In a high-pressure lab experiment, scientists accidentally created a new compound called gold hydride. This particular hydride formed when thin gold foil met dense hydrogen at pressures hundreds of thousands of times Earth’s atmosphere and blazing temperatures.
The discovery challenges gold’s reputation as a nearly inert metal and shows how extreme conditions can push familiar materials into unfamiliar forms.
In late November, airlines around the world were told to urgently ground planes within their Airbus A320 fleets. Investigators had found that intense bursts of solar radiation could corrupt data inside a flight-control computer, potentially causing an aircraft to pitch unexpectedly. Pitch is the movement of the aircraft nose upward or downward.
Approximately 6,000 aircraft from the A320 family, about half of all A320s flying globally, needed immediate software changes before they could carry passengers again.
In Australia, Jetstar canceled around 90 flights and disrupted travel for more than 15,000 passengers, while engineers worked through the night to install the fix.
A tiny percentage of our DNA—around 2%—contains 20,000-odd genes. The remaining 98%—long known as the non-coding genome, or so-called ‘junk’ DNA—includes many of the “switches” that control when and how strongly genes are expressed.
Now researchers from UNSW Sydney have identified the DNA switches that help control how astrocytes work—these are brain cells that support neurons, and are known to play a role in Alzheimer’s disease.
In research published in Nature Neuroscience, researchers from UNSW’s School of Biotechnology & Biomolecular Sciences described how they tested nearly 1,000 potential switches—strings of DNA known as enhancers—in human astrocytes grown in the lab. Enhancers can be located very far away from the gene they control, sometimes hundreds of thousands of DNA letters away—making them difficult to study.
New York State Psychiatric Institute and Columbia University Medical Center investigators, with co-authors across additional US centers, report greater cognitive worsening at 78 weeks with valacyclovir than with placebo among adults with early symptomatic Alzheimer’s disease and herpes simplex virus (HSV) seropositivity.
Infectious diseases may contribute to Alzheimer’s disease pathogenesis. HSV-1 can become latent after oral infection, enter the brain via retrograde axonal transport, infiltrate the locus coeruleus, and migrate to the temporal lobe.
β-amyloid plaques and tau neurofibrillary tangles are neuropathological features of Alzheimer’s disease. Animal models connect HSV-1 infection of neuronal and glial cells with a decrease in amyloid precursor protein, an increase in intracellular amyloid β-protein, and phosphorylation of tau protein.
Renzi et al. identify creatine kinase B (CKB) as a metabolic sensor during white adipocyte differentiation. By modulating AKT, CKB fine-tunes insulin signaling and glycolysis to restrain ChREBP activation, thereby controlling de novo lipogenesis. This work links creatine metabolism to nutrient-responsive transcriptional regulation of lipid accumulation.
One specific state, referred to as State 4, emerged as a key point of difference between the two groups. This state was characterized by strong connections between the left and right hemispheres of the brain. It specifically involved robust communication between the temporal and parietal regions, which are areas often associated with language and sensory processing.
The data showed that children with autism spent considerably less time in State 4 compared to the typically developing children. They also transitioned into and out of this state less frequently. The reduced time spent in this high-connectivity state was statistically distinct.
The researchers then compared these brain patterns to clinical assessments of the children. They found a correlation between the brain data and the severity of autism symptoms. Children who spent the least amount of time in State 4 tended to have higher scores on standardized measures of autism severity.
Here, Qing Zhang & team show targeting kinesin family member KIF20A in vitro and in mice sensitizes stem-like TNBC cells to standard chemotherapy.
1Department of Pathology, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
2Department of Breast and Endocrine Surgery, Nagoya University Graduate School of Medicine, Nagoya, Aichi, Japan.
3Jinfeng Laboratory, Chongqing, China.
4Quantitative Biomedical Research Center, Peter O’Donnell Jr. School of Public Health, University of Texas Southwestern Medical Center, Dallas, Texas, USA.
Toledo, B., González-Titos, A., Hernández-Camarero, P. et al. Impact of pancreatic proenzymes on pancreatic ductal adenocarcinoma associated fibroblasts. Sci Rep 15, 43,750 (2025). https://doi.org/10.1038/s41598-025-24863-2
There has been significant discussion recently on the concept of the “virtual cell.” I want to summarize the key concepts regarding what the field wants from a virtual cell and the challenges we face. In particular, the current trajectory reminds me of the evolution of statistical genetics (GWAS) and Mendelian disorders—analogies that I believe point to the most likely path for the field’s development.
Until AlphaFold’s debut in November 2020, DeepMind had been best known for teaching an artificial intelligence to beat human champions at the ancient game of Go. Then it started playing something more serious, aiming its deep learning algorithms at one of the most difficult problems in modern science: protein folding. The result was AlphaFold2, a system capable of predicting the three-dimensional shape of proteins with atomic accuracy.
Its work culminated in the compilation of a database that now contains over 200 million predicted structures, essentially the entire known protein universe, and is used by nearly 3.5 million researchers in 190 countries around the world. The Nature article published in 2021 describing the algorithm has been cited 40,000 times to date. Last year, AlphaFold 3 arrived, extending the capabilities of artificial intelligence to DNA, RNA, and drugs. That transition is not without challenges—such as “structural hallucinations” in the disordered regions of proteins—but it marks a step toward the future.
To understand what the next five years holds for AlphaFold, WIRED spoke with Pushmeet Kohli, vice president of research at DeepMind and architect of its AI for Science division.