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The study sheds light on the complex molecular mechanisms underlying excitotoxicity, implicating p38 MAPKs and iGluRs as potential therapeutic targets for neuroprotection against excitotoxic injury in cerebral ischemia and other CNS disorders

Methylation Capacity Second, NNMT inhibition affects cellular methylation capacity: SAM is required for hundreds of methyltransferase reactions throughout the cell, and NNMT's consumption of SAM can deplete this critical resource, while the SAH produced by NNMT is a potent product inhibitor of many methyltransferases

Available from: JAMA Network (2020) Autoimmune Thyroid Disease in Women: Prevalence and Risk Factors

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