reMYND’s proprietary APP[V717I] transgenic, modeling a progressive amyloid-o-pathy and therefore serving as an excellent model for Alzheimer’s disease (AD), is also available in combination with PS1[A246E], the bigenic APPxPS1 model showing the same pathological hallmarks but with a different timing of onset and severity and extended into a bigenic APPxTAU model combining both Abeta and tau pathology.


Figure 1. Representative photo collection of anti-Abeta stained sections (proprietary anti-Abeta Nanobody®, reMYND/Ablynx, Belgium)showing total plaque load at different ages in APP[V717I] mice (upper panel) and APP[V717I] x PS1[A246E] mice (lower panel).