Abstract
White matter hyperintensities (WMH) - - areas of increased signal appearing on T2-weighted magnetic resonance imaging - - are associated with Alzheimer’s disease (AD) risk and progression in late onset and genetic forms. Although typically attributable to macrostructural damage due to small vessel cerebrovascular disease or dysfunction, in a paper by Garnier-Crussard and colleagues[1], the authors review recent work suggesting an additional Wallerian-like component to WMH and argue that the elevated WMH seen in AD is a downstream phenomenon secondary to neurodegeneration. Here, we maintain that consideration of pathological correlates, animal work, brain perfusion patterns, longitudinal and incident data, and vascular risk factors provides evidence that is not inconsistent with a vasculogenic source of WMH. Future studies inspired by the consistent observations linking WMH to AD are needed to continue to understand potential vascular contributions to the disease.