Toggle light / dark theme

Synthetic neuroscience grants promote transformative brain tech

The Wu Tsai Neurosciences Institute, Sarafan ChEM-H, and Stanford Bio-X have awarded $1.24 million in grants to five innovative, interdisciplinary, and collaborative research projects at the intersection of neuroscience and synthetic biology.

The emerging field of synthetic neuroscience aims to leverage the precision tools of synthetic biology — like gene editing, protein engineering, and the design of biological circuits — to manipulate and understand neural systems at unprecedented levels. By creating custom-made biological components and integrating them with neural networks, synthetic neuroscience offers new ways to explore brain function, develop novel therapies for neurological disorders, and even design biohybrid systems that could one day allow brains to interface seamlessly with technology.

“The ongoing revolution in synthetic biology is allowing us to create powerful new molecular tools for biological science and clinical translation,” said Kang Shen, Vincent V.C. Woo Director of the Wu Tsai Neurosciences Institute. “With these awards, we wanted to bring the Stanford neuroscience community together to capitalize on this pivotal moment, focusing the power of cutting-edge synthetic biology on advancing our understanding of the nervous system — and its potential to promote human health and wellbeing.”

Sons of mothers with type 1 diabetes show early signs of vascular dysfunction

“Our work shows that vascular function is affected before metabolic dysfunction appears, which challenges current assumptions,” the last author of the study.

The study found that the dysfunction is driven by oxidative stress in endothelial cells, a potential early sign of future cardiovascular disease. The findings could help clinicians better assess risk and focus on preventive measures.

“We observed that early intervention can restore vascular function in affected animals, pointing to new opportunities for disease prevention later in life,” adds the first author.


A new study i reveals that sons born to mothers with type 1 diabetes may develop early vascular dysfunction – independently of metabolic health. The finding, published in Cell Reports Medicine, may help shape future strategies to prevent cardiovascular disease early in life.

Children of women with type 1 diabetes are known to be at increased risk of developing cardiovascular diseases. This new study is, according to the researchers, the first to show that the risk is linked to early dysfunction in blood vessel cells in sons, even before any metabolic issues arise.

Researchers used a combination of animal models, Swedish and Danish health registries, and a small clinical study to explore the link. Results show a sex-specific effect: only sons displayed early vascular changes.

The ‘silent’ brain cells that shape our behaviour, memory and health

Researchers peered through microscopes, hooked up electrodes, and built entire careers around one cell type: neurons. These electrically active cells were clearly the brain’s protagonists, zipping signals through our heads at lightning speed to create thoughts, memories, and movements. Everything else—especially the star-shaped cells called astrocytes that outnumber neurons—was dismissed as mere scaffolding. Glial cells, they were called: “glue.”

Inbal Goshen, a memory researcher at Hebrew University of Jerusalem, remembers feeling like an outsider when she started investigating astrocytes in the early 2010s. “Oh, that’s the weird one who works on astrocytes,” she imagined colleagues whispering at conferences. The skepticism was palpable. Yet new molecular tools had finally given her a way to peek into these mysterious cells, and what she found was too intriguing to ignore.

Unlike neurons, astrocytes don’t fire electrical signals. They were “electrically silent,” which is why they’d been ignored. But they were whispering in another language entirely: calcium. Using advanced imaging, researchers discovered that astrocytes communicate through slow, rhythmic waves of calcium signals—more like a gentle tide than neuron’s lightning strike. And their reach is astonishing: a single human astrocyte can touch up to two million synapses, the junctions where neurons meet. Their bushy tendrils fill every crevice of the brain, each cell nestling against neurons and blood vessels, creating an intimate, three-way relationship.

Memory research revealed another layer. Goshen’s team watched astrocytes in mice navigating toward water rewards. As the animals approached familiar prize locations, astrocyte activity slowly ramped up—but showed no response in new environments. The cells were encoding spatial memories, not just supporting them. Other labs found that astrocytes help stabilize and recall fear memories, their slow calcium signals perfectly suited to bridge the gap between learning something and remembering it days later. As neuroscientist Jun Nagai describes it, “Think of them as the brain’s long-exposure camera: they capture the trace of meaningful events that might otherwise fade too fast.”


Astrocytes make up one-quarter of the brain, but researchers are only now realizing their true value.

Pegcetacoplan—the ‘closest thing to a cure’ for rare, severe kidney disease

A rare and life-threatening kidney disease in children finally has an effective therapy, thanks in large part to pioneering research and clinical leadership from University of Iowa Health Care Stead Family Children’s Hospital.

The disease, known as C3 glomerulopathy (C3G), is an ultra-rare condition that primarily affects children and young adults. Only around 5,000 Americans have C3G, which causes progressive kidney damage, with more than half of patients reaching end-stage kidney failure within a decade of diagnosis.

Unlike previous treatments for C3G that aimed to alleviate the damaging inflammatory process of the disease, the new, first-of-its-kind drug directly targets the root cause of C3G dysfunction in the body’s complement system, a part of the immune response.

