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at low physiological concentrations, zinc serves a twofold function of both neutralizing the negative charge density at the C terminal of α-synuclein and assists other chaperones which work in a concerted manner to prevent aggregation of α-synuclein, whereas at higher concentrations, zinc promotes fibrillation by binding to His50 at the N terminus and lowering its pK a , much like that observed in case of iron (Valiente-Gabioud et al., 2012)
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