Study Finds Mfsd2a Has Critical Role in Protecting Myelin Sheaths

Scientists from Duke-NUS Medical School and the National University of Singapore have discovered the crucial role of a special transporter protein called Mfsd2a in myelination. The research, published in the Journal of Clinical Investigation, may hold the key to reducing the effects of aging on the brain and mitigating the risk of neurological disorders.

Mfsd2a, short for Major Facilitator Superfamily Domain containing 2a, is a protein that transports lysophosphatidylcholine (LPC), a lipid that contains omega-3 fatty acids, into the brain as part of the myelination process. Genetic defects in the Mfsd2a gene have been linked to significantly reduced myelination and microcephaly.

In the study, the team removed Mfsd2a from precursor cells that mature into myelin-producing oligodendrocytes in the brain. This led to deficient myelination after birth. Further research demonstrated that the absence of Mfsd2a caused a reduction in fatty acid molecules, particularly omega-3 fats, in precursor cells. This prevented the cells from maturing into oligodendrocytes that produce myelin.

The findings have significant implications for the development of therapies to improve myelination in aging and disease. According to David Silver, senior author of the study, the study indicates that LPC omega-3 lipids act as factors within the brain to direct oligodendrocyte development, a critical process for brain myelination. Potential avenues for developing therapies and dietary supplements based on LPC omega-3 lipids have been opened up. The research team is now aiming to conduct preclinical studies to determine if dietary LPC omega-3 can help re-myelinate damaged axons in the brain.