In this sense, Figure 1A illustrates an example of the relevant colocalization between PrPC (green) and Aβ (red) in the postmortem frontal cortex of an Alzheimer’s disease (AD) patient in contrast to other prion-like proteins such as α-synuclein with little colocalization with Aβ-positive plaques in the same context; normal endogenous expression and function of PrPC may be largely compromised in NDDs [51,52]. The gene discussed is PRNP; the disease is Alzheimer disease.