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mHTT disrupts mitochondrial function, leading to iron (Fe 2+ ) accumulation in striatal neurons, Fenton reaction-induced ROS, and lipid peroxidation

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Thus, BED appears to involve GLP-1 dysregulation without consistent endocrine abnormalities, implying that GLP-1 RA therapy works through supraphysiological receptor activation and modulation of central reward circuitry, rather than by correcting a hormonal deficit [55]