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Does Treating Brain Edema in Patients with Large Hemispheric Infarction Help?

Brain edema can accompany large ischemic strokes and can increase stroke-related morbidity and mortality. The past few decades have seen no advances in pharmacologic treatment of brain edema. These investigators conducted a manufacturer-funded, randomized, placebo-controlled trial of glibenclamide, a sulfonylurea 1–receptor inhibitor that can decrease brain edema. (Glibenclamide is approved to treat type 2 diabetes.) In a previous study, it was associated with fewer deaths from neurologic causes, but its use in patients with stroke is not widespread.

Eligible patients had large ischemic strokes that could be treated within 10 hours of onset. A large hemispheric infarct in at least the middle cerebral artery territory was defined as either an Alberta Stroke Program Early CT Score of 1 to 5 or lesion volumes of 80 mL to 300 mL on computed-tomography perfusion or diffusion-weighted imaging. Glibenclamide (8.6 mg) was given to half the study participants intravenously over 72 hours.

The study was halted early due to underenrollment. Of 535 enrolled patients, 431 were in the intended age range (18–70) and had complete data (mean age, 58; 33% women; median NIH Stroke Scale [NIHSS] score, 19). Treatment began at an average of 9 hours after symptom onset. No favorable shift with glibenclamide occurred on the primary outcome, the 90-day modified Rankin Scale (mRS). Mortality was similar in the two groups (glibenclamide, 32%; placebo, 29%). Hypoglycemia was seen in 6% of glibenclamide recipients and 2% of placebo recipients. Subgroup analysis revealed a signal of potential benefit with glibenclamide in patients with NIHSS scores of 20 or less.

When Muscles Work Out, they Help Neurons to Grow

The findings suggest that biochemical and physical effects of exercise could help heal nerves. There’s no doubt that exercise does a body good. Regular activity not only strengthens muscles but can bolster our bones, blood vessels, and immune system.

Now, MIT engineers have found that exercise can also have benefits at the level of individual neurons. They observed that when muscles contract during exercise, they release a soup of biochemical signals called myokines. In the presence of these muscle-generated signals, neurons grew 4X farther compared to neurons that were not exposed to myokines. These cellular-level experiments suggest that exercise can have a significant biochemical effect on nerve growth.

Surprisingly, the researchers also found that neurons respond not only to the biochemical signals of exercise but also to its physical impacts. The team observed that when neurons are repeatedly pulled back and forth, similarly to how muscles contract and expand during exercise, the neurons grow just as much as when they are exposed to a muscle’s myokines.

Genetic Mechanism Links Emotional Experiences to Behavior Changes

Summary: Researchers have identified a genetic mechanism that regulates behavioral adaptations to emotional experiences by forming R-loops, unique RNA: DNA structures that activate target genes. The study focused on NPAS4, a gene implicated in stress and drug addiction, showing how blocking R-loops prevents maladaptive behaviors like cocaine seeking and stress-induced anhedonia in mice.

This mechanism demonstrates how emotional experiences influence brain circuits by altering gene expression through enhancer RNA. The findings could pave the way for RNA-based therapies to treat psychiatric disorders linked to stress and substance use.

Brain organoids and assembloids are new models for elucidating, treating neurodevelopmental disorders

But Kelby, who was training to become an operating room nurse, realized Holden’s episodes reminded him of what he was learning about warning signs for stroke. JJ called Holden’s cardiologist in Utah and asked for a detailed neurologic evaluation, which enabled the mysterious episodes to be diagnosed as seizures. Holden began taking anti-seizure medication, which helped, to his parents’ great relief.

A few months after Holden was born, Sergiu Pasca, MD, arrived at Stanford Medicine to pursue a postdoctoral fellowship in the lab of Ricardo Dolmetsch, PhD, then an assistant professor of neurobiology, who was redirecting his research to autism spectrum disorder. At the time, Pasca did not know the Hulet family. But his work soon became focused on the disorder that has shaped Holden’s life.

Light-induced gene therapy disables cancer cells’ mitochondria

Researchers are shining a light on cancer cells’ energy centers—literally—to damage these power sources and trigger widespread cancer cell death. In a new study, scientists combined strategies to deliver energy-disrupting gene therapy using nanoparticles manufactured to zero in only on cancer cells. Experiments showed the targeted therapy is effective at shrinking glioblastoma brain tumors and aggressive breast cancer tumors in mice.

The research team overcame a significant challenge to break up structures inside these cellular energy centers, called mitochondria, with a technique that induces light-activated electrical currents inside the cell. They named the technology mLumiOpto.

“We disrupt the membrane, so mitochondria cannot work functionally to produce energy or work as a signaling hub. This causes programmed followed by DNA damage—our investigations showed these two mechanisms are involved and kill the ,” said co-lead author Lufang Zhou, professor of biomedical engineering and surgery at The Ohio State University. “This is how the technology works by design.”

Molecular motors put significant twists to DNA loops

Astrocytes are star-shaped glial cells in the central nervous system that support neuronal function, maintain the blood-brain barrier, and contribute to brain repair and homeostasis. The evolution of these cells throughout the progression of Alzheimer’s disease (AD) is still poorly understood, particularly when compared to that of neurons and other cell types.

Researchers at Massachusetts General Hospital, the Massachusetts Alzheimer’s Disease Research Center, Harvard Medical School and Abbvie Inc. set out to fill this gap in the literature.

Their paper, published in Nature Neuroscience, provides one of the most detailed accounts to date of how different astrocyte subclusters respond to AD across different brain regions and disease stages, providing valuable insights into the cellular dynamics of the disease.

Breakthrough Study: Natural Compound Could Counter Opioid Addiction Without Sacrificing Pain Relief

Boosting the endocannabinoid 2-AG in the brain can counteract opioid addiction while preserving their pain relief, a Weill Cornell Medicine study finds. This approach, tested in mice using the chemical JZL184, may lead to safer treatments for pain management.

The natural enhancement of chemicals produced by the body, known as endocannabinoids, may mitigate the addictive properties of opioids like morphine and oxycodone while preserving their pain-relieving effects, according to researchers from Weill Cornell Medicine in collaboration with The Center for Youth Mental Health at NewYork-Presbyterian. Endocannabinoids interact with cannabinoid receptors found throughout the body, which play a role in regulating functions such as learning and memory, emotions, sleep, immune response, and appetite.

Opioids prescribed to control pain can become addictive because they not only dull pain, but also produce a sense of euphoria. The preclinical study, published recently in the journal Science Advances, may lead to a new type of therapeutic that could be taken with an opioid regimen to only reduce the reward aspect of opioids.