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They found that oA caused neuronal toxicity with lowered DNMT activity, increased APP and PS1 expression, and decreased cell viability, each consequence of which could be prevented by folic acid via methylation-dependent pathways [145]

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In conclusion, on the basis of these studies, this review speculated that there may be two mechanisms of ferroptosis leading to obesity: (i) In the autonomic nervous system, vagus and parasympathetic nerves in some organs or tissues may be affected by ferroptosis and become dysfunctional, while the inflammatory factors released from adipocytes lead to excessive sympathetic activation and hypothalamic neuronal ferroptosis which promotes the development of obesity through a series of processes

doi:10.1016/0009-8981(79)90364-4 100