An agreement paves the way for hundreds of millions of dollars’ worth of projects to be transferred from the NIH’s institute for infectious diseases to the Department of Defense.
Study shows that the venerable device does not waft bacteria away from workbenches, as is often assumed.
The track and intensity of tropical cyclones can be predicted with high accuracy using an AI model, which has the potential to protect lives if shared responsibly worldwide.
Nature staff discuss the winners of the 2026 Ig Nobel prizes — plus, the isolated energy flash that could be the first glimpse of dark matter. Hear the biggest stories from the world of science | 04 September 2026
The awards highlight weird, funny and improbable research that also makes you think.
India, Peru and Vietnam are rolling out policies that limit opportunities for scientists who fall foul of research-integrity guidelines.
Study shows that psilocybin acts on nerves to prevent the painful condition called peripheral neuropathy.
Many forms of learning, for example, learning a model of the environment or a motor skill, rely on synaptic plasticity that is widely distributed across cell types and network stages. Understanding how this distributed plasticity functions is a central challenge in neuroscience1-5. Here we use connectomics to map the cell types and synaptic connections underlying a form of multi-layer continual learning that cancels predictable sensory responses in a cerebellum-like structure in electric fish6,7. Our analysis shows inhibitory and disinhibitory sensory input pathways that fulfil theoretical requirements for instructing synaptic plasticity8,9, structured synaptic connectivity between network stages that solves a credit assignment problem and structured recurrent connectivity that accelerates sensory prediction and cancellation. A computational model constrained by electrophysiological recordings shows how this synaptic connectivity ensures that multiple sites of plasticity cooperate to overcome their individual limitations, resulting in cancellation that is fast, accurate and robust to noise. Overall, these findings highlight the potential of connectomics, in combination with cell-type-specific physiological recordings and computational modelling, for deciphering learning in neural circuits.
The decarboxylative semi-pinacol rearrangement of β-hydroxy carboxylic acids under electrochemical oxidation conditions was first reported in 19601. However, its further development has remained limited owing to stepwise radical and carbocationic pathways that induce side reactions and result in the loss of stereochemical information at the α-carbon. Herein, we demonstrate that this transformation can instead be realized through a concerted mechanism under Pd(II)/Pd(IV) catalysis. The reaction proceeds via the formation of a six-membered Pd(IV) chelate, which undergoes fragmentation accompanied by β-to-α carbon migration and carbon dioxide extrusion, with Pd(IV) serving as the redox center. This closed-shell pathway enables precise stereochemical control: the migrating carbon retains its absolute configuration, while the α-stereocenter undergoes inversion. For unsymmetrical ketones, the reaction displays markedly higher migrating-group selectivity than the classical Tiffeneau–Demjanov2 and Büchner–Curtius–Schlotterbeck reactions3. Broadly applicable to cyclic and acyclic ketones and aldehydes, this method avoids hazardous diazo reagents. Its utility is illustrated by a concise total synthesis of (+)-rupestine D, where the rearrangement serves as a key carbon-skeleton-editing step.
Mice on GLP-1s also performed better on cognitive tasks than those on a calorie restricted diet . Plus, satellite images showed early warning signs of glacier collapse near the Nepal–Tibet border and the impact of people saying fewer words aloud.
Results from a small trial suggest a modified virus can instruct the immune system to wipe out disease-causing cells.
Results bolster hopes that the drug daraxonrasib could prove effective against a variety of tumours.
Researchers identify more than 1,200 personality-linked genetic variants, with effects largely independent of family background.
The causes of Nepal’s deadly flash flood, evidence that the shingles vaccine might cut the risk of heart disease, and the future of nuclear power.
Marvel at the month’s best science images. Plus, why timekeepers are rushing to get rid of the leap second and whether Meta’s legal settlement will make social media safer for kids.
Individual mammalian mRNAs and proteins are typically believed to originate from single genomic loci, with isoform diversity arising through cis-splicing of pre-mRNA. Whether mRNA from distant genes can undergo trans-splicing to generate functionally relevant chimeric transcripts has remained unclear. Here we develop a pipeline combining long-read direct RNA sequencing with non-targeted and targeted validation to identify chimeric transcripts in macrophages. Chromatin conformation capture studies reveal that inflammation induces interchromosomal DNA interactions, positioning parent genes proximally to facilitate the formation of chimeric mRNA. Notably, we identify a protein-coding chimeric mRNA representing a fusion between the pore-forming protein gasdermin D (GSDMD)1,2 and a C-terminal domain translated out of frame from Tmem106a (Gsdmd-Tmem106a) in mice. We show that inflammasome priming upregulates Gsdmd-Tmem106a, with the protein localizing to the plasma membrane. After activation of the inflammasome, GSDMD-TMEM106A directly interacts with canonical GSDMD N termini to accelerate and enhance pore formation and IL-1β release. Finally, we show that GSDMD-TMEM106A balances host defence and immunopathology in vivo: its loss protects against lethal sepsis but compromises antibacterial defence, whereas overexpression enhances host protection while increasing sepsis lethality. We establish that protein-coding chimeric mRNAs formed by regulated transcript fusion events are operative during inflammation and immunity.
Researchers are hunting for ways to enhance DNA repair with the hopes that this will keep people healthier for longer. Listen to an audio version of a recent Nature Feature.
El Niño events have been powering up since the Industrial Revolution. Plus, a visit to the Robot Olympics and an introduction to the Nancy Grace Roman Space Telescope.
Neurodegeneration is a major driver of disability in multiple sclerosis (MS), the most common chronic inflammatory disease of the central nervous system (CNS)1. Retinal ganglion cells (RGCs), a heterogeneous neuronal population in the eye, undergo degeneration in MS and provide a model to study neuronal subtype-specific resilience to inflammatory injury2. However, the neuron-intrinsic mechanisms underlying differential vulnerability remain unclear. Here we identify a neuroprotective role for intracellular complement factor H (CFH) in neurons. Using single-nucleus RNA-sequencing analysis of RGCs from donors with MS and control individuals, we found that CFH expression was strongly correlated with intrinsic resilience to RGC degeneration. Mechanistically, CFH was induced in retinal and other CNS neurons in response to inflammatory and oxidative stress, where it limited reactive oxygen species accumulation and lipid peroxidation. CFH localized to the endoplasmic reticulum, a major site of lipid peroxidation during neuronal ferroptosis. Its protective activity was dependent on its C-terminal SCR20 domain, was independent of CFH secretion and was preserved in the absence of complement component C3. These findings reveal a non-canonical intracellular function of CFH in neurons. Together, our results identify CFH as a key mediator of neuronal resilience across the CNS in mice and humans and provide mechanistic insight into inflammatory neurodegeneration with implications for MS therapy and neuroprotection more broadly.
