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* Correspondence: Haoyu Wang, [email protected] These authors share first authorship Disclaimer All claims expressed in this article are solely those of the authors and do not necessarily represent those of their affiliated organizations, or those of the publisher, the editors and the reviewers

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It was discussed that this may be due to the possibility that other pathological mechanisms could underlie the progression of PDD, rather than amyloid-beta burden (Gomperts et al., 2012)

The association of APR-246 with induction of ferroptosis (either by pharmacological compounds, or genetic inactivation of SLC7A11 or GPX4) had a synergistic effect on the promotion of cell death, both in vivo and ex vivo