The fountain of youth may not be a fountain at all, but an area of the brain the controls growth, reproduction and metabolism. According to a study recently published in Nature, a molecule that controls DNA transcription—and controls the body’s reaction to stress—in the hypothalamus becomes more active as laboratory mice grow older. When scientists at the Albert Einstein School of Medicine in New York injected mice with a substance that inhibited the stress-related hormone, they lived 20-percent longer. Not only did the mice live longer, but their muscle strength, bone density and skin retained more youthful qualities, even when middle-aged mice were injected.

If the experiment garnered similar results in humans, it could mean an extra 20 years of life. It’s long been known that stress and inflammation make people look and feel older. But the study actually shows that it may be our brains initiating these reactions rather than external stimuli.

“We have provided scientific evidence for the concept that systemic aging is influenced by a particular tissue in the body,” said Donghsheng Cai, a physiologist at Albert Einstein College of Medicine.

According to Richard Miller, a scientist at the University of Michigan in Ann Arbor, previous studies have noted how long mice lived after treatment, but the Albert Einstein experiment actually looks at different aspects of age-specific functions. “It makes a much stronger case that the whole aging process has in some ways been decelerated.”

Researchers tested the mental and physiological abilities of the mice six months after their initial injections. They found mice injected with the inhibitor performed better than control subjects on tasks designed to test both cognition and movement.

Should the research ultimately be applicable to humans, scientists hope it will be stimulate new treatments in age-related illnesses linked to inflammation, such as Alzheimer’s, diabetes and arthritis.

“If we’re going to translate this research into medicines that can help people, clearly we cannot start very early in life,” David Sinclair, a molecular biologist at Harvard Medical School, said.