Things Worth Knowing About

Researchers in Germany took young blood cells from an 80-year-old donor and converted them directly into stem cells that make brain cells. This happened only in a laboratory dish, not inside a person.

The chemical marks that show how old a cell is were reset during the change. Cells that started at age 80 ended up acting like they were under 20. The process unfolded slowly over about 50 days, which lets scientists watch how cells get younger step by step.

Age is the biggest risk for brain diseases like Alzheimer's, so this could help researchers study ways to keep brain cells young. Earlier tests in mice showed similar cells can connect with existing brain cells, but that has not been tried in people yet.

A NASA-supported team took the plastic used in water bottles, broke it into tiny pieces, and fed those pieces to specially designed yeast. The yeast turned the pieces into proteins, fats and other nutrients.

Just as a cow turns grass into milk without grass remaining in the milk, the plastic itself does not end up in the cookie. The researchers added sweetener, fiber and starch to the yeast's output and baked a protein-rich cookie.

This was done only in the laboratory. The method could let astronauts make food from waste on long space trips or help people after disasters on Earth. It is still early and not yet ready as everyday food.

Lab researchers found two everyday chemicals that turn ordinary skin cells into muscle-repair cells in just 10 days. These cells can keep making copies of themselves and become any kind of muscle cell the body needs.

They tested the cells in mice with torn muscles. Some mice were young, some were old, and some had a gene change like a human muscle-wasting disease. Four weeks after the cells were placed in the damaged muscle, the mice moved better and their muscles worked stronger.

A second method skipped growing cells in a dish. Tiny dissolving particles carried the chemicals straight into the injured muscle and woke up the mouse’s own repair cells. That also worked, even in old mice. Everything was done in mice, not people.

Spinal cord injuries destroy the nerve cells that carry signals between brain and body, and the resulting scar from support cells called astrocytes often blocks any chance of repair. Researchers built a two-part genetic system called TRANsCre-DIONE that activates only in the reactive scar astrocytes at the injury site, flipping on a gene that reprograms them into motor neurons capable of sending electrical signals.

Two weeks after injury, treated mice showed 87 percent of the targeted cells becoming neurons that fired impulses and connected with existing circuits. Eight weeks later those animals scored an average 3.88 on a nine-point walking scale versus less than 1 for untreated controls; temporarily silencing the new neurons erased the gains, proving they were driving recovery. The same conversion improved movement in rats and showed early signs of working in monkey brain tissue.

Because the method uses cells already present in the tissue, it skips the need for transplants. Scientists believe it could one day help people with spinal injuries, ALS or stroke rebuild circuits from the inside, though safety and long-term effects still need years of study before human trials.

In a small first-in-human trial, 15 people with stubborn, medication-resistant high cholesterol and triglycerides received a single infusion of an experimental CRISPR-Cas9 therapy called CTX310. The treatment travels to the liver and permanently switches off a gene called ANGPTL3, which normally keeps cholesterol and triglycerides elevated. People born with a naturally inactive version of this gene tend to have low lifelong cholesterol without health problems, which is what inspired the approach.

A year after the single infusion, patients on the highest dose still had LDL ("bad") cholesterol down about 52.5% and triglycerides down about 47.8% from baseline, with no serious safety issues related to the therapy. It's very early, small-scale research, but it hints at a future where one treatment could replace a lifetime of daily pills.

A UCLA-led team discovered that a mix of forskolin (from a plant root) and the molecule RepSox efficiently produces genuine, self-renewing muscle stem cells from dermal cells in only 10 days instead of months. These cells were transplanted into injured muscles of adult mice, 18-month-old mice, and mice with a genetic mutation similar to Duchenne muscular dystrophy.

Four weeks later the transplanted cells had integrated into the damaged tissue and significantly improved muscle function in every group. In a second approach, the same cocktail was loaded into tiny biodegradable nanoparticles and injected directly into injured muscle, where it activated the animal’s own quiescent stem cells and triggered robust repair without any lab-grown cells.

