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Elon Musk Holds Surprise Talk At The World Economic Forum In Davos

The musk blueprint: navigating the supersonic tsunami to hyperabundance when exponential curves multiply: understanding the triple acceleration.

On January 22, 2026, Elon Musk sat down with BlackRock CEO Larry Fink at the World Economic Forum in Davos and delivered what may be the most important articulation of humanity’s near-term trajectory since the invention of the internet.

Not because Musk said anything fundamentally new—his companies have been demonstrating this reality for years—but because he connected the dots in a way that makes the path to hyperabundance undeniable.

[Watch Elon Musk’s full WEF interview]

This is not visionary speculation.

This is engineering analysis from someone building the physical infrastructure of abundance in real-time.

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Neutrophil extracellular trapping network-associated biomarkers in liver fibrosis: machine learning and experimental validation

The diagnostic and therapeutic potential of neutrophil extracellular traps (NETs) in liver fibrosis (LF) has not been fully explored. We aim to screen and verify NETs-related liver fibrosis biomarkers through machine learning.

In order to obtain NETs-related differentially expressed genes (NETs-DEGs), differential analysis and WGCNA analysis were performed on the GEO dataset (GSE84044, GSE49541) and the NETs dataset. Enrichment analysis and protein interaction analysis were used to reveal the candidate genes and potential mechanisms of NETs-related liver fibrosis. Biomarkers were screened using SVM-RFE and Boruta machine learning algorithms, followed by immune infiltration analysis. A multi-stage model of fibrosis in mice was constructed, and neutrophil infiltration, NETs accumulation and NETs-related biomarkers were characterized by immunohistochemistry, immunofluorescence, flow cytometry and qPCR. Finally, the molecular regulatory network and potential drugs of biomarkers were predicted.

A total of 166 NETs-DEGs were identified. Through enrichment analysis, these genes were mainly enriched in chemokine signaling pathway and cytokine-cytokine receptor interaction pathway. Machine learning screened CCL2 as a NETs-related liver fibrosis biomarker, involved in ribosome-related processes, cell cycle regulation and allograft rejection pathways. Immune infiltration analysis showed that there were significant differences in 22 immune cell subtypes between fibrotic samples and healthy samples, including neutrophils mainly related to NETs production. The results of in vivo experiments showed that neutrophil infiltration, NETs accumulation and CCL2 level were up-regulated during fibrosis. A total of 5 miRNAs, 2 lncRNAs, 20 function-related genes and 6 potential drugs were identified based on CCL2.

Peripheral cancer attenuates amyloid pathology in Alzheimer’s disease via cystatin-c activation of TREM2

Now online! Peripheral cancer inhibits amyloid pathology and rescues cognition of Alzheimer’s disease through secretion of cystatin-c (Cyst-C), which binds amyloid oligomers and activates TREM2 in microglia and enables microglia to degrade pre-existing plaques.

Can Aging Be Measured—and Eventually Reversed?

A former professor at the University of California, Los Angeles, Horvath is now principal investigator of the U.K. research arm of Altos Labs, a longevity biotech company that says it is developing therapies that could reverse age-related diseases and disabilities.

Having precise and meaningful ways to measure aging could make it possible for drug developers like Altos Labs to test longevity treatments in people, Horvath says: “It’s a quintessential tool to find interventions for rejuvenation.”

As part of TIME’s series interviewing longevity leaders and influencers, we spoke to Horvath about his pioneering invention and what he thinks might be possible for human life extension.

Scientists May Have Discovered a Way to Rejuvenate The Immune System

As we age, the immune system gradually declines in function, leaving the body more vulnerable to disease. Scientists have discovered a new way to rejuvenate a key component of immune function, potentially boosting health in later years.

A team from the Broad Institute of MIT and Harvard focused on the thymus, a small organ in front of the heart that’s crucial for the development of T cells. These immune cells act as guards, identifying and fighting threats such as cancer and infections.

From early adulthood, the thymus shrinks and slows, limiting T cell production. In mouse models, the researchers were able to repurpose part of the liver as a thymus substitute, sending the molecular signals that stimulate T-cell production.

Using lab-grown lung tumors as test subjects for tailored cancer therapies

Lung cancer varies widely from patient to patient, and that diversity makes it hard to find effective treatments. Researchers at the Berlin Institute of Health at Charité (BIH) have developed a method to evaluate multiple therapeutic approaches on patient-derived “tumoroids”—miniature tumors grown from tissue removed during surgery at Charité

By testing drug responses across these tumoroids, the team showed that therapeutic success depends on a complex interplay of tumor characteristics rather than a single factor. Their results suggest that tumoroid-based testing could help physicians tailor treatments to individual patients and improve clinical decision-making.

The BIH researchers have published their findings in Nature Biomedical Engineering.

