How xenon gas is offering hope for Alzheimer's patients and their families

Researchers found that xenon can penetrate the blood-brain barrier

Back in 1898, William Ramsay, then chair of inorganic chemistry at University College, London, alongside his colleague, Morris Travers, embarked on a quest to uncover the secrets of the air we breathe. They devised an elaborate process to extract gases from liquid air, and extracted neon, argon and krypton. They found support from wealthy industrialist Ludwig Mond, who sponsored a new liquid-air machine. They used it to extract more of krypton. By repeatedly distilling this, they eventually isolated a heavier gas. When they examined it in a vacuum tube, it emitted a beautiful blue glow. They named the new gas xenon.

Fast forward to 2025: xenon, an odourless noble gas in Group 18 of the periodic table, is now offering hope for Alzheimer’s patients and their families.

Researchers from Mass General Brigham and Washington University School of Medicine in St. Louis have shown that inhaling xenon gas can reduce neuroinflammation, minimise brain atrophy, and promote protective neuronal states in mouse models of Alzheimer’s disease. Their groundbreaking findings were recently published in Science Translational Medicine.

Alzheimer’s disease is a complex neurodegenerative disorder marked by the progressive decline of cognitive functions, particularly memory. While its exact causes remain unclear, the hallmark of the disease is the abnormal accumulation of proteins in the brain―amyloid plaques outside neurons and tau tangles within them. These disruptions impair communication between nerve cells, leading to neuronal loss over time.

In Alzheimer’s disease, the brain’s primary immune cells, microglia, can become overactive or dysfunctional, leading to chronic inflammation. Researchers have developed a method to study microglial responses to neurodegeneration, observing that certain microglial characteristics can be modulated to provide protective effects against Alzheimer’s.

A significant challenge in Alzheimer’s research and treatment is designing medications that can cross the blood-brain barrier―a vital protective structure that regulates the movement of substances between the bloodstream and the central nervous system (CNS). However, the researchers found that xenon can penetrate this barrier, travelling directly from the bloodstream into the fluid surrounding the brain.

Upon entering the brain fluid, xenon induced and enhanced a protective microglial response linked to clearing amyloid plaques and improving cognition. In Alzheimer’s disease mouse models, nest-building behaviours―a key marker for assessing cognitive function―are significant for understanding disease progression. Impairments in these behaviours signal early cognitive dysfunction.

Notably, inhalation of xenon reduced brain atrophy and neuroinflammation while improving nest-building behaviour in mice. The researchers also observed xenon’s protective effects in mouse models exhibiting both amyloid and tau pathologies.

Building on these successful results, a clinical trial will now commence at Brigham and Women’s Hospital, initially enrolling only healthy volunteers to establish safety and dosage. Meanwhile, the researchers plan to investigate the mechanisms underlying xenon’s protective effects and explore its potential in treating other diseases, such as multiple sclerosis, amyotrophic lateral sclerosis, and neurodegenerative eye diseases.

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