A groundbreaking study published in *Nature Neuroscience* has demonstrated that faulty mitochondria, the cell's energy generators, may be directly responsible for cognitive decline in neurodegenerative diseases. Researchers from Inserm and the University of Bordeaux, in collaboration with the Université de Moncton, developed a tool to temporarily boost mitochondrial activity in mouse models of dementia, resulting in restored memory performance. This suggests that energy deficits in neurons could occur before brain cells die, potentially providing a new target for Alzheimer's treatments. The study establishes a crucial cause-and-effect relationship between mitochondrial dysfunction and cognitive symptoms, challenging the traditional view that mitochondrial issues are merely a consequence of neuronal degeneration. The researchers created an artificial receptor, mitoDreadd-Gs, which activates G proteins within mitochondria to enhance their function. While the findings are promising, further research is necessary to assess the safety and efficacy of similar approaches in humans. The study adds to a growing body of evidence that emphasizes the importance of mitochondrial health in the early stages of Alzheimer's disease and could pave the way for innovative therapeutic strategies.