Determining how brain glial cells and myelin age and get sick in neurodegenerative diseases (e.g., Alzheimer´s and multiple sclerosis) is essential to unveil drugable targets to develop new therapeutic strategies with drugs that slow the progression of these diseases and improve patients' quality of life. To do so, we are currently exploring the potential of human brain organoids derived from Alzheimer´s patients and neuroprotective drugs targeting myelin and glial neurotransmitter receptors.

Recent MRI studies led by our laboratory revealed that marathon runners experience a significant decrease in myelin water fraction (MWF) after completing a marathon, affecting both white and gray matter. This MWF reduction, involving key brain areas, recovers within two months, suggesting a novel metabolic plasticity where myelin serves as an energy source during extreme conditions. These findings challenge the traditional view that neuronal function depends solely on glucose and oxygen, highlighting myelin's role in brain energy metabolism. Understanding this process could provide insights into brain aging and neurodegenerative diseases, where diminished glial support might lead to metabolic deficits and neuronal damage.