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In a new study, Broad Institute researchers report that two small-molecule chemicals that reduce oxygen delivery to cells improved symptoms of neurodegeneration in a mouse model of Parkinson's disease. The scientists had previously found that excess oxygen in the brain is associated with neuronal death in Parkinson's—and that reducing the oxygen that mice breathe could help reverse symptoms.

The new study, published in the Proceedings of the National Academy of Sciences, also revealed that the two-drug combination extended life span and alleviated symptoms in a mouse model of Leigh syndrome and helped delay progression of neurological symptoms in a mouse model of Friedreich's ataxia. Leigh syndrome and Friedreich's ataxia are rare genetic disorders that occur when mitochondria, which generate energy in the cell, malfunction, often leading to high levels of unused oxygen that can damage tissues.

Vamsi Mootha, an institute member at the Broad Institute who led the new study, has found over the last decade that exposure to low-oxygen conditions improved symptoms in mouse models of these two rare diseases, which in humans affect the nervous system, are debilitating and can be fatal.

Mootha and his team say that the new drug regimen merits further preclinical and eventually clinical testing as a potential treatment for Parkinson's and some mitochondrial disorders.

"Mitochondrial dysfunction is associated with many different conditions, ranging from rare diseases to universal, age-related diseases," said Mootha, who is also a professor of systems biology and medicine at Harvard Medical School and a Howard Hughes Medical Institute investigator in the Department of Molecular Biology at Massachusetts General Hospital (MGH), a founding member of the Mass General Brigham health care system.

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