Science finds way to reverse memory loss

A groundbreaking study by a team of scientists at INSERM (French National Institute of Health and Medical Research), the University of Bordeaux (France) and the University of Moncton (Canada) has established for the first time a direct causal link between mitochondrial dysfunction and memory loss in neurodegenerative diseases.

Not only that, they also created a new tool that increases mitochondrial activity in a mouse model of the disease, thereby restoring memory ability.

Mitochondria are tiny organelles inside cells that are responsible for producing the energy needed for all life activities. The brain is the largest energy consumer in the body, and nerve cells (neurons) rely heavily on this energy to transmit signals. When mitochondria are not functioning properly, neurons are starved of energy, leading to decreased function.

In Alzheimer’s disease and many other neurodegenerative diseases, neuronal degeneration is often accompanied by mitochondrial dysfunction. However, scientists have long debated whether this is the cause of the disease or just a consequence of the pathological process, due to a lack of tools to directly verify it.

The team developed a new artificial receptor called mitoDreadd-Gs, which directly activates G proteins in mitochondria, thereby enhancing energy production. When applied to mice with amnesia, the results showed that mitochondrial activity was restored and their memory ability was significantly improved.

"This is the first time we have shown that mitochondrial dysfunction can be the root cause of neuronal degeneration, not just a consequence," said Giovanni Marsicano, research director at INSERM, who led the study.

Scientists have previously been unclear whether mitochondrial dysfunction in the brain is a cause or a consequence of neurodegenerative disease. New research has made it clear that mitochondrial “malfunction” occurs very early and is the cause of the onset of neurodegeneration, not just a consequence of the disease’s progression.

Professor Étienne Hébert Chatelain (University of Moncton) commented: "This discovery helps us better understand the key role of mitochondria in brain function. This new tool could pave the way for identifying the molecular mechanisms that cause dementia and developing more effective treatments."

The team is now continuing to test long-term mitochondrial stimulation to assess whether this approach can slow or prevent neurodegeneration.

If future trials prove long-term effectiveness and safety in humans, mitochondrial activation could become the basis for a range of new therapies that not only treat Alzheimer's, but also many other neurological diseases such as Parkinson's, spinal muscular atrophy, and traumatic brain injury.

Enhancing mitochondrial function may even have applications in preventing age-related cognitive decline, helping to extend “brain longevity” and improve quality of life for millions of people.