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Selenoprotein P (Sepp1) and its receptor, apolipoprotein E receptor 2 (apoER2), account for brain retaining selenium better than other tissues, Sepp1-apoER2 interactions supply selenium for maintenance of brain neurons, to protect the severe neurodegeneration and death in mild selenium deficiency [33]

reported plasticity of CA3-CA1 synapses after pairing of GDPs with Schaffer collateral stimulation in hippocampal slices during the first postnatal week of development (Mohajerani et al

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CagriSema shows less discontinuation, however increased rates of vomiting and nausea

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