The depletion of GSH in the brain is a common finding and is linked to loss of neurons, resulting in neurological diseases such as PD, stroke, and AD.[203, 204] GSH maintains redox homeostasis through binding to Fe2+ in the LIP to inhibit the iron‐dependent oxidization[205] and functions as the substrate of GPX4‐mediate lipid detoxification.[63, 64] Decreased levels of GSH in the brain were found in both animal models[206, 207] and autopsy specimens[208, 209] of AD. This evidence concerns the gene GPX4 and Parkinson disease.