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Category: biotech/medical – Page 14

Vascular Control Of Aging And Regeneration (Featuring Anjali Kusumbe, PhD)

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Light-triggered arrhythmia reveals rapid brain oxygen shifts in mice

An irregular heartbeat, or arrhythmia, leads to inefficient pumping of blood by the heart, which then prevents blood and oxygen from getting to the body’s other organs. When blood and oxygen flow poorly to the brain, the risk of stroke and cognitive decline increases.

A team of researchers based at Washington University in St. Louis used cardiac optogenetics to noninvasively study arrhythmia and its impact on the brain. Using highly sensitive imaging in a mouse model, they found that arrhythmia in a mouse heart alters oxygen concentration in the brain during and after arrhythmia.

Results of the research are published in Science Advances.

Fragile X deficits in mice respond to gene therapy

A gene therapy designed to replace a missing brain protein restored normal brain activity and improved behavior in a mouse model of fragile X syndrome (FXS), according to a study led by researchers at the University of California, Riverside. The findings, published in Molecular Therapy Nucleic Acids, suggest that gene therapy may one day address the underlying cause of FXS rather than simply treating its symptoms.

FXS affects approximately 2–3% of individuals diagnosed with autism and is one of the best-defined genetic causes of neurodevelopmental disability. The condition occurs when a mutation in the FMR1 gene prevents the production of fragile X messenger ribonucleoprotein (FMRP), a protein that regulates communication between brain cells.

“In a typical brain, FMRP acts like a brake or a volume control,” said Iryna Ethell, the paper’s senior author and a professor of biomedical sciences in the UCR School of Medicine. “Without it, neural circuits become overactive and less efficient, which contributes to many of the developmental and behavioral challenges associated with FXS.”

Scientists uncover a genetic ‘shield’ that lowers the risk of colorectal cancer

A team of scientists from the Barbara Ann Karmanos Cancer Institute, Wayne State University and institutions across the U.S. have published a new paper on the role of TGFBR1*6A, a naturally occurring genetic mutation in the TGFBR1 gene found in approximately 14% of the general population.

The study, “TGFBR1*6A and risk for colorectal cancer,” published June 9, 2026, in Cancer Communications, focuses on TGFBR1*6A and how it influences a person’s risk of developing colorectal cancer. Dr. Boris Pasche, president and CEO of the Karmanos Cancer Institute and chair of the Wayne State University Department of Oncology, was the first to discover TGFBR1*6A as a cancer risk allele.

“This mutation has often been overlooked by genome-wide association study chips, which cannot detect TGFBR1*6A, and is commonly missed by next-generation sequencing platforms due to the complexity of the region,” said Dr. Allan Johansen, a postdoctoral fellow and first author of the paper.

Faster aging, chronic disease linked to WTC responders with PTSD

Post-traumatic stress disorder (PTSD) remains a common condition affecting World Trade Center (WTC) responders 25 years after the attack on the Twin Towers. While the condition is considered mainly psychological, a new study sheds light on changes in the biological processes of WTC patients with PTSD that may explain why PTSD is associated with a variety of chronic diseases that ultimately contribute to aging.

Completed by a team of researchers affiliated with the Stony Brook World Trade Center Health and Wellness Program, which monitors the health of and provides patient care to some 10,000 WTC responders, and scientists at Duke University, the study is published in Nature Communications.

The work represents more than a decade of research led by Benjamin J. Luft, MD, senior author, the Edmund D. Pellegrino Professor of Medicine in the Renaissance School of Medicine (RSOM) at Stony Brook University and director of the WTC Health and Wellness Program; and Pei-Fen Kuan, Ph.D., first author and professor in the Department of Applied Mathematics and Statistics in the College of Engineering and Applied Sciences at Stony Brook University.

Better heart ‘digital twins’ could help target treatment for atrial fibrillation

A cross-university paper led by researchers at Queen Mary University of London, published in the Journal of Physiology, shows how better “digital twins” could help doctors treat people with atrial fibrillation.

