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In animal models, studies show that the lack of PINK1 resulted in abnormal mitochondrial morphology, loss of SNpc DA neurons, reduction in complex I activity, and enhanced vulnerability to oxidative stress (Yang et al., 2006

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doi: 10.1016/j.scib.2021.01.008 160 ZhangLHuangCCDaiYLuoQJiYWangKet al

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