If, upon the elicitation of the ISR in the current transgenic animal AD models (and, as discussed above, the ISR is elicited in these models via the accumulation of AβPP-derived iAβ), the RNA-dependent mRNA amplification-competent RdRp complex is assembled (and, as discussed above, it is highly plausible that it is), it could be argued that since human AβPP mRNA is the eligible RdRp template, and because it is human AβPP mRNA, which is expressed from the transgenes in the current animal AD models, its amplification should occur. Here, APP is linked to Alzheimer disease.