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Degradation or autophagy of ferritin in response to other regulators such as autophagy-associated protein (Atg) and Nuclear receptor coactivator 4 can result in release of Fe2+ from ferritin into the LIP [52]

Therefore, investigating subcellular dysfunction, particularly mitochondrial abnormalities, is critical for understanding how these risk factors converge to drive oxidative stress and metabolic derangements

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Furthermore, transport of GSH and/or GSH precursors via astrocytederived extracellular vesicles to neurons has been proposed as a process to supply neurons with GSH precursors (PrezSala and Pajares 2023)

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