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Several independent reports have indicated that -synuclein exerts its action by associating with -synuclein and subsequently a) elongating the lag phase of fibrillation (Jain et al., 2018) and b) arresting secondary nucleation (Hayashi and Carver, 2022)

Maintaining high intracellular GSH expression preserves redox status, allowing cells to respond to proliferative and differentiation signals in tissue after toxin injury (22) and rapidly supplement GSH during pro-oxidant anticancer therapy

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