By using mice expressing APP and presenilin-1 (PS1) to increase Aβ production as a model for AD, they found that deleting the gene encoding for AQP4 resulted in a significant decrease in glymphatic clearance and extracellular accumulation of Aβ, but not this was severe enough to reach the point of Aβ plaque formation. This evidence concerns the gene PSEN1 and Alzheimer disease.