Studies by a growing number of labs have identified neurological health benefits from exposing human volunteers or animal models to light, sound and/or tactile stimulation at the brain’s “gamma” frequency rhythm of 40Hz. In the latest such research at The Picower Institute for Learning and Memory and Alana Down Syndrome Center at MIT, scientists found that 40Hz sensory stimulation improved cognition and circuit connectivity and encouraged the growth of new neurons in mice genetically engineered to model Down syndrome.
Li-Huei Tsai, Picower Professor at MIT and senior author of the new study in PLOS ONE, said that the results are encouraging but also cautioned that much more work is needed to test whether the method, called GENUS (for Gamma Entrainment Using Sensory Stimulation), could provide clinical benefits for people with Down syndrome. Her lab has begun a small study with human volunteers at MIT.
“While this work, for the first time, shows the beneficial effects of GENUS on Down syndrome using an imperfect mouse model, we need to be cautious as there is not yet data showing whether this also works in humans,” said Tsai, who directs The Picower Institute and The Alana Center, and is a member of MIT’s Brain and Cognitive Sciences faculty.
Karolinska Institutet researchers report that children born before 34 weeks of gestation show persistent deficits in cognitive abilities at ages 9 to 10. Impairments appear independent of socioeconomic status, genetic predisposition, and prenatal or child-specific risk factors. Lower scores were observed in vocabulary, working memory, episodic memory, and recall tasks. Children born late preterm (34–36 weeks) or early term (37–38 weeks) performed comparably to those born full term.
Preterm birth affects approximately 13 million infants worldwide each year and remains a leading cause of childhood morbidity and mortality. Although advances in perinatal care have increased survival, cognitive deficits in these children continue to present major public health concerns.
Critical brain development processes that occur between 24 and 40 weeks of gestation may be disrupted by premature birth. Prior research has mostly focused on extremely or very preterm infants, often overlooking those born moderately or late preterm, who constitute a large portion of preterm births.
Cancer creates an immunosuppressive environment that hampers immune responses, allowing tumors to grow and resist therapy. One way the immune system fights back is by inducing ferroptosis, a type of cell death, in tumor cells through CD8 + T cells. This involves lipid peroxidation and enzymes like lysophosphatidylcholine acyltransferase 3 (Lpcat3), which makes cells more prone to ferroptosis. However, the mechanisms by which cancer cells avoid immunotherapy-mediated ferroptosis are unclear. Our study reveals how cancer cells evade ferroptosis and anti-tumor immunity through the upregulation of fatty acid-binding protein 7 (Fabp7).
To explore how cancer cells resist immune cell-mediated ferroptosis, we used a comprehensive range of techniques. We worked with cell lines including PD1-sensitive, PD1-resistant, B16F10, and QPP7 glioblastoma cells, and conducted in vivo studies in syngeneic 129 Sv/Ev, C57BL/6, and conditional knockout mice with Rora deletion specifically in CD8+ T cells, Cd8 cre; Rorafl mice. Methods included mass spectrometry-based lipidomics, targeted lipidomics, Oil Red O staining, Seahorse analysis, quantitative PCR, immunohistochemistry, PPARγ transcription factor assays, ChIP-seq, untargeted lipidomic analysis, ROS assay, ex vivo co-culture of CD8+ T cells with cancer cells, ATAC-seq, RNA-seq, Western blotting, co-immunoprecipitation assay, flow cytometry and Imaging Mass Cytometry.
PD1-resistant tumors upregulate Fabp7, driving protective metabolic changes that shield cells from ferroptosis and evade anti-tumor immunity. Fabp7 decreases the transcription of ferroptosis-inducing genes like Lpcat3 and increases the transcription of ferroptosis-protective genes such as Bmal1 through epigenetic reprogramming. Lipidomic profiling revealed that Fabp7 increases triglycerides and monounsaturated fatty acids (MUFAs), which impede lipid peroxidation and ROS generation. Fabp7 also improves mitochondrial function and fatty acid oxidation (FAO), enhancing cancer cell survival. Furthermore, cancer cells increase Fabp7 expression in CD8+ T cells, disrupting circadian clock gene expression and triggering apoptosis through p53 stabilization. Clinical trial data revealed that higher FABP7 expression correlates with poorer overall survival and progression-free survival in patients undergoing immunotherapy.
The first genetically engineered synapses have been implanted in a mammal’s brain. Chemical brain signals have been bypassed in the brains of mice and replaced with electrical signals, changing their behaviour in incredible ways. Not only did they become more sociable, they were also less anxious and exhibited fewer OCD-like symptoms. This work has sparked hope that one day we could use this technology to help humans with mental health conditions. But would you want someone making permanent edits to your brain?