One of the leading causes of stroke, atrial fibrillation (AF) is an erratic, quivering heartbeat that affects more than 1.5 million people in the U.K. The most common treatment is a procedure called ablation, in which doctors use heat or cold energy to destroy the small patches of heart tissue that trigger the chaotic rhythm. It works, but not for everyone and not always the first time.

Repeat ablation is common in persistent AF partly because the condition involves complex, distributed electrical changes that are hard to map in a single procedure.

Quantum-inspired AI could tailor patients’ cancer treatment to their entire molecular background

For a child diagnosed with neuroblastoma—the most common infant cancer, occurring when early nerve cells grow out of control—the path to treatment isn’t simple. Some types of neuroblastoma resolve on their own, while others require aggressive intervention. Researchers have tried matching treatments to patients based on one-gene mutations with limited success. This is because patients’ outcomes depend on their entire molecular background, containing millions or even billions of features, such as DNA and RNA from tissues and blood.

“It’s much more than just one gene—everything that’s happening in the cells of the patient matters,” said Orly Alter, an associate professor of biomedical engineering at the University of Utah’s Scientific Computing & Imaging Institute.

Current artificial intelligence and machine learning (AI/ML) approaches require massive amounts of training data and, specifically, vastly more patient samples than genetic features.

Intracellular mechanisms promote tumor survival during hypoxia

Northwestern Medicine scientists have, for the first time, described the underlying mechanisms that regulate how cells rapidly change gene expression in response to hypoxia, a key feature of many treatment-resistant tumors, according to a recent study published in Science Advances.

Ali Shilatifard, Ph.D., the chair and Robert Francis Furchgott Professor of Biochemistry and Molecular Genetics, was the senior author of the study.

Scientists found an 8-year-old Neanderthal child in a Belgian cave, and the molar DNA found is said to be the oldest human genetic code ever sequenced, turning one hillside into a rare window on our deep past

Scientists have uncovered the oldest human genetic code from an 8-year-old Neanderthal child in Belgium, offering profound insights into our evolutionary past and Neanderthal development.

A selective, brain-penetrant GalR1 antagonist restores cholinergic signaling in vitro and rescues cholinergic cognitive deficits in mice

In this study, we characterized PAC-832, a small-molecule GalR1 antagonist with sub-micromolar potency (IC50 = 0.28 μM), 30-fold selectivity over GalR2 and GalR3, and excellent brain penetration and drug-like properties. In functional cell-based assays, PAC-832 reversed galanin-mediated suppression of acetylcholine release. In a scopolamine challenge model, PAC-832 attenuated cognitive deficits in the Y-maze and NOR tasks, with effect sizes comparable to donepezil.

The scopolamine model is widely used in behavioral mouse research to evaluate compounds for procognitive activity. However, because scopolamine impairs cognition by blocking muscarinic receptors rather than by reducing acetylcholine release, our behavioral results do not directly assess whether PAC-832 acts by restoring cholinergic signaling in vivo, or whether it acts through an alternative downstream mechanism. Establishing the former will require direct measurement of acetylcholine release in the CNS (e.g. using microdialysis or biosensor-based approaches) and/or GalR1-dependent in vivo validation (e.g. using transgenic GalR1-knockout mice).

Nonetheless, our work addresses a longstanding pharmacological gap in the galanin field. Despite decades of work implicating galanin signaling in CNS function and disease, translational progress has been limited by a lack of subtype-selective, brain-penetrant small molecule galanin modulators. Recent therapeutic development within the galanin field has largely focused on GalR2 agonism, while GalR1-targeting approaches have remained dependent on peptide tools unable to pass the blood-brain barrier. PAC-832 is, to our knowledge, the first GalR1-selective small molecule antagonist with sufficient brain exposure to test the effects of GalR1 antagonism following peripheral administration.

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