A consistently slower and weaker blood-oxygenation-level-dependent (BOLD) fMRI response is consistently seen in patients with cerebral amyloid angiopathy (CAA).However, our mechanistic understanding of why this occurs in CAA is lacking. To improve our mechanistic understanding, we propose a hypothesis testing framework for simulating the relationship between of impaired microvascular function and the associated abnormal fMRI response. We use BOLD biophysical modeling to link microvascular dynamics with fMRI signals. Here we test whether reduced arteriolar reactivity predicts abnormal BOLD response in early- and late-stage CAA.
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