The hypothesised role of PVS in the removal of metabolic and neurotoxic waste products, including Amyloid-β (Aβ) and tau [15–17]—key proteins in the pathogenesis of Alzheimer’s disease (AD)—proposes that PVS enlargement reflects compromised PVS function and, by extension, potentially dysregulated glymphatic fluid exchange and clearance (for review see [2, 15, 18, 19]). This evidence concerns the gene MAPT and Alzheimer disease.