For the first time, climate scientists can now link specific fossil fuel companies to climate-related economic damages in particular places. A new method has been developed that can show the exact impact these companies are having on our environment — which the world’s top five emitters linked to trillions of dollars of economic losses. Find out how scientists have managed to piece this together — and whether these companies are about to face massive lawsuits.
As we reflect on the death of Pope Francis, we explore his legacy on scientific issues and his transformative stance on climate change. As the spiritual leader of 1.4 billion Catholics, he became an influential figure in advocating for better care to be taken of our planet. Will his legacy continue with the next Pope?
Chapters: 00:00 Intro. 00:28 First brain engineering in a mammal. 10:57 Landmark in fossil fuel lawsuits. 19:33 Climate legacy of Pope Francis.
Hosted by Rowan Hooper and Penny Sarchet, with guests Alexandra Thompson, James Dinneen, William Schafer, Chris Callahan, Justin Mankin and Miles Pattenden. – Learn more ➤ https://www.newscientist.com/podcasts.
A new study found that a gene recently recognized as a biomarker for Alzheimer’s disease is actually a cause of it, due to its previously unknown secondary function. Researchers at the University of California San Diego used artificial intelligence to help both unravel this mystery of Alzheimer’s disease and discover a potential treatment that obstructs the gene’s moonlighting role.
The research team published their results on April 23 in the journal Cell.
About one in nine people aged 65 and older has Alzheimer’s disease, the most common cause of dementia. While some particular genes, when mutated, can lead to Alzheimer’s, that connection only accounts for a small percentage of all Alzheimer’s patients. The vast majority of patients do not have a mutation in a known disease-causing gene; instead, they have “spontaneous” Alzheimer’s, and the causes for that are unclear.
Advances in high-throughput phenotyping (HTP) platforms together with genotyping technologies have revolutionized breeding of varieties with desired traits relying on genomic prediction. Yet, we lack an understanding of the expression of multiple traits at different time points across the entire growth period of the plant.
A research team, including IPK Leibniz Institute and the Max Planck Institute of Molecular Plant Physiology, has developed a computational approach to solve this problem. The results were published in the journal Nature Plants.
The phenome of a plant comprises the entirety of traits expressed at any given time, and is the integrated outcome of the effects of genetic factors, environmental conditions and their complex interactions. Understanding how the crop phenome changes over time can help predict individual traits at specific time points in crop development. However, this problem is challenging not only because of the intricate dependence between individual traits, but also due to differences in how the phenomes of specific genotypes change over the plant life cycle.
A groundbreaking gene therapy has restored sight in four young children born with severe blindness due to a rare genetic deficiency. Scientists at UCL and Moorfields Eye Hospital successfully injected healthy copies of the defective gene into the retina, leading to life-changing improvements. Gr
Human cyborgs are individuals who integrate advanced technology into their bodies, enhancing their physical or cognitive abilities. This fusion of man and machine blurs the line between science fiction and reality, raising questions about the future of humanity, ethics, and the limits of human potential. From bionic limbs to brain-computer interfaces, cyborg technology is rapidly evolving, pushing us closer to a world where humans and machines become one.
Alternative RNA splicing is like a movie editor cutting and rearranging scenes from the same footage to create different versions of a film. By selecting which scenes to keep and which to leave out, the editor can produce a drama, a comedy, or even a thriller—all from the same raw material. Similarly, cells splice RNA in different ways to produce a variety of proteins from a single gene, fine-tuning their function based on need. However, when cancer rewrites the script, this process goes awry, fueling tumor growth and survival.
In a recent study reported in the Feb. 15 issue of Nature Communications, scientists from The Jackson Laboratory (JAX) and UConn Health not only show how cancer hijacks this tightly regulated splicing and rearranging of RNA but also introduce a potential therapeutic strategy that could slow or even shrink aggressive and hard-to-treat tumors. This discovery could transform how we treat aggressive cancers, such as triple-negative breast cancer and certain brain tumors, where current treatment options are limited.
At the heart of this work, led by Olga Anczuków, an associate professor at JAX and co-program leader at the NCI-designated JAX Cancer Center, are tiny genetic elements called poison exons, nature’s own “off switch” for protein production. When these exons are included in an RNA message, they trigger its destruction before a protein can be made—preventing harmful cellular activity. In healthy cells, poison exons regulate the levels of key proteins, keeping the genetic machinery in check. But in cancer, this safety mechanism often fails.
