Sporadic cerebral amyloid angiopathy (CAA) denotes a common form of microangiopathy in the brain—its pathologic hallmark is vascular amyloid-β protein deposition affecting small vessels in the cerebral cortex and overlying leptomininges.1 Although CAA often does not result in clinically recognizable symptoms and might be diagnosed only at autopsy, it is now considered as a major risk factor for spontaneous lobar intracerebral hemorrhage in elderly people and an important contributor to age-related cognitive decline and dementia.1, 2 In vivo knowledge on CAA has developed largely as a result of progress in neuroimaging, which has allowed the characterization of the spectrum of hemorrhagic and ischemic brain injury associated with CAA as well as different clinical phenotypes.1, 3 The entity of CAA now encompasses not only a specific cerebrovascular pathologic trait and disorder, but also a clinical syndrome (or syndromes) and brain parenchymal lesions seen on neuroimaging (including a set of validated imaging diagnostic criteria—the Boston criteria).4