Given both the predicted and observed modulatory effects of AQP4 inhibition and facilitation on perivascular ISF drainage, it is crucial to investigate whether this influence also extends to the clearance of soluble Aβ, to what extent, and how it relates to the turnover of insoluble Aβ species (such as Aβ42) and amyloid plaque formation in Aβ‐overexpressing mouse models. Here, AQP4 is linked to amyloidosis.