Core Insights - The acceleration of aging society has led to increased attention on neurodegenerative diseases such as Alzheimer's and Parkinson's, with nearly 10 million new cases of Alzheimer's reported annually by the World Health Organization [1] - Recent research from French and Canadian institutions has demonstrated that enhancing mitochondrial function can reverse memory deficits in mice, providing new insights into the mechanisms of neurodegenerative diseases and potential treatment pathways [1][2] Group 1: Research Findings - Mitochondrial dysfunction is closely related to neuronal damage, as mitochondria are responsible for energy production in high-energy cells like neurons [1] - The newly developed DREADD tool allows for direct manipulation of mitochondrial function, leading to a 10% increase in mitochondrial activity in activated neurons, which significantly improves memory deficits in mouse models of Alzheimer's and frontotemporal dementia [2][3] - Activation of the mitochondrial "switch" enhances energy metabolism, increases synaptic activity, and reduces inflammation, collectively promoting memory function recovery [3] Group 2: Implications and Future Directions - The study highlights the potential of targeting mitochondria for therapeutic interventions, contrasting with previous indirect methods that yielded limited effects [3] - Clinical application of these findings faces challenges, including reliance on viral vectors for activation and the complexity of human diseases compared to mouse models [3] - Future research will explore the mechanisms in different brain regions and cell types, as well as assess the long-term effects of enhanced mitochondrial activity on disease progression and neuronal survival [3]