‘Mount Everest air’ offers clues to potential Parkinson’s breakthrough

A low-oxygen environment, similar to air at Mount Everest base camp, could slow or even reverse Parkinson’s symptoms, new research suggests, offering hope for new therapies.

The study found that faulty cellular processes in the brain cause oxygen molecules to build up, damaging neurons and triggering symptoms. Restricting oxygen intake appeared to slow or even reverse this process.

Scientists from Harvard Medical School tested the idea by creating Parkinson’s-like conditions in mice using injections of α-synuclein proteins, which form toxic clumps called Lewy bodies inside brain cells. Lewy bodies are protein deposits that build up in neurons and are a hallmark of the disease.

Mice were split into two groups: one breathed normal air with 21 per cent oxygen, while another was kept in chambers with 11 per cent oxygen, similar to living at 4,800 metres altitude.

After three months, mice breathing normal air had high levels of Lewy bodies, neuron loss and severe movement problems.

By contrast, those in low-oxygen conditions developed Lewy bodies but showed no neuron loss or movement difficulties.

The findings suggest hypoxia did not prevent Lewy bodies forming, but it protected neurons from their damaging effects.

Parkinson’s affects more than 10 million people worldwide, causing a progressive loss of neurons that leads to tremors and slowed movement.

Anecdotal reports also suggest people with Parkinson’s sometimes fare better at high altitudes.

Study author Fumito Ichinose said: “Based on this evidence, we became very interested in the effect of hypoxia on Parkinson’s disease.”

Hypoxia refers to reduced oxygen levels in tissues.

Vamsi Mootha, another author, said: “We first saw that low oxygen could alleviate brain-related symptoms in some rare diseases where mitochondria are affected, such as Leigh syndrome and Friedreich’s ataxia.

“That raised the question: Could the same be true in more common neurodegenerative diseases like Parkinson’s?” said

Mitochondria are cell structures that generate energy, often described as the powerhouse of the cell.

The low-oxygen treatment also worked when introduced six weeks after injection, when symptoms had already appeared.

At that stage, the mice’s motor skills rebounded, their anxiety-like behaviours faded and neuron loss stopped.

Brain scans revealed that mice with symptoms had much higher oxygen levels in certain brain regions than control mice or those kept in low-oxygen air.

Scientists believe this excess oxygen resulted from mitochondrial dysfunction. With mitochondria unable to use oxygen efficiently, oxygen was building up to harmful levels.

Dr Mootha said: “Too much oxygen in the brain turns out to be toxic. By reducing the overall oxygen supply, we’re cutting off the fuel for that damage.”

Researchers are now developing “hypoxia in a pill” drugs to replicate the effects of low oxygen for treating mitochondrial disorders.

However, they caution that more research is needed before the findings can be applied to humans.

Dr Mootha said: “It may not be a treatment for all types of neurodegeneration, but it’s a powerful concept – one that might shift how we think about treating some of these diseases.”