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Notably, in addition to trying to block potential downstream detrimental effects, new therapies need to be designed that preserve and boost astrocytic defences and improve astrocytic homoeostasis

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While failure of these compensatory mechanisms could ultimately cause ferroptotic cell death, more subtle changes in intracellular redox balance could also enhance signaling pathways, including those associated with T2 inflammation (10)

activation of cytochrome c and the apoptotic machinery

However, from postnatal days 10 to 14, dendrites of PCs grow extensively and the presence of GluR2 becomes exclusively abundant at their dendritic spines, leading to synaptic targeting [16, 49]

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