A New Way of Looking at Aging Brain: Could a Common Supplement Be the Key to Treating MS And Alzheimer’s?

A recent study shows alternative therapies that may be better at treating neurological diseases, such as multiple sclerosis and Alzheimer’s disease as we get older.

Researchers from Duke-NUS Medical School and the National University of Singapore have identified a crucial role played by a special transporter protein in regulating brain cells that protect nerves with myelin sheaths.

The findings, reported in the Journal of Clinical Investigation, could help reduce the detrimental effects of aging on the brain.

Myelin sheaths, which act as an insulating membrane surrounding nerves, facilitate the rapid and efficient transmission of electrical signals throughout the body’s nervous system.

Damage to myelin sheaths can cause neurological disorders and a loss of nerve function. As people age, the natural degeneration of myelin sheaths can contribute to the decline of physical and mental abilities in older individuals.

“Loss of myelin sheaths occurs during the normal aging process and in neurological diseases, such as multiple sclerosis and Alzheimer’s disease,” explains lead author Dr. Sengottuvel Vetrivel. “Developing therapies to improve myelination—the formation of the myelin sheath—in aging and disease is of great importance to ease any difficulties caused by declining myelination.”

To lay the groundwork for potential therapies, the researchers aimed to comprehend the function of Mfsd2a, a protein that transfers lysophosphatidylcholine (LPC) — a lipid containing an omega-3 fatty acid — into the brain during the myelination process.

Studies have shown that genetic mutations in the Mfsd2a gene result in significantly lower myelination and a birth defect known as microcephaly, which causes the baby’s head to be smaller than normal.

Using preclinical models, the team demonstrated that the removal of Mfsd2a from precursor cells that develop into oligodendrocytes — cells that generate myelin in the brain — leads to inadequate myelination following birth.

Further analyses, including single-cell RNA sequencing, revealed that the lack of Mfsd2a caused a decrease in the pool of fatty acid molecules, particularly omega-3 fats, in precursor cells, preventing their maturation into oligodendrocytes that create myelin.

This study shows “that LPC omega-3 lipids act as factors within the brain to direct oligodendrocyte development, a process that is critical for brain myelination,” says senior author Professor David Silver.

“This opens up potential avenues to develop therapies and dietary supplements based on LPC omega-3 lipids that might help retain myelin in the aging brain,” adds the author, “and possibly to treat patients with neurological disorders stemming from reduced myelination.”

Previously, Professor Silver and his research team made a groundbreaking discovery of Mfsd2a, and collaborated with other research groups to study the role of LPC lipids in the brain and other organs.

The latest research has provided further insights into the crucial role of lipid transport in the development of oligodendrocyte precursor cells.

Professor Silver commented that their next step is to carry out preclinical studies to investigate whether dietary LPC omega-3 can aid in re-myelinating damaged axons in the brain.

The hope is that supplements containing these fats can potentially help maintain or even enhance brain myelination and cognitive function during aging.

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