Periventricular white matter hyperintensities co‐localize with deep intramedullary venules, sparing compact fiber tracts and can increase or decrease over time in Alzheimer's disease

Confluent pWMH clearly mapped to visualizable DMVs, suggesting venous insufficiency due to collagenosis. Compact fiber tract sparing and reversible progression of pWMH provided in vivo evidence of chronic edema. Our findings support the notion that venous insufficiency of DMVs is the main substrate of pWMH, reflecting vasogenic edema induced from increased venous pressure and extracellular fluid accumulation from reduced interstitial fluid circulation along the glymphatic perivenous spaces.