If, indeed, oxidative stress is implicated in Parkinson’s disease, finding a way to relieve it might slow mitochondrial deterioration. Typically, antioxidant dietary supplements don’t help, probably because they can’t get through the mitochondrial membrane into the matrix, where free radicals are produced. To address that problem, Mike Murphy designed MitoQ with a positive charge so that it would be drawn in by the mitochondria’s negative charge.

Now the larger Phase II trials should show how well MitoQ, a powerful antioxidant, works in humans and help determine whether oxidative stress does play a major causative role in Parkinson’s—and, potentially, in a number of other diseases, including Alzheimer’s, amyotrophic lateral sclerosis (ALS) and even migraines. If MitoQ works for Parkinson’s, it might also prove effective against those other diseases.

In the case of type 2 diabetes, one of today’s most prevalent diseases, evidence for a possible mitochondrial link stems from the observation that mitochondria of diabetics have a reduced ability to produce energy. In 2003, Vamsi Mootha, a systems biologist at the Massachusetts General Hospital and the Broad Institute in Cambridge, decided to test whether a genetic approach, using a device known as a gene chip, could help isolate the problem. (Gene chips are quartz plates the size of a postage stamp spotted with every human nuclear gene, but not mitochondrial DNA. Manufacturers chemically attach more than 20,000 bits of DNA at specified coordinates on the plate.)

In his study, Mootha and his team poured a batch of RNA—the intermediary molecule DNA uses to make proteins—from the muscles of diabetics over 17 chips. To 18 others they applied RNA from the muscles of nondiabetics. He knew that if the RNA stuck to the DNA on the chip and fluoresced under a special light, the genes were actively producing proteins.

The results were striking. The dots for genes involved in energy production pathways—and linked to mitochondria—were much dimmer in diabetics than in those without the disease. It appeared whole sets of energy-production genes were associated with diabetes. “No single gene showed a striking difference in expression between the diabetics and the controls, probably because diabetes is a complex disease,” Mootha says. “Rather, we’re seeing a general decline in mitochondrial numbers and activity,” suggesting diabetic muscles can’t produce energy as well as nondiabetic muscles.

Mootha and others don’t yet know whether dysfunctional mitochondria cause diabetes, are a by-product of the disease or are simply an unrelated correlative condition. Still, these results strengthen the hope for one simple remedy. “It has long been known that exercise increases mitochondrial content and efficiency,” Mootha says.