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Multiple sclerosis—oligodendrocytes from stem cells

October 19th, 2017
multiple sclerosis
Demyelination by MS. The CD68 colored tissue shows several macrophages in the area of the lesion. Original scale 1:100. Credit: CC BY-SA 3.0 Marvin 101/Wikipedia

Multiple sclerosis is an autoimmune disease of the central nervous system (CNS) with unknown aetiology, characterized by a loss of a particular glial cell type, the oligodendrocytes. These cells are highly specialized and provide electrical insulation to neuronal connections, thereby speeding up signal propagation in the brain and spinal cord.

If these oligodendrocytes are damaged or destroyed, the axons, the signalling projections of neurons, are unsheathed, becoming vulnerable and functionally impaired. It is therefore of considerable interest to repair such lesions and to support the diseased CNS in generating new oligodendrocytes.

Within the brain and spinal cord are immature cell types that could be activated and redistributed, and which have the potential to become oligodendrocytes, among them the adult neural stem cells. Unfortunately, this repair process is far from efficient, and in many cases, fails to provide regeneration and functional recovery to patients with MS. Such limitations unfortunately also account for neural stem cells.

Janusz Jadasz, the first author of a study published in the journal GLIA, reports that the interaction and communication of two stem cell types can strongly promote oligodendrogenesis—mesenchymal stem cells originating from bone, and adult neural stem cells. The team looked at different subprocesses, investigated a number of molecular markers and studied conservation in both humans and rats. They clearly demonstrated that the mechanism is valid for the generation of human oligodendrocytes, which makes their observations interesting regarding clinical translation.

More information:
Janusz J. Jadasz et al, Human mesenchymal factors induce rat hippocampal- and human neural stem cell dependent oligodendrogenesis, Glia (2017). DOI: 10.1002/glia.23233

Provided by Heinrich-Heine University Duesseldorf

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