You are here

Researchers generate a brain cell type crucial to support neural activity

MÁLAGA (ES), November 2020 — The loss of oligodendrocytes (OLs) – highly specialized cells of the brain that produce myelin, an essential structure enabling an efficient transmission of electrical signals and the support of neural activity – is a frequent condition in patients suffering neurodegenerative diseases. Researchers in the Department of Cellular Biology, Genetics and Physiology at the University of Malaga (UMA) have succeeded in generating human OLs from pluripotent stem cells derived from patients with nervous system diseases, specifically multiple sclerosis or ALS.

This is a new method that is faster and more efficient, because it enables the generation of OLs in just three weeks. The study is published in Nature Protocols.

"So far, no one has developed any treatment that reverts the loss of myelin and OLs in these patients, probably because there hasn't been an appropriate platform available to study these phenomena," said Juan Antonio García-León, Ph.D., the study’s main author.

The generated cells are equivalent to the OLs of a human brain, and they produced myelin around neurons when transplanted in the brain of an animal model, according to Dr. García-León. The cells could be used to advance the search for efficient treatments that favor myelination. A biotechnology company already uses this new method to develop a drug to revert myelin loss involved in multiple sclerosis, something crucial to counteract its symptoms and pathologies.

Although the studies on the alteration of OLs and myelin in patients with neurological diseases such as Alzheimer's disease or schizophrenia are still limited, some recent studies argue its fundamental role in these conditions. The UMA is working in collaboration with other national and international R&D&I groups on the application of this new technology in those diseases in which its exact involvement is unknown.

Learn more:
https://www.eurekalert.org/pub_releases/2020-11/uom-rga111220.php
DOI: 10.1038/s41596-020-0395-4