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Future success will likely hinge on multi-target strategies that simultaneously inhibit -syn toxicity, rectify iron dyshomeostasis, and harness the supportive functions of gliaall tailored to disease stage and individual patient profiles

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To help answer this fundamental question, we have proposed and provided evidence for an adaptive exchange model: the limited pool of CUL1 constantly and rapidly scans the entire population of F-boxSKP1, ensuring timely recruitment of substrate bound F-boxSKP1 and the subsequent degradation of the substrates

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