Animal stroke models show evidence of increased GFAP-positive astrocytes observed around the lesion days after vessel occlusion in models of small vessel and white matter stroke76,77 and white matter hypoperfusion increases tau hyperphosphorylation in mouse models.12 Taken together, we speculate that there is an endogenous cerebrovascular component to Alzheimer’s disease pathogenesis that likely is not due to amyloid and tau pathology but instead interacts with inflammatory processes to promote tauopathy and subsequent neurodegeneration. The gene discussed is MAPT; the disease is tauopathy.