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Project

To boost lesion repair in MS by promoting fatty acid uptake (R-12706)

Failure of remyelination underlies the progressive nature of demyelinating diseases such as multiple sclerosis (MS). Why endogenous repair mechanisms fail in these disorders is poorly understood, however, there is now strong evidence that this is related to the inability of oligodendrocyte precursor cells (OPCs) to differentiate into mature myelinating cells. Our preliminary findings indicate that fatty acid transporters are potent drivers of CNS repair by promoting the differentiation of myelin-forming oligodendrocytes. This project will use innovative techniques, transgenic mouse models and unique patient samples to identify the impact of fatty acid transporters on metabolic changes during oligodendrocyte differentiation and investigate whether these identified mechanisms can be used to promote CNS repair. The results of this study will provide further insight into the role of fatty acid transporters in OPC maturation and CNS repair and the therapeutic applicability of fatty acid transporter modulators in demyelinating diseases such as MS
Date:1 Jan 2022 →  31 Dec 2023
Keywords:Fatty acid transporter, multiple sclerose, Remyelination
Disciplines:Neurosciences not elsewhere classified