Scientists from Singapore have demonstrated the crucial role that a special transport protein plays in regulating brain cells that protect nerves with sheaths called myelin sheaths.
The findings, published in the Journal of Clinical Investigation by researchers from the Duke-NUS School of Medicine and the National University of Singapore, could help reduce the damaging effects of aging on the brain.
The myelin sheath, the insulating membrane surrounding nerves, facilitates the rapid and efficient conduction of electrical signals throughout the body’s nervous system. When the myelin sheath is damaged, nerves can lose their ability to function and cause neurological disorders.
As we age, the myelin sheaths can naturally begin to degenerate, which is often why seniors lose their physical and mental abilities.
“Loss of myelin sheaths occurs during the normal aging process and in neurological diseases such as multiple sclerosis and Alzheimer’s disease,” said Dr. Sengottuvel Vetrivel, senior research fellow in Duke-NUS’ Cardiovascular & Metabolic Disorders (CVMD) program and principal investigator of the study.
“The development of therapies to improve myelination – the formation of the myelin sheath – in aging and disease is very important to alleviate any problems caused by declining myelination.”
To pave the way for the development of such therapies, researchers sought to understand the role of Mfsd2a, a protein that transports lysophosphatidylcholine (LPC) a lipid that contains omega-3 fatty acids into the brain as part of the myelination process.
From what is known, genetic defects in the Mfsd2a gene lead to severely reduced myelination and a birth defect called microcephaly, which causes a baby’s head to be much smaller than it should be.
In preclinical models, the team showed that removing Mfsd2a from precursor cells that mature into myelin-producing cells – known as oligodendrocytes – in the brain led to insufficient myelination after birth. Further research, including single-cell RNA sequencing, showed that the absence of Mfsd2a caused a reduction in the amount of fatty acid molecules particularly omega-3 fats in the precursor cells, preventing these cells from maturing into myelin-producing oligodendrocytes.
“Our study shows that LPC omega-3 lipids act as factors in the brain that control the development of oligodendrocytes, a process that is critical for brain myelination,” explained Professor David Silver, lead author of the study and deputy director of the CVMD program.
“This opens up potential avenues for the development of therapies and dietary supplements based on LPC omega-3 lipids that could help maintain myelin in the aging brain—and possibly treat patients with neurological disorders resulting from reduced myelination.”
Previously, Professor Silver and his lab discovered Mfsd2a and worked closely with other teams to determine the function of LPC lipids in the brain and other organs. Current research provides further insights into the importance of lipid transport for the development of oligodendrocyte precursor cells.
“Prof Silver has been tireless in exploring the far-reaching role of Msdf2a since discovering this important lipid transport protein, hinting at many potential treatments not only for the aging brain but also for other organs in which the protein plays a role. ” said Professor Patrick Casey, Senior Associate Dean for Research. “It is exciting to watch Professor Silver and his team shape our understanding of the roles these specialized lipids play through their many discoveries.”
Written by: Vaishali verma
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