New research from King’s College London and the University of Porto has mapped the histamine system in the brain. Histamine, a molecule more commonly associated with allergies, plays a separate but poorly understood role in brain function. This study addresses this gap, building the first multiscale map of the histamine system that spans from genetics to behavior and related mental health conditions.
The findings provide a new framework for understanding how this often-overlooked chemical system contributes to brain function and could point toward new treatment strategies for histamine-related conditions such as depression, ADHD, and schizophrenia. The study is published in Nature Mental Health.
Histamine is a neurotransmitter, a molecule crucial for neurons to communicate with one another. Neuroscience research has classically focused on understanding other neurotransmitter systems such as dopamine and serotonin.
Gene editing can repair a DNA error in mice that causes Dravet syndrome, a rare, incurable, and potentially deadly form of childhood epilepsy. After the edit, the mice have far fewer seizures and live much longer. As published in Science Translational Medicine, the results suggest that a one-time genetic correction could someday treat the root cause of the disease rather than just managing its symptoms. The work represents a major step for genetic medicine, as restoring disease-relevant brain function with gene editing tools remains a major challenge.
The study also reflects growing momentum behind gene editing as a therapeutic platform for rare diseases. In February 2026, the Food and Drug Administration issued its Plausible Mechanism Framework guidance, outlining a regulatory pathway for individualized therapies targeting specific genetic conditions. It recognizes that for rare genetic diseases, a well-characterized biological mechanism can serve as the foundation for approval where large clinical trials are not feasible.
“For families affected by Dravet syndrome, our study provides proof of concept that a genetic correction approach could have real impact, a future with treatments that don’t just manage the disease but actually address its cause,” said Matthew Simon, a senior study director at The Jackson Laboratory (JAX) Rare Disease Translational Center (RDTC) who co-led the study. “We’re at an inflection point in genetic medicine, where we can now actually repair the DNA itself.”
Researchers at the University of Rochester showed that one of those biological advantages can be moved into another mammal. By transferring a gene linked to the naked mole rat’s unusually high levels of high molecular weight hyaluronic acid (HMW-HA), the team improved health and modestly extended lifespan in mice.
The work, published in Nature in 2023, suggested that at least some longevity traits that evolved in long-lived animals may be adaptable beyond the species that developed them. The genetically modified mice lived healthier lives and had an approximate 4.4 percent increase in median lifespan compared with ordinary mice.
“Our study provides a proof of principle that unique longevity mechanisms that evolved in long-lived mammalian species can be exported to improve the lifespans of other mammals,” says Vera Gorbunova, the Doris Johns Cherry Professor of biology and medicine at Rochester.
Biermeier et al. use live imaging in zebrafish to show that microglia alternate between distinct morphological states that support brain surveillance and phagocytosis. By optogenetically controlling cytoskeletal contractility, they demonstrate programmable, reversible control of microglial behavior in the living brain.
Engineered microorganisms are widely used in industrial biotechnology and biopharmaceutical applications, including the production of biofuels, sustainable chemicals, and therapeutic compounds. However, concerns remain regarding the unintended environmental release and uncontrolled proliferation of genetically engineered microbes. For this reason, biocontainment technologies, which are designed to prevent microorganisms from surviving outside controlled environments, have become increasingly important in both academia and industry.
Conventional biocontainment strategies have relied on auxotrophy-based approaches, toxin–antitoxin systems, or DNA cleavage-based technologies such as CRISPR-Cas9. However, these methods often suffer from environmental dependency, genetic instability, and the risk of unintended mutations and cellular stress caused by DNA double-strand breaks.
In particular, DNA cleavage-based systems may compromise genomic stability and allow certain mutant cells to escape survival control. In addition, CRISPR interference (CRISPRi)-based systems are inherently reversible, posing challenges for achieving complete and permanent control of cell viability.
In a recently published review, researchers led by Prof. Wu Qingfeng at the Institute of Genetics and Developmental Biology of the Chinese Academy of Sciences explored the ongoing process of neural cell competition (NCC), a fundamental mechanism that shapes the brain across the lifespan.
The review is published in National Science Review, and provides fresh insights into how brain cells continuously “compete” for survival and how this competition impacts brain development, wiring, function, and aging.
Although neural cell competition is widely recognized for its role during early brain development, Prof. Wu’s team demonstrated that this process continues to be vital throughout life. They revealed that NCC not only helps maintain healthy brain function but also contributes to age-related cognitive decline when disrupted.
Cas12a2 enzyme is programmed to identify specific RNA sequences rather than DNA. Upon successful recognition and binding to its target RNA, the protein undergoes a conformational change that unleashes indiscriminate collateral cleavage of intracellular DNA, effectively shredding the genetic material and inducing rapid cell death. In preclinical in vitro and in vivo models, a single administration of this targeted Cas12a2 system suppressed the proliferation of KRAS-mutated cancer cells by 50% and eliminated human papillomavirus (HPV)-infected cells with an efficacy exceeding 90%. Crucially, the intervention demonstrated high specificity, displaying no significant off-target cytotoxicity or damage to healthy tissue. This RNA-triggered DNA-shredding mechanism provides a highly adaptable and potent platform for oncology and virology, shifting the CRISPR paradigm from localized genetic correction to the targeted apoptosis of diseased cells, with future applications potentially expanding to target HIV and other robust infections.
Kadin Crosby, Ryan Jackson and colleagues report newly discovered details demonstrating how CRISPR Cas12a2 can be repurposed to discriminately kill cancer cells in the petri dish and in mice.
Autoimmune diseases, where the body’s own immune system mistakenly goes on the attack, are much more common in women – and a new study analyzing more than 1.25 million blood cells goes a long way to explaining why.
The analysis, led by a team from the Garvan Institute of Medical Research in Australia, revealed over 1,000 genetic ‘switches’ in immune cells that work differently depending on sex.
In short, these variations in gene activity mean that inflammatory pathways that respond to threats are likely to be busier in women, leading to a greater risk of conditions like lupus and multiple sclerosis.
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Imagine a civilization reaches something like a Type II level, advanced enough to move through interstellar space and keep large populations alive for generations. At that stage, the challenge is developing ships that can cross the void, and also making sure the people inside them can survive radiation, isolation, and extreme travel times. That could mean heavy genetic engineering before the journey begins, changing bone density, metabolism, resistance to disease, tolerance for low gravity, or even sensory systems and respiration. But when they finally arrive, they may still find that the planet is wrong for them, maybe the air is toxic, the gravity is crushing, the temperatures are extreme, or the native chemistry is incompatible with human biology.
At that point, they face two paths. One is terraforming, which means trying to remake an entire planet into something closer to Earth. That could involve thickening or thinning an atmosphere, warming a frozen world, cooling a hot one, importing water, altering soil chemistry, introducing engineered microbes, building orbital mirrors or shades, and managing the planet for centuries or even millennia. The scale of that project is absurdly expensive, not just in money but in energy, infrastructure, labor, time, and raw materials. You are not changing a city or even a continent, you are trying to rewrite a whole world.
The other option is pantropy. Instead of forcing the planet to become Earth-like, the colonists change themselves to fit the planet. They might alter their lungs to breathe a different atmospheric mix, redesign their skin to handle harsher radiation, reduce their size for lower resource use, strengthen their bodies for higher gravity, or even become something so biologically different that they no longer look fully human. That is the core idea of pantropy, adapting the colonists to the world rather than adapting the world to the colonists.
The term was coined by James Blish, and he used it in connection with the stories collected in The Seedling Stars, especially “Surface Tension.” which was first published in 1952 in Galaxy Science Fiction.
