Living in a low-oxygen environment, like the thin air found at the base of Mount Everest, may slow or even reverse the progression of Parkinson’s disease, according to a new study in mice.
Researchers at the Broad Institute of MIT and Harvard and Mass General Brigham report that breathing air with just 11% oxygen, compared to the usual 21%, prevented motor decline and brain cell death in a mouse model of Parkinson’s. The findings suggest that excess oxygen in the brain, caused by mitochondrial dysfunction, may be fueling neurodegeneration—and that reducing oxygen intake can interrupt the process.
Low Oxygen, Big Results
In the study, published August 6 in Nature Neuroscience, mice with Parkinson’s-like brain changes were either kept in normal air or placed in hypoxia chambers replicating conditions at 16,000 feet. After three months, mice in the low-oxygen group had normal movement and no loss of dopamine neurons, despite forming the characteristic protein clumps known as Lewy bodies.
“The fact that we actually saw some reversal of neurological damage is really exciting,” said co-senior author Vamsi Mootha, a systems biologist at the Broad Institute and Harvard Medical School. “It tells us that there is a window during which some neurons are dysfunctional but not yet dead—and that we can restore their function if we intervene early enough.”
Even when hypoxia treatment was delayed until six weeks after symptoms began, the results held. The mice recovered motor function, showed fewer anxiety-like behaviors, and had halted loss of dopamine-producing neurons in the brain.
Why Oxygen Matters in Parkinson’s
Parkinson’s disease affects more than 10 million people worldwide. It causes the gradual death of neurons in the brain, especially in the substantia nigra, a region critical for movement control. Accumulated α-synuclein protein aggregates (Lewy bodies) are a hallmark of the disease, and mounting evidence suggests that these clumps impair mitochondria—the cellular powerhouses that also consume most of the body’s oxygen.
“Too much oxygen in the brain turns out to be toxic,” said Mootha. “By reducing the overall oxygen supply, we’re cutting off the fuel for that damage.”
Using specialized sensors, the researchers showed that Parkinson’s-model mice had elevated brain oxygen levels (hyperoxia) in areas with mitochondrial dysfunction. This oxygen buildup was linked to increased lipid peroxidation—a damaging oxidative process that kills neurons. But when oxygen levels were reduced via hypoxia, lipid peroxidation dropped dramatically and neurodegeneration slowed or stopped.
Key Findings
- Mice exposed to 11% oxygen showed no loss of dopamine neurons, despite Lewy body formation.
- Delayed hypoxia still reversed movement symptoms and halted neuron loss.
- Brain tissue from Parkinson’s-model mice had higher oxygen levels and more oxidative damage.
- Low-oxygen breathing reduced both tissue oxygen and markers of lipid peroxidation.
- These neuroprotective effects were also seen in a worm model of Parkinson’s (C. elegans).
A New Therapeutic Path?
Co-senior author Fumito Ichinose, an anesthesiologist at Massachusetts General Hospital, said the findings point to “an entirely new paradigm” for Parkinson’s research. Rather than focusing solely on blocking α-synuclein aggregation, the study suggests it may be possible to preserve neurons by managing the cellular environment in which that aggregation becomes toxic.
But the researchers are quick to caution against unsupervised attempts at hypoxia. “Breathing low-oxygen air, especially intermittently such as only at night, can be dangerous and may even worsen the disease,” the authors wrote.
Instead, the team is working on “hypoxia in a pill”—a class of experimental drugs that mimic the effects of low oxygen without altering atmospheric conditions. Early candidates are already being tested for mitochondrial diseases like Leigh syndrome and Friedreich’s ataxia. Parkinson’s may be next.
Why This Matters
Anecdotal reports have long hinted that Parkinson’s patients feel better at high altitudes. Smokers, too—who experience lower oxygen delivery due to carbon monoxide—have a statistically lower risk of Parkinson’s, though the reasons remain unclear. This study may offer a scientific explanation for those observations.
“It may not be a treatment for all types of neurodegeneration,” said Mootha, “but it’s a powerful concept—one that might shift how we think about treating some of these diseases.”
The research adds to a growing body of evidence that hypoxia, properly harnessed, could one day be used to preserve brain function in diseases that currently have no cure.
Journal Information
Journal: Nature Neuroscience
DOI: 10.1038/s41593-025-02010-4
Article Title: Hypoxia ameliorates neurodegeneration and movement disorder in a mouse model of Parkinson’s disease
Authors: Eizo Marutani, Vamsi K. Mootha, Fumito Ichinose, et al.
Publication Date: August 6, 2025
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