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In the early stages of AD, ferroptosis may act as a co-trigger of A aggregation and tau hyperphosphorylation by promoting neuronal degeneration, driving microglial polarization, and compromising the integrity of the bloodbrain barrier (BBB)

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doi: 10.1007/BF00297496

or spontaneous oxidation of free GSH to GSSG) if plasma is not analyzed on the same day as collection

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Its core design aims to preserve the bone metabolism regulatory activity of hGH and eliminate its side effects such as growth promotion, hyperglycemia, and IGF-1 elevation