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[...]despite a successful recanalization being achieved in more than 70% of patients treated with mechanical thrombectomy +/– intravenous tissue recombinant plasminogen activator, functional independence (modified Rankin score 0–2 at 3 months after ischemic stroke) is obtained only in ~45% of cases. No reflow can occur within 5–10 minutes of ischemia in the brain, and may, therefore, contribute to neuronal death, whereas in the heart it only occurs after 30+ minutes and its contribution to cell death is less clear. [...]the time window for neuroprotection at reperfusion is presumably wider than that for cardioprotection. GLP-1 is known to be a growth factor with its classical inherent effects, i.e. activation of the expression of genes responsible for cell growth, repair and replacement, increase of cell metabolism, and inhibition of apoptosis and inflammatory responses (Hölscher, 2014). Regarding the rationale of using the same pharmacological approach based on GLP-1 analogues for neuroprotection as for cardioprotection, there are important data from in vitro studies, which indicate that the GLP-1R agonists possess a neurotrophic property, reduce oxidative stress, and protect cortical neurons from hypoxia-triggered cell death (Salcedo et al., 2012).