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Why we must stop talking about artificial general intelligence — and instead build ‘pro-worker’ AI
Briefing Chat: New narcolepsy drug could unlock host of novel brain therapies
Neurologist with MAHA ties to lead NIH’s child health institute
Appointment of John Gaitanis increases concern that scientific qualifications are no longer driving leadership picks
Deadly tick-borne virus gains ground in Europe as climate warms
Kosovo shows how surveillance can uncover hidden circulation—and help countries prepare before human cases appear
Scientists discover how gut bacteria “train” the intestine to fight inflammation
A compound made when gut bacteria break down dietary fiber may do more than briefly calm inflammation—it could leave a lasting protective “memory” in the gut. Northwestern Medicine researchers found that butyrate can reprogram intestinal lining cells so they continue encouraging anti-inflammatory immune responses even after the compound is gone. In mice, this effect boosted production of the immune-calming molecule IL-10 and reduced the severity of colitis-like disease.
Ozempic does something unexpected to the brain’s hunger neurons
Ozempic may work in the brain in almost the opposite way scientists expected, activating hunger-linked neurons that appear essential for sustaining fat loss. The surprising discovery in mice could reveal new targets for developing even more effective obesity drugs.
Footprints may reveal biggest known mammal from age of the dinosaurs
Beefy tracks point to a Cretaceous critter as big as a large dog or mountain lion
Knee osteoarthritis isn’t inevitable — here’s what you can do
Knee osteoarthritis can seriously affect mobility and quality of life, but its progression isn’t completely out of your control. Exercise, stronger leg muscles, a healthier diet, and even modest weight loss can dramatically reduce stress on the knees and help keep pain in check.
Schizophrenia’s lost brain connections follow a surprising pattern
Specialized brain scans reveal that schizophrenia is linked to widespread loss of the synapses that connect brain cells, with the left side of the brain hit especially hard. The damage follows a surprisingly organized pattern tied to the brain’s chemistry and wiring. Researchers also identified a left frontal region that may serve as a starting point for the loss.
Scientific spat erupts over claim that bones have key immune vessels
Discovery of lymphatic tubes suggested new possibilities for bone healing, but challenge has prompted dueling papers and publication delay in prominent journal
NASA abandons orbit-boosting rescue mission for space observatory
Novel rescue craft unable to connect with doomed Swift Observatory
The hallmarks of skeletal muscle health
Skeletal muscle is a central determinant of organismal health. Preserving muscle quality is therefore critical for preventing disease and sustaining quality of life across the lifespan. Despite its central role, the field lacks a unifying framework that defines the core properties of skeletal muscle health. Here, we propose a conceptual framework for muscle homeostasis built around seven interconnected hallmarks-metabolism and bioenergetics, proteostasis, genomics, excitability, structure,...
Inhibiting cyclin D1-CDK6 suppresses senescence-associated inflammatory gene expression and age-related functional decline
Cellular senescence contributes to aging and age-related diseases by driving chronic inflammation through the senescence-associated secretory phenotype (SASP), including interferon-stimulated genes (ISGs). Here we confirm and extend previous observations that cyclin D1 (CCND1), a key cell cycle regulator, is paradoxically upregulated across models of nonproliferating senescent cells. We show that CCND1 and its kinase partner CDK6 drive SASP and ISG expression in senescent cells by promoting DNA...
Turning CDK4/6 inhibitors against the dark side of senescence
No abstract
STINGing the brain: S-nitrosylation drives neuroinflammation in Alzheimer's disease
Neuroinflammation is a major secondary driver of Alzheimer's disease (AD). In this issue of Cell Chemical Biology, Carnevale et al.¹ demonstrate that S-nitrosylation of the cyclic GMP-AMP synthase (cGAS) stimulator of interferon genes (STING) pathway sustains pathological neuroinflammation in AD, identifying a promising therapeutic target for this devastating disease.
Risk of transmission of amyloid β pathology via transfused blood products
Seeded protein misfolding and aggregation are relevant to many neurodegenerative diseases. The archetype are prions: protein-only infectious agents that cause fatal neurodegenerative diseases including Creutzfeldt-Jakob disease (CJD). The recent recognition of iatrogenic amyloid β cerebral amyloid angiopathy (CAA) and Alzheimer's disease, caused by inadvertent seeding of amyloid β pathology following historical medical procedures, raises concerns that these conditions might also be transmitted...
Neurodegeneration as a dysregulation of neuroimmune crosstalk
Neurodegeneration is increasingly recognized not only as a disorder of neurons but also as a breakdown of dialogue between the nervous and immune systems. Recent discoveries reveal that immune cells and inflammatory signals are deeply interwoven with brain function across the lifespan. Far from passive responders, immune cells act as sentinels and shapers of neuronal resilience, vulnerability, and repair. Together, robust data support a model in which neurodegeneration emerges from complex...
Multimodal evidence for bone lymphatics in skeletal health and repair
Previous studies predominantly associated lymphatics with skeletal disease and bone loss. However, building on our work, bone lymphatics are emerging as a paradigm-shifting component of the skeletal microenvironment, illustrating their role as positive regulators of bone mass and repair. Here, we present a comprehensive analysis integrating spatial transcriptomics, single-cell RNA sequencing, and imaging across murine and human bones. Spatial transcriptomics identifies Prox1^(+) endothelial...
Making zombies to kill cancer
Genotoxic drugs induce apoptosis-resistant senescent "zombie" cells. In this issue of Cell Chemical Biology, Gallagher Aldave et al.¹ show that these cells acquire dependence on BCL-xL and MCL-1, creating a therapeutic vulnerability to their inhibitors and degraders.
Cell-type-specific damage scores reveal kidney and liver disease trajectories in single-cell and spatial transcriptomics
Degenerative diseases progress through gradual cell-intrinsic damage that is difficult to resolve with bulk transcriptomics or discrete cell-state analysis. We introduce a generalizable single-cell and spatial transcriptomics framework that quantifies continuous damage trajectories in vivo using cell-type-specific scores. Applied to chronic kidney disease and metabolic dysfunction-associated steatotic liver disease, the podocyte damage score (PDS) and hepatocyte damage score (HDS) place...