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It's an essential cofactor that helps transport long-chain fatty acids into the mitochondria so that they can be oxidized to produce energy in the form of adenosine triphosphate (ATP)

Previously, OPN was shown to be up-regulated in MS lesions and in several experimental animal models for demyelination including the cuprizone model (Chabas et al., 2001

This suggests that a pre-existing deficit in the oxytocinergic system may be a prerequisite for beneficial outcomes of oxytocin treatment

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