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One interpretation is that brain iron elevation in AD could be a reactive, possibly protective sequestration mechanism (for instance, immobilizing iron in plaques or ferritin)

doi: 10.1016/j.pbiomolbio.2021.05.010

10.1038/tp.2012.143 12 FryeR

Similarly, SF pretreatment protected neural cells against A-fragment cytotoxicity and apoptosis in part through upregulation of Bcl-2 [169]

Flip-flop pharmacokinetics was present in the model and the apparent half-life of approximately 6 h was determined by the absorption rate (Table 2)

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