https://www.selleckchem.com/pr....oducts/Pomalidomide(
It has been proposed that Amyloid β Precursor Protein (APP) might act as a rheostat controlling neuronal excitability, but mechanisms have remained untested. APP and its catabolite Aβ are known to impact upon synapse function and dysfunction via their interaction with the prion protein (PrPC), suggesting a candidate pathway. Here we test if PrPC is required for this APP function in vivo, perhaps via modulating mGluR5 ion channels. We engineered zebrafish to lack homologs of PrPC and APP, allowing us to assess their purport
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