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While SCA3 has an adult onset, alterations in the CNS precede symptom appearance [166, 167]: therefore, correcting the mutation in ATXN3 in the disease state might not be fully beneficial, as neurons could already have irreversible changes
In biochemical and cellular research, GHK-Cu is widely studied for its role in peptidemetal interactions, extracellular matrix signaling, copper-dependent molecular regulation, and cellular communication pathways
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Experiments using FITC-phalloidin staining have revealed that BPC-157 is a potent stimulator of F-actin formation in fibroblasts [11]
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