Reply to Altered Monoaminergic Systems and Depressive-like Behavior in Congenic Prion Protein Knock-out Mice

Nuvolone and Aguzzi (1) ascribed to the effect of a 129-Sirpa polymorphism, a macrophage phenotype we had previously attributed to PrP, and we acknowledge that comparisons of wild-type and Prnp-null mice are subject to the flanking gene problem, as are many other studies of genetically modified mice. However, our current suggestion of a PrPmonoaminergic link, consistent with the scaffold hypothesis, additionally relies on the binding of PrP to monoaminergic markers.