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This pathophysiological dichotomy presents a significant therapeutic challenge, wherein the essential intervention of reperfusion simultaneously triggers molecular cascades that can potentially exacerbate tissue damage and compromise clinical outcomes (Chen et al

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Thus, the whole results strengthen the hypothesis that Semax could interfere with oligomeric species formed by Aβ 1–40 , which in turn are responsible for the kinetics of fiber formation and the consequent disruption of model membranes