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Particular focus should be placed on interactions between mHTT, the ironmetabolism axis (such as transferrin receptor 1 and hepcidin), and key ferroptosis mediators (GPX4 and Nrf2) to build a dynamic model linking mHTT aggregation, iron dysregulation, and neuronal ferroptosis, and to define subtype-specific vulnerability of MSNs
I mean, the brain isits a small part of the body, but its massively outsized in terms of the energy that it consumes
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