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Recently, we found that semaglutide therapy post-stroke can prevent ischemia-induced neurotoxicity and normalize neurogenesis and proliferation of stem cells in the brain via inhibition of p38 MAPK/MKK/c-Jun activity, regulation of Bcl-2/Bax pathways, and C-raf/ERK/caspase-3, restoration of insulin signaling sensitivity, and normalization of the ERK1 and IRS1 pathways ( DMB (GLP-1Ragonist/Modulator) The GLP-1R agonist quinoxaline 6,7-dichloro-2-methylsulfonyl-3-N-tert-butylaminoquinoxaline (DMB
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