Remarkably, this in-body method still worked in elderly mice whose natural stem-cell environment had deteriorated, suggesting a possible one-time treatment for age-related muscle loss, traumatic injury, or certain muscular dystrophies.

UCLA scientists created a “mathematical microscope” that reduced the brain’s billions of neurons to a simple two-neuron model and then tested it against real electrical recordings from sleeping or anesthetized animals. They discovered that neurons in the entorhinal cortex (the memory hub where Alzheimer’s first appears) can enter a state of spontaneous persistent inactivity — remembering recent information by doing nothing at all.

This “do-nothing” memory costs virtually zero energy, unlike the classic persistent-firing method that burns a lot of fuel. Combining both states more than doubles working-memory capacity while cutting metabolic cost in half. The same efficient mechanism operates during sleep, when the neocortex sends oscillating waves to the entorhinal cortex.

Because metabolic failure is a hallmark of Alzheimer’s, mild cognitive impairment and other memory disorders, the finding offers a new window into early diagnosis and possible therapies that restore this low-energy memory mode.

The JADES team announced two record-breaking galaxies, JADES-GS-z14-0 and JADES-GS-z14-1, whose light has traveled more than 13.5 billion years to reach us. The more distant one existed only 300 million years after the Big Bang and is surprisingly large and bright, meaning it was already assembling huge numbers of young stars far earlier than most models predicted.

Because the universe’s expansion has stretched their ultraviolet light all the way into the infrared, only Webb’s sensitive instruments could detect them. The size of JADES-GS-z14-0 proves most of its light comes from stars rather than a central black hole, challenging ideas about how quickly the first galaxies grew.

These discoveries give scientists a direct look at the first billion years of cosmic history and will help refine theories of galaxy formation in the infant universe.

An international team including Nobel laureate Roger Penrose cooled rubidium atoms to near absolute zero and used a custom atom chip to put each atom into a quantum superposition of two paths. Magnetic fields held one path stationary while the other followed a free-fall trajectory, exactly as a dropped ball would.

When the two waves were reunited they interfered, revealing a tiny quantum-phase difference that matched the prediction of Einstein’s equivalence principle applied to a quantum object — the first direct observation of this effect. The experiment does not yet unify quantum mechanics and general relativity, but it shows Einstein’s rule still holds in the quantum realm.

The technique paves the way for similar tests with much heavier objects such as nanodiamonds, which could eventually reveal where the two great theories of physics begin to disagree.

All known life uses the four-letter DNA alphabet A, T, C and G. UC San Diego researchers showed that E. coli’s RNA polymerase — the enzyme that transcribes DNA into RNA — can faithfully read a synthetic eight-letter “hachimoji” system that adds the extra letters P, Z, B and S.

Atomic-resolution cryo-electron microscopy revealed the enzyme recognizes the unnatural base pairs using the same chemical and structural signals it uses for natural letters, although transcription of one pair was about twice as slow. The work was done in test tubes, not living cells, but it demonstrates that existing cellular machinery can process genetic information evolution never produced.

This is a crucial step toward synthetic organisms whose expanded DNA could store far more information or produce entirely new proteins, potentially transforming biotechnology and our understanding of life’s chemical possibilities.

A randomized controlled trial found that combining vitamin D3 with the omega-3 fatty acid DHA (from fish oil) was significantly more effective at slowing mild cognitive impairment than either nutrient taken separately. Participants receiving the pair showed greater gains on memory and thinking tests, suggesting the two nutrients work together to protect brain cells and reduce inflammation.

The study adds to growing evidence that targeted nutritional combinations can be more powerful than single supplements for brain health. Because both vitamin D and DHA are inexpensive, widely available and already recommended for other health reasons, the finding points to a practical, low-risk strategy that could help delay the progression toward dementia.

Larger and longer trials are still needed, but the results offer hope that simple dietary additions might buy extra years of clearer thinking for millions of older adults.