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These mechanisms could potentially explain A aggregation but they require further investigation, although difficult due to the high sensitivity of A aggregation to experimental conditions such as pH and oxygenation, and the influence of other factors in vivo such as A binding to lipids and cell surface gangliosides (Morgado and Garvey, 2015), ApoE (Xia et al., 2024), and potentially bacterial amyloids (Elkins et al., 2024)

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Moreover, Nrf2a key regulator of iron homeostasisis robustly activated by BL (Yao et al., 2020a,b), leading to increased production of NAD(P)H-dependent enzymes such as NQO1, suppression of NF-B signaling, and reduction of both -Syn aggregation and oxidative stressmediated neuroinflammatory damage (Lastres-Becker et al., 2016

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