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G., Pasternak, M., Wachter, A., Cobbett, C

These structural changes further support the notion that chronic ethanol exposure disrupts the neural circuits involved in mood regulation and cognitive function, ultimately contributing to the onset of depressive symptoms

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Mechanistically, GHK-Cu preserved mitochondrial function by increasing mitochondrial membrane potential, alleviating age-related mitochondrial network fragmentation, shifting mitochondrial dynamics toward fusion via regulating drp-1 and fzo-1 expression, and promoting ATP biosynthesis