Lifeboat Foundation

“Badass”. That was the word Harvard University neuroscientist Steve Ramirez used in a Tweet to describe research published online by fellow neuroscientist Ali Güler and colleagues in the journal Nature Neuroscience last March. Güler’s group, based at the University of Virginia in the US, reported having altered the behaviour of mice and other animals by using a magnetic field to remotely activate certain neurons in their brains. For Ramirez, the research was an exciting step forward in the emerging field of “magnetogenetics”, which aims to use genetic engineering to render specific regions of the brain sensitive to magnetism – in this case by joining proteins containing iron with others that control the flow of electric current through nerve-cell membranes.

By allowing neurons deep in the brain to be switched on and off quickly and accurately as well as non-invasively, Ramirez says that magnetogenetics could potentially be a boon for our basic understanding of behaviour and might also lead to new ways of treating anxiety and other psychological disorders. Indeed, biologist Kenneth Lohmann of the University of North Carolina in the US says that if the findings of Güler and co-workers are confirmed then magnetogenetics would constitute a “revolutionary new tool in neuroscience”

The word “if” here is important. In a paper posted on the arXiv preprint server in April last year and then published in a slightly revised form in the journal eLife last August, physicist-turned-neuroscientist Markus Meister of the California Institute of Technology laid out a series of what he describes as “back-of-the-envelope” calculations to check the physical basis for the claims made in the research. He did likewise for an earlier magnetogenetics paper published by another group in the US as well as for research by a group of scientists in China positing a solution to the decades-old problem of how animals use the Earth’s magnetic field to navigate – papers that were also published in Nature journals.

A study led by Umeå University, Sweden, presents new insights into how stem cells develop and transition into specialized cells. The discovery can provide increased understanding of how cells divide and grow uncontrollably so that cancer develops.

“The discovery opens a new track for future research into developing new and more effective treatments for certain cancers,” says Francesca Aguilo, associate professor at the Department of Molecular Biology at Umeå University and leader of the study in collaboration with various institutions including the University of Pavia, University of Texas Health Science Center at Houston, Universidad de Extremadura, and others.

All cells in the body arise from a single fertilized egg. From this single origin, various specialized cells with widely differing tasks evolve through a process called cellular differentiation. Although all cells share the same origin and share the same genetic information, specialized cells use the information in different ways to perform different functions. This process is regulated by genetic and epigenetic mechanisms.

Researchers tracked the health of nearly one thousand mice on a variety of diets to see if these diets would extend the mice’s lifespan. The study was designed to ensure that each mouse was genetically distinct, which allowed the team to better represent the genetic diversity of the human population. By doing so, the results are made more clinically relevant, elevating the study to one of the most significant investigations into aging and lifespan to date.

For nearly a century, laboratory studies have shown consistent results: eat less food, or eat less often, and an animal will live longer. But scientists have struggled to understand why these kinds of restrictive diets work to extend lifespan, and how to best implement them in humans. Now, in a long-awaited study to appear in the Oct. 9 issue of Nature, scientists at The Jackson Laboratory (JAX) and collaborators tracked the health of nearly one thousand mice on a variety of diets to make new inroads into these questions.

The study was designed to ensure that each mouse was genetically distinct, which allowed the team to better represent the genetic diversity of the human population. By doing so, the results are made more clinically relevant, elevating the study to one of the most significant investigations into aging and lifespan to date.

Imagine doctors being able to predict how a disease might progress in your body based on your genetic makeup, or which treatments would be most effective for you.

This research could bring us one step closer to that reality.

To sum it all up, this new research is shaking up how we think about evolution. Instead of seeing it as a series of random events, the study suggests there’s a level of predictability influenced by gene families and genetic history.

Bioengineers propose “electro-agriculture,” a method that replaces photosynthesis with a solar-powered reaction converting CO₂ into acetate, potentially reducing U.S. agricultural land needs by 94% and supporting controlled indoor farming.

Initial experiments focus on genetically modified acetate-consuming plants like tomatoes and lettuce, with potential future applications in space agriculture.

Revolutionary Electro-Agriculture

Potential therapies could include precise genetic targeting of the GLUT4 pathway or dietary modifications to fine-tune glucose levels, ensuring an optimal environment for neurogenesis.

Stanford research uncovers glucose’s role in boosting neurogenesis, offering insights into brain aging interventions.

Cirrhosis, hepatitis infection and other causes can trigger liver fibrosis—a potentially lethal stiffening of tissue that, once begun, is irreversible. For many patients, a liver transplant is their only hope. However, research at Cedars-Sinai in Los Angeles may offer patients a glimmer of hope. Scientists there say they’ve successfully reversed liver fibrosis in mice.

Reporting in the journal Nature Communications, the team say they’ve discovered a genetic pathway that, if blocked, might bring fibrosis to a halt.

The three genes involved in this fibrotic process are called FOXM1, MAT2A and MAT2B.

Discovery advances development of new therapeutic options for cancer and other diseases. A research team led by the University of California, Irvine has engineered an efficient new enzyme that can produce a synthetic genetic material called threose nucleic acid. The ability to synthesize artificial chains of TNA, which is inherently more stable than DNA, advances the discovery of potentially more powerful, precise therapeutic options to treat cancer and autoimmune, metabolic and infectious diseases.

A paper recently published in Nature Catalysis describes how the team created an enzyme called 10–92 that achieves faithful and fast TNA synthesis, overcoming key challenges in previous enzyme design strategies.

Inching ever closer to the capability of natural DNA synthesis, the 10–92 TNA polymerase facilitates the development of future TNA drugs.

CRISPR is a way off being using in human treatment – but a new discovery could unlock its potential. Here’s what’s new.