The summit of human endurance may also hold clues to preserving the brain. Scientists at the Broad Institute and Mass General Brigham have discovered that exposing Parkinson’s disease models to low-oxygen environments—the kind found at Mount Everest base camp—can both protect and restore brain function. The finding challenges one of neuroscience’s long-held assumptions: that oxygen is always good for the brain.

Parkinson’s disease affects more than 10 million people worldwide, eroding motor control as neurons die and toxic protein clumps called Lewy bodies accumulate. Traditional therapies try to address symptoms, but they do little to preserve the neurons themselves. What the Broad-MGH team found is that too much oxygen may be part of the problem. Damaged mitochondria, the energy factories of brain cells, stop using oxygen efficiently, leading to dangerous buildup. This excess oxygen appears to act more like a toxin than a nutrient, fueling the neurodegeneration that underpins Parkinson’s.

By housing mice in chambers with oxygen levels around 11%—roughly the same as at 16,000 feet of altitude—the researchers saw remarkable results. Mice that should have developed severe motor problems stayed mobile. Neurons that would have died remained alive. Even more compelling, mice already showing symptoms rebounded when moved into the low-oxygen environment. Their movement improved, anxiety behaviors faded, and brain cell death halted. This suggests that neurons can be rescued if the intervention comes early enough—an insight that reframes the way researchers think about “irreversible” damage in Parkinson’s.

The effect wasn’t due to stopping Lewy bodies from forming; the clumps were still there. Instead, hypoxia appeared to make neurons resilient to their toxic effects. This opens the door to a radical new strategy: treating Parkinson’s not by eliminating protein clumps, but by making neurons resistant to them.

The work builds on a decade of research showing hypoxia’s protective role in other mitochondrial diseases, such as Leigh syndrome and Friedreich’s ataxia. Anecdotal hints already existed: people with Parkinson’s sometimes feel better at high altitudes, and long-term smokers—whose tissues operate with lower oxygen levels due to carbon monoxide exposure—appear less likely to develop Parkinson’s.

The researchers caution, however, that this doesn’t mean patients should start restricting oxygen on their own. Intermittent or unsupervised hypoxia can be dangerous, even accelerating disease progression. Instead, the real promise lies in “hypoxia in a pill”—drug compounds that could mimic the protective effects of low oxygen safely and consistently.

If successful, this approach could mark a paradigm shift in how neurodegeneration is treated. Instead of chasing after tangled proteins or symptom management, medicine might learn to protect neurons by adjusting one of biology’s most fundamental variables: oxygen.

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