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Some experimental models indicate that GHK-Cu may regulate fibrosis-related gene pathways, suggesting a possible role in conditions involving abnormal tissue scarring

One possible explanation is that the host environment resulting from a localized excitotoxic lesion differs fundamentally from that of a chronically degenerating brain burdened with aggregated proteins such as alpha-synuclein or huntingtin

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LASSO regularized partial correlation network analyses were performed to model unique interactions between symptoms