Increasing evidence suggests that cerebrovascular dysfunction is one of the pathological hallmarks of Alzheimer’s disease (AD). AD patients suffer from cerebral microinfarcts and a damaged cerebral vasculature, and a majority of patients with dementia present with both AD and vascular pathologies. Furthermore, some cerebrovascular symptoms such as white matter hyperintensity and carotid artery wave intensity start to increase 5 – 10 years prior to cognitive impairment onset. Circulatory deficiencies could therefore play an important role in AD progression, but the mechanism underlying the vascular contribution to AD is still unclear. Based on this idea, we are investigating the crosstalk between the cerebrovascular system and the nervous system to identify molecular targets and biomarkers underlying cerebrovascular deficits in AD.