COPPER, which like all metals can have a toxic effect, appears to play a role in multiple sclerosis. To suggest it is an Italian study of the RCCS San Raffaele Hospital in Milan led by Cinthia Farina and published on the pages of Pnas.
The discovery
Multiple sclerosis is an autoimmune-based disease characterized by the loss of myelin, the sheath that covers neurons, which is essential for the transmission of nerve impulses. As the researchers write, it is astrocytes (cells that support neurons in the nervous system) that are involved in regulating copper in the central nervous system (CNS), and in particular the TrkB receptors on their surface. The “crazy” action of the TrkB receptors ultimately leads to an excessive release of copper outside the cells, which has been linked to the loss of myelin.
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An important receptor
TrkB is a receptor for neurotrophins, substances involved in the development and protection of the nervous system. However, the researchers explain, these substances are not present at the level of the lesions observed in multiple sclerosis. So there must be something else that makes the receptor active. Thing? “We have shown that TrkB receptors can be activated, in the pathological context of MS, even in the absence of neurotrophins, because they respond to other signals, both inflammatory and toxic”, he replies Emanuela Colombo, first author of the research. And, thus unregulated, they contribute to the demyelination process: mice lacking the receptor on the astrocytes are in fact resistant to the process. The administration of a diet capable of inducing the loss of oligodendrocytes (the cells that produce the myelin sheath in the central nervous system) also confirmed the role of the receptor in animal models: mice without TrkB suffered less losses.
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The balance of copper and the loss of myelin
Thanks to observations in animals (without the receptor and subjected to the experimental diet), the researchers demonstrated that the expression of copper transporters depends on the TrkB receptor of astrocytes. The final effect observed is an increase in the release of copper by astrocytes and the loss of oligodendrocytes.
What has been observed leads us to believe that this receptor plays a fundamental role in contributing to the process of demyelination and damage, we read in the conclusions. And, perhaps, by acting at this level and influencing the balance (homeostasis) of the copper downstream, the damage itself could – conditionally obligatory, given the preliminary level of research – be contained.
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