A novel mechanism for cancer-associated weight loss

Combined metabolomics and transcriptomics analysis in eight different organs of tumor-bearing mice with and without cachexia allowed researchers to create metabolic signatures typical of cancer-associated weight loss. High-throughput analyses identified a cachexia-specific metabolic and genetic signature that provides insight into the progression of these metabolic changes.

The researchers found that all organs showed increased activation of the so-called “one carbon cycle”, a biochemical process essential for the synthesis of nucleotides, amino acids, and cell regeneration. Products of this cycle, such as sarcosine or dimethylglycine, could potentially serve as biomarkers for cachexia in the future.

The study also revealed that hyperactivation of the one carbon cycle in muscle is associated with increased glucose metabolism (glucose hypermetabolism) and muscle atrophy. Early experiments suggest that inhibiting this process could prevent muscle loss. Comparative analyses across eight different mouse tumor models (lung, colon, and pancreatic cancer) confirmed that the one carbon signature represents a universal cachexia signature, independent of cancer type.

Currently, there is no approved drug for cancer cachexia in Germany. New approaches are being explored to address cancer-related appetite loss. This study provides the first evidence of how metabolism itself could potentially be normalized. Early experiments in cell cultures show that interventions targeting the one carbon cycle can have positive effects. sciencenewshighlights ScienceMission.

Cachexia is a metabolic disorder that causes uncontrolled weight loss and muscle wasting in chronic diseases and cancer. A new study shows that cachexia affects more than just muscles. Numerous organs respond in a coordinated manner, ultimately contributing to muscle loss. Analysis of metabolome and transcriptome data, along with glucose tracing in tumor-bearing mouse models, identified a novel mechanism that plays a key role in cancer-associated weight loss.

A loss of 10% of body weight within six months – what may sound desirable in some contexts – often causes uncertainty and frustration in cancer patients with cachexia, as they are unable to maintain or gain body weight despite wanting to. Cachexia (from the Greek kakós, “bad,” and héxis, “condition”) affects 50–80% of all cancer patients, reduces quality of life, diminishes the effectiveness of cancer therapies, and increases mortality.

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Wood burning in homes drives dangerous air pollution in winter, study finds

Throwing another log into a crackling fireplace on a cold winter’s night might seem like a cozy, harmless tradition. But Northwestern University scientists have found residential wood burning is a major—yet often overlooked—contributor to winter air pollution across the United States.

Although only 2% of U.S. homes rely on wood as their primary heating source, residential wood burning accounts for more than one-fifth of Americans’ wintertime exposure to outdoor fine particulate matter (PM2.5), the new study found.

These tiny airborne particles can penetrate deep into the lungs and enter the bloodstream, where they are linked to increased risks of heart disease, lung disease and even premature death. Among their findings, the scientists calculated that pollution from residential wood burning is associated with about 8,600 premature deaths per year.

The human advantage: Stronger brains in the age of AI

Stronger brains strengthen resilience, productivity, and shared prosperity. It is time to invest accordingly.

The brain is the body’s most complex and vital organ, regulating everything from basic life functions to complex decision-making. It is also the foundation of how people live, work, and connect, making it central to individual well-being, high-performing organizations, and resilient economies. Despite rapid technological advances, nothing yet replicates the brain’s capacity to contribute to society.

AI will reshape work, and competitiveness will hinge on combining human and machine strengths. Countries and companies must evolve their strategies to enable collaboration and harness the complementary strengths of human intelligence and technology, or risk slower growth and being left behind in the next era of the global economy. And while the stakes are high if we fail to invest in the health of our brains and the skills that make us uniquely human, the potential gains—individually, socially, and economically—are even greater if we choose to do so.

In this report, brain health is defined as a state of optimal brain functioning, supported by the promotion of healthy brain development and the prevention or treatment of mental, neurological, and substance use disorders in people of all ages. But health alone is not enough. Brain skills—the foundational cognitive, interpersonal, self-leadership, and technological literacy abilities that enable people to adapt, relate, and contribute meaningfully—are equally critical to societal progress. Together, these form what is called brain capital.

Underinvestment in the brain has a substantial cost. The global disease burden of brain health conditions is rising, driven by an aging population, increased stressors, and elevated uncertainty about the future. When societies overlook the brain’s central role in health and productivity, the impact is felt in disrupted lives, lost potential, and a heavy toll on families and caregivers. Scaling cost-effective interventions to prevent, treat, and help people recover from brain health conditions could avert 267 million disability-adjusted life years (DALYs) globally by 2050, generating up to $6.2 trillion in cumulative GDP gains.1 Investing early can create even greater returns—quality early-childhood programs have demonstrated annual returns of 7 to 13 percent and delivered benefit-to-cost ratios of up to nine to one in low-and middle-income countries.

In this report by the McKinsey Health Institute, in collaboration with the World Economic Forum, the authors make the case for investing in the brain, introduce five levers for action, and offer a road map for next steps. While specific actions may vary by stakeholder, region, or sector, there is a need for a shared aspiration and framework for change. This report aims to fill that gap.

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