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Category: health

New antibody may boost KRAS-targeted lung cancer treatment after resistance emerges

An experimental antibody treatment that binds to a protein known as PCDH7 shrank tumors in preclinical models of non-small cell lung cancer (NSCLC), including those resistant to a targeted therapy, a study led by UT Southwestern Medical Center researchers showed. The findings, published in Science Advances, could eventually lead to a new class of drugs to treat NSCLC and potentially other cancers.

“Overcoming resistance to molecularly targeted therapies is a critical unmet need for lung cancer patients. We are excited that these antibodies may open another therapeutic avenue for lung cancer, especially for patients whose cancers have become resistant to KRAS inhibitors,” said Kathryn O’Donnell, Ph.D., associate professor of molecular biology and a member of the Harold C. Simmons Comprehensive Cancer Center at UT Southwestern. O’Donnell co-led the study with first author Nicole Novaresi, Ph.D., a postdoctoral researcher in the O’Donnell Lab, and collaborators at the University of Texas Health Science Center at Houston.

NSCLC accounts for about 85% of lung cancer cases in the U.S. and is the leading cause of cancer-related deaths. The O’Donnell Lab focuses on identifying and characterizing proteins on the surface of NSCLC and other cancer cells because of their potential as therapeutic targets. In 2017, O’Donnell and her colleagues identified PCDH7 as a driver of NSCLC, especially in tumors with mutations in a gene called KRAS. Found in about 25% of NSCLC cases, these mutations cause uncontrolled cell proliferation that propels tumor growth.

Faulty protein cleanup gene tied to severe early-onset neurological disorders

Though protein clumps associated with Alzheimer’s and Parkinson’s were discovered more than a century ago, researchers remain largely unable to prevent them from forming or eliminate them from the brain. And though a variety of therapies have taken aim at tau tangles, beta-amyloid plaques and Lewy bodies, among other notorious aggregates, none have been very effective at stopping disease progression.

Rockefeller’s Hermann Steller and his team in the Strang Laboratory of Apoptosis and Cancer Biology have long been focused on understanding how the cell’s protein-degrading machines, called proteasomes, are regulated. His lab discovered that a transporter protein termed PI31 shuttles proteasomes over long distances from the nerve cell body to synapses. When this system fails, synapses become depleted of degradative capacity, and proteins that should have been eliminated accumulate. As a result, synaptic communication breaks down, protein clumps form and neuronal health deteriorates.

Now a new study in Nature Communications, led by researchers from University College London and contributed to by Steller’s lab, has identified mutations in PSMF1, the gene that produces PI31, that cause the protein to malfunction. Moreover, the scientists demonstrated that these mutations cause a spectrum of severe, very early-onset neurological disorders.

Genomes from Oceania offer new clues to human evolution

A new Yale-led study provides one of the most detailed and comprehensive analyses to date of genetic variation in human populations in Oceania, filling a major gap in representation in genomics research. Despite harboring remarkable diversity, populations in this vast region in the South Pacific historically have been overlooked in global human genetic studies, which have often focused largely on people of European descent, researchers say. The study is published in the journal Science.

“The drastic underrepresentation of Oceanians limits our understanding of human evolution and could exacerbate health inequalities as genomic research is used to develop novel medical treatments,” said lead author Serena Tucci, assistant professor of anthropology in Yale’s Faculty of Arts and Sciences and principal investigator of the Yale Human Evolutionary Genomics Laboratory. “To fill that gap, my research team embarked on a large-scale project to expand what is known about human genetic variation, including genetic variants inherited from extinct hominins.”

The work shows how the genes that ancient humans acquired after mating with extinct hominins continue to shape the biology, health and survival of our species today.

Gut microbes unlock hormone signaling that regulates gut movement, study suggests

Millions of people worldwide are periodically or chronically affected by gut-related conditions, such as irritable bowel syndrome (IBS), gastroesophageal reflux disease (GERD) and gastroenteritis. Uncovering the physiological and biological processes that contribute to gut health could thus be highly valuable, as it might help devise more effective interventions to prevent and treat these ailments.

The transit of food, fluids and waste through the intestine is known to be coordinated by various interacting systems in the body, including gut wall muscles, neurons in the gastrointestinal tract and hormones. A growing body of research has also been exploring the crucial contribution of bacteria and other microorganisms residing in the digestive tract, which are collectively referred to as the gut microbiome.

Researchers at Boston Children’s Hospital, Harvard Medical School, the University of North Carolina at Chapel Hill and Laval University recently carried out a study aimed at better understanding how these gut microbes interact with specific sex hormones and nerve cells that control the movement of muscles in the intestines.

Promote Neurogenesis and Neuroplasticity with Exercise, Diet, and more

You may have heard the phrase “neurons that fire together wire together.” This short phrase summarizes the synaptic plasticity theory of learning described by Canadian psychologist Donald Hebb in his 1949 book The Organization of Behavior.

Hebb explained how the connections between neurons (brain cells) change as a result of repetitive firing. So when you repeat a movement like swinging a golf club over and over, the neural pathways involved in controlling that movement become stronger and faster. Not only do existing synapses (junctions between neurons) begin to fire more efficiently, but new synapses are formed and other neurons are recruited to get in on the action. As a result, your golf swing becomes more automatic, reliable, and forceful the more often you practice.

