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Historically, cerebrovascular abnormalities were recognized as prominent in the pathology of age-related dementia. In more recent decades, however, research and funding for development of therapeutics has almost entirely been focused on β-amyloid and tau deposits (as described by Alzheimer in pre-senile dementia), despite a lack of conclusive evidence of a causal relationship or efficacy of targeted treatment on cognitive decline or dementia. Here we present a brief history of the evidence for a dominant vascular component of Alzheimer’s Disease and highlight a potential target for slowing the functional progression of the disease.