What is it about?

Here we describe a novel astrocyte-dependent mechanism contributing to CNS demyelination. The key molecular and functional checkpoint is the receptor TrkB, which enhances copper distribution mediated by the astrocyte in response to inflammatory and toxic signals, thereby fostering myelin and oligodendrocyte loss.

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Why is it important?

This is the first description of copper transport dysregulation in multiple sclerosis.


Restoration of copper homeostasis is a necessary therapeutic goal to hamper demyelinating processes.

Cinthia Farina
IRCCS San Raffaele Scientific Institute

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This page is a summary of: Dysregulated copper transport in multiple sclerosis may cause demyelination via astrocytes, Proceedings of the National Academy of Sciences, June 2021, Proceedings of the National Academy of Sciences,
DOI: 10.1073/pnas.2025804118.
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