Brain damage caused by devastating inherited diseases can be reversed simply by breathing thin air, an early study suggests.

The results, from research on mice, hint at the possibility of using oxygen deprivation to prevent or even reverse mitochondrial disorders, say scientists.

Mitochondrial diseases are caused by defective DNA in the mitochondria - tiny rod-like power plants in cells that supply energy.

They are only passed on to children from their mothers and can cause a wide range of conditions including muscle wasting, heart, liver and kidney damage, visual and hearing problems, and learning disability.

One type of mitochondrial disorder is known as Leigh syndrome and affects muscles and growth, leading to early death from respiratory failure.

Scientists studying mice genetically engineered to develop a form of Leigh syndrome found that halving the amount of oxygen in their air more than quadrupled the animals' lifespan from 58 to 270 days.

Scans showed no evidence of tell-tale lesions, or sites of damage, in mouse brains associated with neural degeneration.

Lead researcher Dr Vamsi Mootha, from Howard Hughes Medical Institute in the US, said: "We found, much to our surprise and delight, that we could actually reverse advanced disease.

"I don't think anybody thought that these types of neurological diseases could be reversible."

The air the mice breathed contained 11% oxygen, compared with the 21% found in normal air at sea level. This is similar to what climbers would encounter at Mount Everest base camp, at an altitude of about 17,000 ft.

While certainly not "super comfortable", a healthy person would be able to tolerate it, said Dr Mootha.

Previous research from the same team published in the journal Science last year showed that hypoxia, or oxygen deficiency, appeared to improve the health of mice with defective mitochondria.

The new research, reported in the journal Proceedings of the National Academy of Sciences, goes much further and indicates that oxygen deprivation actually reverses existing brain damage caused by mitochondrial disease.

Magnetic resonance imaging (MRI) scans revealed that after a month of breathing low-oxygen air, lesions in the mouse brains had disappeared.

Dr Mootha said the findings were "profound and striking" but stressed the research was still at an early stage and a long way from benefiting patients.

"We are not ready yet to go into the clinic," he added.

Exactly how being deprived of oxygen counteracts the effects of mitochondrial disease is still unknown.

The team plans to investigate molecular pathways triggered by low-oxygen conditions that may help to protect and repair the brain.

The findings have wider implications because neurodegenerative conditions associated with ageing are linked to weakened mitochondria.

"As all of us age, our mitochondrial activity declines," said Dr Mootha. "Hypoxia, or a drug that mimics a key aspect of it, might one day be able to rejuvenate flagging mitochondria, and perhaps the ageing body, too."

Mitochondrial disorders are at the heart of the controversy over so-called "three parent baby" treatments.

Doctors in Newcastle plan to replace damaged mitochondria in human embryos using healthy egg cells from the "third" parent, a female donor.

The UK is the first country in the world to support mitochondrial replacement treatment (MRT), which crosses an important line by altering human DNA that is passed onto future generations.

Scientists stress that mitochondrial DNA accounts for only around 0.1% of a person's genetic material and does not affect key human characteristics such as personality and eye colour.