Many describe this as the experience of seeing their life ‘flash before their eyes.’

The recording was made when an 87-year-old patient underwent cardiac arrest while being treated for epilepsy.

Doctors had strapped a device on his head to monitor brain activity, but the man died during the process.

Xenon gas inhalation reduced neurodegeneration and boosted protection in preclinical models of Alzheimer’s disease. Most treatments being pursued today to protect against Alzheimer’s disease focus on amyloid plaques and tau tangles that accumulate in the brain, but new research from Mass General Brigham and Washington University School of Medicine in St. Louis points to a novel — and noble — approach: using Xenon gas. The study found that Xenon gas inhalation suppressed neuroinflammation, reduced brain atrophy, and increased protective neuronal states in mouse models of Alzheimer’s disease. Results are published in Science Translational Medicine, and a phase 1 clinical trial of the treatment in healthy volunteers will begin in early 2025.

“It is a very novel discovery showing that simply inhaling an inert gas can have such a profound neuroprotective effect,” said senior and co-corresponding author Oleg Butovsky, PhD, of the Ann Romney Center for Neurologic Diseases at Brigham and Women’s Hospital (BWH), a founding member of the Mass General Brigham healthcare system. “One of the main limitations in the field of Alzheimer’s disease research and treatment is that it is extremely difficult to design medications that can pass the blood-brain barrier — but Xenon gas does. We look forward to seeing this novel approach tested in humans.”

“It is exciting that in both animal models that model different aspects of Alzheimer’s disease, amyloid pathology in one model and tau pathology in another model, that Xenon had protective effects in both situations,” said senior and co-corresponding author David M. Holtzman, MD, from Washington University School of Medicine in St. Louis.

Weill Cornell Medicine investigators have identified in a preclinical model a specific brain circuit whose inhibition appears to reduce anxiety without side effects. Their work suggests a new target for treating anxiety disorders and related conditions and demonstrates a general strategy, based on a method called photopharmacology, for mapping drug effects on the brain.

In their study, published Jan. 28 in Neuron, the researchers examined the effects of experimental drug compounds that activate a type of brain-cell receptor called the metabotropic glutamate receptor 2 (mGluR2). While these receptors are found on neurons within many brain circuits, the team showed that activating them in a specific circuit terminating in an emotion-related brain region called the amygdala reduces signs of anxiety without apparent adverse side effects. Current treatments for anxiety disorders, panic disorder and associated conditions can have unwanted side effects including cognitive impairments.

“Our findings indicate a new and important target for the treatment of anxiety-related disorders and show that our photopharmacology-based approach holds promise more broadly as a way to precisely reverse-engineer how therapeutics work in the brain,” said study senior author Dr. Joshua Levitz, an associate professor of biochemistry at Weill Cornell Medicine.