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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
It has also been confirmed that AD pathologic markers, oligomeric A and A plaque load, could be reduced by LG and microglial activation is decreased and memory behaviors are improved in APP swe /PS1_E9 (APP/PS1) mouse model after using LG (74)
Unlike some other diabetes medications, GLP-1 drugs are smart enough to only trigger insulin release when you actually need it
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