That is neuroplasticity: your brain’s ability to change and adapt based on input and use. The concept of neuroplasticity had been previously proposed by others, most notably American psychologists William James and Karl Lashley, and Polish neuroscientist Jerzy Konorski, but it was largely ignored by the scientific community until Hebb brought the concept to the forefront in his groundbreaking book.

Researchers trigger sleep’s restorative effect in parts of the awake brain

Scientists from the University of Wisconsin-Madison have successfully replicated some of the restorative effects of deep sleep in awake mice by artificially inducing slow-wave brain activity. Using optogenetics to control specific neurons, researchers triggered localized cortical activity that mimics the NREM sleep phase responsible for synaptic homeostasis and the reorganization of neural connections. This targeted stimulation significantly reduced signs of fatigue and improved memory retention and cognitive performance in the mice following prolonged wakefulness. While the researchers caution that this technique is not a substitute for natural sleep, the findings suggest that localized neural stimulation can effectively preserve brain function during extended periods of wakefulness. Future research aims to explore whether similar cognitive benefits can be achieved in humans through non-invasive methods, such as transcranial electrical stimulation.

NIH-funded study in animals offers new details about how the brain resets during sleep.

By inducing specific patterns of activity in small portions of the brain in awake mice, researchers supported by the National Institutes of Health (NIH) have triggered a recalibration of neural connections that normally only occurs during sleep. This new approach offset the effects of sleep deprivation in memory tasks and revealed features of sleep that are key to its restorative effect.

“What we’re essentially doing is forcing sleep in a local region of the brain. While that part is solidifying memories and restoring learning capacity, other parts stay aware/vigilant and connected to environment,” said corresponding author Chiara Cirelli, M.D., Ph.D., a professor of psychiatry at the University of Wisconsin-Madison. “Dolphins do something similar, sleeping with only one brain hemisphere at a time.”

Renin–angiotensin system: a novel target for brain health

Emerging evidence highlights the brain renin–angiotensin system (RAS) as a key regulator of reward, memory, and stress. While these discoveries established the brain RAS as a promising therapeutic target for interventions in neurological and neuropsychiatric disorders, translational progress is hampered by the lack of an integrative mechanistic framework. Here, we consolidate accumulating evidence on the molecular and system-level roles of the brain RAS in reward, memory, and stress pathways, and its dual regulatory architecture. Pharmacological RAS modulation regulates domain-specific signaling in frontostriatal reward circuits, hippocampal–prefrontal memory networks, and frontolimbic fear networks. We evaluate the transdiagnostic therapeutic potential in neurological and neuropsychiatric disorders (e.g.

Why this $10 spectrometer chip could bring real-time chemical sensing to wearables

Researchers from the University of Cambridge and GlitterinTech, a startup founded by the same research group, have unveiled a fundamentally new type of optical spectrometer that delivers laboratory-grade precision in a device small enough to be embedded in portable and wearable technologies. By rethinking how spectra are measured and processed, the team has demonstrated a spectrometer costing only around $10, operating at a centimeter scale, and capable of applications ranging from industrial quality control to real-time health care monitoring.

Optical spectrometers underpin countless technologies, from chemical analysis and manufacturing to environmental sensing and medicine. Yet shrinking these instruments has historically involved painful trade-offs: Miniaturized devices typically sacrifice bandwidth, resolution or accuracy, limiting them to rough identification rather than true metrological measurements. The newly reported convolutional spectrometer overcomes these barriers by introducing a conceptually elegant operating principle grounded in the convolution theorem, offering unprecedented performance metrics compared with existing dispersive, Fourier-transform and reconstructive spectrometers.

Major surgery may accelerate memory loss in 1 in 7 older adults

Going through surgery can take a significant toll on a patient’s physical health and capabilities, especially if they are elderly. A recent study found that the effects extend far beyond mobility and pain management, as the operation may also lead to a significant loss of overall cognitive sharpness.

Researchers tracked 560 adults over 70 with no signs of dementia for six years after major surgeries such as hip replacements and abdominal procedures, watching how their memory and thinking skills changed over time. They found that nearly 15% of participants experienced a sharp decline in memory and thinking abilities shortly after surgery, with their condition continuing to deteriorate over time.

The three biggest warning signs that made a person more likely to fall into a severe decline were: being older, having lower mental test scores before the surgery, and developing postoperative delirium, which is a mental state where a person has episodes of confusion and disordered thinking that can develop over hours or days after the surgery.

The Brain Health Accelerator Seeks to Revolutionize Neuroscience Research

For decades, researchers across institutions have peered into microscopes and dived into data to try to understand how diseases like Alzheimer’s disease, Parkinson’s disease, and amyotrophic lateral sclerosis (ALS) affect the brain. While scientists have made many important insights into these conditions, breakthrough therapies to cure or even treat them remain out of reach.

To expedite understanding of and treatments for neurodegenerative diseases, the Allen Institute launched the Brain Health accelerator. The project, announced today, is a global initiative that will leverage cutting-edge technology with the goal of improving modeling, therapeutic development, and the understanding of disease mechanisms. With funding support from the Allen Institute, the Bezos family, Amazon Web Services, the National Institutes of Health, EverythingALS, and other partners, the project financial contribution is $400 million.

One of the challenges in studying diseases in the human brain and identifying treatment strategies has been the scale and complexity of the organ. The brain consists of many distinct parts, and studying disease mechanisms requires samples from large numbers of individuals. Additionally, while technological advancements in transcriptomics, proteomics, neuroimaging, and AI have helped researchers study the brain in finer detail, researchers have not always integrated many of these approaches into the same project.

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