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In Alzheimers disease, the production of pro-inflammatory factors and A can over-activate microglia, secrete inflammatory factors and neurotoxins, and then induce neuronal damage and even apoptosis, thereby triggering Alzheimers disease

doi: 10.1017/S0029665110000042

We thought that a more nucleophilic site, to accommodate with selenium catalyst temporarily, might be helpful for competing with the deactivation

930 These findings suggest that inhibition of TRPM2 may provide an effective treatment strategy for diseases associated with ferroptosis

Documentation was readily accessible

Symptoms include nausea, increased intracranial pressure, coma, and even death (20)