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Any increases in iron uptake or reduced capacity for iron storage contributes to iron overload and the potential to generate highly reactive hydroxyl radicals through the Fenton reaction

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The mechanism is well-characterized and scientifically sound NNMT overexpression in obese adipose tissue is well-documented, and its inhibition does restore metabolic function in cell culture and animal models

Excessive iron promotes hydroxyl radical (OH) generation via the Fenton reaction, thereby exacerbating lipid peroxidation and oxidative injury, which in turn facilitates A aggregation, tau hyperphosphorylation, and neuronal degeneration (Pei et al., 2025