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We now demonstrate that GIPR agonist administration critically relies on Gipr expression in the hindbrain, while GIPR antagonism relies on hypothalamic Gipr expressionboth are probably neuronal populations, given that we used hSyn-driven Cre-expression for the region-specific knockout studies
In addition, given that microglia clearly exhibit functional NRF2 signalling [315], it could be an important target for NRF2 induction in neurodegeneration
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