Multiple sclerosis (MS) is a chronic complex neurological disease of the central nervous system (CNS), which affects 2.3 million people worldwide. One of the main pathological characteristics of multiple sclerosis is demyelination, which involves the injury and loss of myelin sheaths. Myelin is a material that surrounds the part of the neurons that transmit electric impulses from one neuron to the next one (axons). When myelin is intact, axons are insulated, and the electric impulses are transmitted efficiently. However, during demyelination, myelin is damaged, and these nerve impulses are slowed down causing different symptoms in the patients. There is a natural process in the brain, called remyelination, that can partly or completely repair these demyelinated lesions. However, this process is often disrupted in multiple sclerosis patients.
The cause of MS is still unknown, but it has been proposed that some genetic and environmental factors are related to MS pathology. microRNAs (miRNAs) are involved in the interaction between these genetic and environmental factors. miRNAs are molecules that can regulate the expression of different genes and have been found altered in several diseases. Specifically in MS, miRNAs have been found to be dysregulated in different tissues and biological fluids.
All current disease-modifying therapies in MS are unable to prevent the progressive accumulation of disability and to induce the endogenous repair of the brain. Thus, it is critical that innovative therapeutics that can promote remyelination are designed to address this deficit to treat MS patients. The main research goal of MiRepair project was to identify potential miRNAs related to demyelination and remyelination and to study their therapeutic potential to enhance remyelination in MS.
The findings of the project suggests that a specific miRNA and its target genes are potential candidates to enhance remyelination, neurorepair and reduce neuroinflammation in MS.
