Alzheimer’s disease (AD) is a neurodegenerative disease that affects more than 4 million people in the US alone. To date, efforts at understanding the disease process have been primarily directed towards studies of amyloid accumulation and cerebral blood flow (CBF) deficits. Despite consistent findings of temporopariental hypoperfusion in patients with AD, there is a possibility that reduction in CBF may not be an indication of vascular dysfunction, but may merely reflect a reduction in metabolic demand.
In our lab, we seek to clarify this by using a more direct approach to assess vascular function (the vasodilatory capacity of vessels) in AD. We applied BOLD fMRI under hypercapnia (5% CO2 breathing) challenge to measure cerebrovascular reactivity (CVR) in a group of AD and normal control (NC) subjects. Baseline CBF was determined using pseudo-continuous arterial spin labeling (PCASL) technique. Spatial patterns of CVR and CBF deficits were compared. We found that regions of CVR deficits were restricted to anterior regions of the brain. This spatial pattern is drastically different from the patterns of CBF deficit measured in the same groups, which showed predominantly temporoparietal regions. Thus, CVR may be a better marker of vascular dysfunction. In the future, we hope to further investigate vascular dysfunction systematically in AD so that we can achieve a better understanding of the disease process.