 million Americans take it each year.
For extra nuances and all the references, please see the newsletter: https://staycuriousmetabolism.substack.com/p/can-we-become-l…a?r=40ekz2… StayCurious Human Enhancement Series.
The StayCurious Human Enhancement Series.
We’re launching a new series at StayCurious Metabolism called Peptides Plus, where we’ll explore the most promising tools available today—and the innovations that may shape tomorrow. We have dozens of deep dives planned, covering everything from emerging therapeutics to cutting-edge performance and longevity interventions.
GO HERE: https://staycuriousmetabolism.substac…
Chapters.
0:00 — Superhuman Biology Is Already Starting.
2:40 — Beyond GLP-1: Fat Loss Without Muscle Loss.
7:28 — Gene Editing, CRISPR, and the Future of Disease Cure.
14:57 — Cellular Reprogramming and Biological Age Reset.
18:49 — MicroRNAs, Mitochondria, and What Comes Next.
Video Description.
Brain–machine interfaces (BMIs) are no longer just science fiction; they are the gateway to a future where thought itself can interact directly with technology. These systems read the brain’s electrical activity and, in turn, stimulate neurons — forming a two-way communication link between biology and machines.
In just a few decades, BMIs have evolved from laboratory curiosities into one of the fastest-growing frontiers in science and engineering. The possibilities are staggering. In the future, neural interfaces could restore vision to the blind, enable paralyzed individuals to move again, facilitate seamless communication between human brains and artificial intelligence, and ultimately power virtual realities that are indistinguishable from the physical world.
This convergence of biology, computing, and neuroscience marks the dawn of a new era — one where the boundaries between human and machine begin to blur.
Research from CCR scientists points toward a strategy for making chimeric antigen receptor (CAR) T-cell therapy, the cell-based immunotherapy that has revolutionized the treatment of some blood cancers, safer and more effective for treating solid tumors.
The study, led by Grégoire Altan-Bonnet, Ph.D., Deputy Chief of the Laboratory of Integrative Cancer Immunology, Naomi Taylor, M.D., Ph.D., Senior Investigator in the Pediatric Oncology Branch, and Paul François, Ph.D., at the University of Montréal, shows how adding certain receptors to CAR T cells can prevent the cells from attacking healthy tissue while simultaneously enhancing their activity against cancer cells. The findings appeared April 10, 2025, in Cell.
CAR T-cell therapy reprograms patients’ immune cells to be effective cancer killers using genetically engineered chimeric antigen receptors (CARs) that are added to their T cells. CARs are designed to recognize molecules on the surface of cancer cells called antigens, which can usually be found on some healthy cells, too. This leads to manageable side effects for patients with blood cancer, but when CAR T cells designed to target solid tumors attack healthy tissue, the effects can be severe.
A new Yale-led study provides one of the most detailed and comprehensive analyses to date of genetic variation in human populations in Oceania, filling a major gap in representation in genomics research. Despite harboring remarkable diversity, populations in this vast region in the South Pacific historically have been overlooked in global human genetic studies, which have often focused largely on people of European descent, researchers say. The study is published in the journal Science.
“The drastic underrepresentation of Oceanians limits our understanding of human evolution and could exacerbate health inequalities as genomic research is used to develop novel medical treatments,” said lead author Serena Tucci, assistant professor of anthropology in Yale’s Faculty of Arts and Sciences and principal investigator of the Yale Human Evolutionary Genomics Laboratory. “To fill that gap, my research team embarked on a large-scale project to expand what is known about human genetic variation, including genetic variants inherited from extinct hominins.”
The work shows how the genes that ancient humans acquired after mating with extinct hominins continue to shape the biology, health and survival of our species today.