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It has been shown to be secondary to intramuscular NH3 accumulation, resulting in activation pathways that contribute to sarcopenia.45 In that line of thought, it is easy to imagine that the inhibition of ActRIIB or the minimization of GDF-8 expression could be new treatment alternatives

Unfortunately, the majority of promising therapies in animals have failed to successfully translate into clinical therapies for HT (66), and we are still lacking applicable translational therapeutic options to reach the CNS

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