Therefore, the dual action of ThA in targeting Aβ/tau proteins and activating the Nrf2/GPX4 pathway affects multiple pathological processes, from oxidative stress and mitochondrial dysfunction to neuroinflammation and ferroptosis, implicated in AD underscoring its therapeutic potential in mitigating AD pathology by preventing ferroptosis and neuronal cell death. This evidence concerns the gene NFE2L2 and Alzheimer disease.