Cracking the code of Parkinson’s: How supercomputers are pointing to new treatments

More than 1 million Americans live with tremors, slowed movement and speech changes caused by Parkinson’s disease—a degenerative and currently incurable condition, according to the Parkinson’s Foundation and the Mayo Clinic. Beyond the emotional toll on patients and families, the disease also exerts a heavy financial burden. In California alone, researchers estimate that Parkinson’s costs the state more than 6 billion dollars in health care expenses and lost productivity.

Scientists have long sought to understand the deeper brain mechanisms driving Parkinson’s symptoms. One long-standing puzzle involved an unusual surge of brain activity known as beta waves—electrical oscillations around 15 Hertz observed in patients’ motor control centers. Now, thanks to supercomputing resources provided by the U.S. National Science Foundation’s ACCESS program, researchers may have finally discovered what causes these waves to spike.

Using ACCESS allocations on the Expanse system at the San Diego Supercomputer Center—part of UC San Diego’s new School of Computing, Information, and Data Sciences—researchers with the Aligning Science Across Parkinson’s (ASAP) Collaborative Research Network modeled how specific brain cells malfunction in Parkinson’s disease. Their findings could pave the way for more targeted treatments.

Cancer-promoting DNA circles hitchhike on chromosomes to spread to daughter cells

Small, cancer-associated DNA circles “hitchhike” on chromosomes during cell division to spread efficiently to daughter cells by co-opting a process used to maintain cellular identity through generations, Stanford Medicine-led research has found.

These circles, known as extrachromosomal or ecDNA, are major drivers in human cancers. Blocking their ability to associate with chromosomes causes the loss of the circles during cell division and the death of lab-grown cancer cells. Targeting this weak link in the circles’ proliferation could lead to new classes of cancer therapies, the researchers predict.

“Unfortunately, ecDNAs have developed a crafty mechanism that allows them to wreak havoc on human health,” said professor of pathology Paul Mischel, MD. “They are using nature’s own method of gene expression and cell fate to ensure they are safely distributed into the next generation of cells and not lost into the cytoplasm or extracellular space when a cell divides.”

Hormone-disrupting chemicals from plastics shown to promote a chronic inflammatory skin condition

A Johns Hopkins Medicine study involving a dozen people with the inflammatory skin disease hidradenitis suppurativa (HS), which mostly affects skin folds, is believed to be the first to provide evidence that hormone-disrupting chemicals commonly found in ultra-processed food and single-use water bottles may contribute to the development of or worsen the condition in some people.

The new findings about the disorder build on previous reports about the role of endocrine-disrupting chemicals, a common environmental contaminant known to mimic, block or alter the body’s hormones, in human health. Researchers believe their findings suggest that reducing exposure could ease HS symptom severity and provide a new avenue of relief for a disease with limited FDA-approved treatment options that include biologic therapy and surgery.

The full report on the study was published in Nature Communications on Nov. 28 and includes insights into the molecular mechanisms that are involved in the disease.

How statins harm muscles—and how to stop it

Statins have transformed heart health, saving millions of lives by lowering cholesterol and reducing the risk of heart attacks and strokes. But for many patients, these drugs come with a troubling downside: muscle pain, weakness and, in rare cases, severe muscle breakdown that can lead to kidney failure.

University of British Columbia researchers and their collaborators at the University of Wisconsin-Madison have now pinpointed the cause. Their findings, published last week in Nature Communications, could pave the way for a new generation of statins without these side effects.

FLASH-AWAY: Intrabody-Directed Targeting of Optogenetic Tools for Protein DegradationClick to copy article linkArticle link copied!

Protein homeostasis, or proteostasis, is essential for cellular proteins to function properly. The buildup of abnormal proteins (such as damaged, misfolded, or aggregated proteins) is associated with many diseases, including cancer. Therefore, maintaining proteostasis is critical for cellular health. Currently, genetic methods for modulating proteostasis, such as RNA interference and CRISPR knockout, lack spatial and temporal precision. They are also not suitable for depleting already-synthesized proteins. Similarly, molecular tools like PROTACs and molecular glue face challenges in drug design and discovery. To directly control targeted protein degradation within cells, we introduce an intrabody-based optogenetic toolbox named Flash-Away integrates the light-responsive ubiquitination activity of the RING domain of TRIM21 for protein degradation, coupled with specific intrabodies for precise targeting. Upon exposure to blue light, Flash-Away enables rapid and targeted degradation of selected proteins. This versatility is demonstrated through successful application to diverse protein targets, including actin, MLKL, and ALFA-tag fused proteins. This innovative light-inducible protein degradation system offers a powerful approach to investigate the functions of specific proteins within physiological contexts. Moreover, Flash-Away presents potential opportunities for clinical translational research and precise medical interventions, advancing the prospects of precision medicine.

/* */