Zimmerman et al. show loss of behavioral inhibition correlated with attenuated theta activity in the primary visual cortex, hippocampus, and deficient top-down control from the prefrontal cortex in the Fmr1 KO mice. These findings shed light on circuit-level impairments underlying behavioral deficits in Fragile X syndrome for potential therapeutic interventions.
A New Era for SMA — Dr. Tracey Dawson, PhD, — SVP and U.S. Therapeutic Area Head of Neuroscience, Novartis.
Spinal muscular atrophy (SMA) has undergone one of the most remarkable transformations in modern medicine. A disease that once carried devastating consequences, particularly in its most severe forms, can now be treated with therapies designed to dramatically alter its course — especially when treatment begins early.
But medical progress creates a fascinating new question. What happens when you don’t just change the disease — you change what’s possible for the person living with it?
Because today’s SMA community includes children treated before symptoms emerge, young adults who have grown up in this new treatment era, and adults who have lived with SMA for decades and carry the consequences of disease that occurred before these therapies existed.
And that’s where our conversation today gets particularly interesting. Because the next challenge may not simply be developing better medicines. It may be helping people take full advantage of the lives those medicines make possible.
The Hidden Organ Transplant Threat — CMV — Dr. Neil Inhaber, MD, FRCPC — Head, Marketed Products and Neuroscience, Global Medical Affairs, Takeda.
Every year, hundreds of thousands of people around the world receive life-saving organ transplants — new hearts, kidneys, lungs, and livers that offer patients a second chance at life.
But transplantation is only the beginning of the journey.
Because preventing organ rejection requires suppressing the immune system, transplant recipients become vulnerable to infections that most healthy people never even notice.
One of the most important — and least understood — is cytomegalovirus, or CMV.
Scientists discovered that human microglia, immune cells that help shape developing brain circuits, can take four to eight years to mature instead of just weeks as they do in mice. The unusually slow process may help explain how the human brain develops its remarkable complexity and cognitive abilities.
P2RX7 may be linked to severe suicidal thoughts and recovery, but researchers still need to confirm the pattern in living people.
Severe suicidal thoughts may leave a detectable biological signal in the brain, and that signal could also change when people recover. Researchers at the Netherlands Institute for Neuroscience have identified a receptor that may be linked to these shifts, providing a possible new direction for studying resilience and suicide prevention.
In the Netherlands, nearly five people die by suicide each day, and there may be about twenty suicide attempts for every death. Despite the enormous consequences for individuals and families, scientists still understand relatively little about the biological processes associated with suicidal thoughts. Effective medications specifically targeting suicidal thoughts are also urgently needed.
Rice University and collaborators in Switzerland have developed a platform to grow human-derived nerve cells and Schwann cells, supporting cells that form a protective coating called myelin around nerve fibers. This platform enables the formation of functional myelin in a three-dimensional, lab-grown environment. Researchers confirmed that it worked by measuring an increase in the speed of electrical signals traveling across networks of connected nerve cells.
Developed at Rice and ETH Zurich, the platform combines human-derived cells, tissue-like materials and electrical measurements in one system. Because nerves contain many cell types and can be difficult to access without damage, researchers can use the model to study how myelin develops, how injury or exposure to toxins affects it and whether drugs or electrical stimulation can prevent its loss or promote repair. The platform can also be adapted to model the brain and measure complex cellular processes. The study was published Aug. 26 in Advanced Healthcare Materials.
“While the formation of myelin is exciting to see, we are even more excited that it is functional and changes how the nerve communicates,” said Christina Tringides, corresponding author and assistant professor of materials science and nanoengineering at Rice.
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Scientists have identified a protein that acts like a brake on the nervous system’s ability to repair damaged connections. Blocking AHR helped injured nerve fibers regrow and improved movement and sensation in mice with nerve or spinal cord injuries. The discovery could eventually point toward new treatments designed to shift neurons from simply surviving an injury to actively rebuilding themselves.
Do you ever feel like sometimes you can master a new dance step almost immediately, while other times you struggle to nail it despite repeated practice? This might be due to skill or effort, but also to something less obvious: whether the brain is in a state that allows learning to take hold.
The brain does not learn in isolation from the rest of the body. Signals from internal organs continuously reach the brain through a key part of our nervous system called the vagus nerve. Researchers at Tohoku University specializing in super-network brain physiology have now demonstrated in mice that stimulating this nerve after training can promote lasting motor learning. This study reveals a previously underappreciated way in which body-to-brain signaling may support long-term learning.
The findings were published in iScience on August 25, 2026.