Published in the scientific journal EMBO Reports, the new research in fruit flies suggests that, at the right dose and in the right form, a "brief release of these unstable and reactive molecules, produced by glial cells, the brain's supporting tissue, may actually help in brain repair."

The discovery comes after decades in which molecules called reactive oxygen species – free radicals – were considered the "villains of the brain, responsible for mechanisms associated with ageing, neurodegeneration, and damage caused by strokes or trauma," the FC added.

In a statement, the foundation explained that "oxidative stress" is a direct consequence of an excess of so-called free radicals in the body, which can be caused by lifestyle, environmental, and biological factors such as smoking, high alcohol consumption, poor diet, stress, pollution, radiation, industrial chemicals, and chronic inflammation.

When this occurs, an imbalance arises between the production of free radicals and the body's antioxidant defences, which neutralise them.

"When we hear about oxidative stress in the brain, it's almost always bad news, associated with ageing, Alzheimer's disease, and other neurodegenerative diseases," the FC stated, adding that the study released today "shows that a brief and well-controlled pulse of oxidative stress, immediately after an injury, can actually help the brain repair itself."

In this investigation, Christa Rhiner, principal investigator at the CF Stem Cell and Regeneration Laboratory, and her team demonstrated that, following a small brain injury in adult flies, a specific group of brain support cells, known as glia, rapidly release a pulse of chemically reactive forms of oxygen, including hydrogen peroxide.

“This controlled ‘oxidative spark’ does two things at once: it activates protective antioxidant processes in the glia and, crucially, acts as an activation signal for cells that are normally inactive, leading them to divide and replace lost tissue,” the statement said.

The team identified the enzyme responsible for this pulse of free radicals as Duox, a membrane-bound enzyme present in glial cells that produces hydrogen peroxide outside the cells.

“This was surprising, as we initially thought that mitochondria – the tiny batteries of cells – would be the main generators of oxidative stress in the injured brain,” explained first co-author Carolina Alves.

When researchers genetically reduced Duox activity or decreased reactive oxygen levels with antioxidant treatments, the injured brains of flies produced fewer new cells, and the regenerative response was substantially attenuated.

Conversely, stimulating glia to increase Duox activity was sufficient to trigger additional cell divisions, even in the absence of injury, the FC noted, highlighting that this means that, in particular, glial-derived hydrogen peroxide is a “powerful driver of brain plasticity.”

“These results challenge the simplistic idea that oxidative stress in the brain is always harmful and may help explain why broad-spectrum antioxidant therapies largely fail to improve brain recovery in patients after injury,” the FC emphasised.

In the future, more targeted strategies that mitigate harmful chronic oxidative stress by preserving – or even harnessing – these short-lived oxidative signals “could open new avenues for promoting brain repair,” the researchers considered.