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Figure 9 In summary, although current studies demonstrate that ferroptosis plays a central regulatory role in the pathogenic cascade of HD—linking mHTT aggregation, neuroinflammation, and neuronal loss—and provide a new mechanistic basis for understanding the sequence of basal ganglia iron accumulation, striatal atrophy, and motor dysfunction, several fundamental limitations remain

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One key player in this response is posited to be MST1, a protein that increases its activity in the presence of oxidative stress