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Indeed, CNTF was shown to prevent disease associated denervation and axon pruning in the ALS SOD1-G93A mouse line discussed above [44]

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On the one hand, in some in vitro or animal models, enhanced BCAA catabolism has been reported to upregulate certain M2-related markers and support alternative activation programs, whereas inhibition of BCAA metabolism may impair the establishment of M2-like phenotypes (62)