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Although astrocyte dysfunction and iron dysregulation are increasingly recognized in AD pathology, their direct causal link to disease progression—and particularly to hypothesized central mechanisms such as ferroptosis—requires further validation in human contexts
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Vega et al., 1998), as well as subsequent disruption of the active GSTP1-1 dimer (Jenkins et al., 2007), which is also explained by its importance in dimerization (Chang et al., 1997a,b
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