In our laboratory, we focus on studying the neurological component of demyelinating pathologies, with a specific emphasis on investigating the molecular mechanisms responsible for myelination processes in the Central Nervous System (CNS). We know that proper myelination is crucial for the correct transmission of nerve impulses. In the CNS, oligodendrocytes play a fundamental role in myelinating neuronal axons, a complex process involving multiple cellular interactions. Diseases resulting from improper myelination, such as Multiple Sclerosis or leukodystrophies, currently lack effective treatments.

Therefore, understanding the molecular mechanisms responsible for oligodendrocyte maturation and how oligodendrocyte-neuron interaction is established is crucial for advancing the study of these myelin diseases. Our group has demonstrated the importance of R-Ras1 and R-Ras2 GTPases, essential proteins in oligodendrocyte differentiation and survival, as well as in maintaining energy homeostasis.

Our experimental models, lacking R-Ras1 and/or R-Ras2, faithfully reproduce the symptomatic characteristics of myelin diseases, suggesting that they could be used as models for the development of new treatments based on the neurological component. Overall, our work seeks to shed light on the molecular processes underlying demyelinating pathologies and open new avenues for the development of effective therapies.