Myelin is an essential biological structure that allows the nervous system to transmit information rapidly and efficiently. It is produced by specialised glial cells called oligodendrocytes in the central nervous system. When myelin is damaged, lost, or not properly maintained, neurological function can be severely affected. This is relevant to several neurodevelopmental, neurodegenerative and demyelinating conditions, including multiple sclerosis.
SUMOMyePath addressed an important knowledge gap in myelin biology: whether SUMOylation, a reversible molecular modification that regulates protein function, localisation and interactions, contributes to oligodendrocyte development, myelin formation and demyelinating pathology. While SUMOylation is known to regulate many cellular processes, its role in oligodendrocyte biology and myelin-related disease mechanisms remains insufficiently understood.
The overall objective of the project was to explore SUMOylation as a novel regulatory pathway in myelin biology, with the long-term aim of identifying new molecular mechanisms that may contribute to demyelinating disease and future remyelination-oriented strategies. The project combined molecular and cellular biology, glial-cell models, myelin biology and training in advanced neuroscience approaches. Its pathway to impact was based on generating mechanistic knowledge, developing experimental know-how and enabling resources, and strengthening future research capacity in the field of oligodendrocyte and myelin biology.
In the wider European context, the project contributes to the need for better understanding of chronic neurological diseases, improved research capacity in neurobiology, and training of highly skilled researchers able to work across molecular neuroscience, disease modelling, open science, communication and responsible research practice.
