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In PD models, the use of dependent sodium channel blockers reduces glutamatergic hyperactivity and inhibits abnormal glutamate release, suggesting that amino acid metabolism disturbances may contribute to neurotoxicity and oxidative toxicity, ultimately resulting in dopaminergic neuron death [85]

The findings of some of the clinical trials in which lipoic acid administration has been tested in diabetic patients during the last 10 years are summarized

10.1126/science.1164382 211 PasiniB.StratakisC

This suggests that the cells rely on GPX4 to resist oxidative stress, and this could potentially increase their sensitivity to RSL3, a ferroptosis inducer that targets GPX4

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