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In vitro experiments confirmed that A 25-35 treatment significantly inhibited the activation of the NRF2/SLC7A11/GPX4 signaling pathway in HT22 cells, upregulated the expression of Fe 2+ , TFR1, ACSL4, MDA, and GSSG, and decreased the expression of FTH1, SOD, and GSH, as well as the GSH/GSSG ratio, resulting in dysregulated neuronal iron metabolism, impaired amino acid antioxidant systems, mitochondrial dysfunction, and ferroptosis, which ultimately promoted neuronal injury

Ensuring adequate vitamin B12 intake can help prevent these issues

[93] In a more recent study, uPAR was found to improve physical aging phenotypes and alleviate metabolic syndrome

As mentioned, it is able to neutralize the reactive oxygen species that damage cells