Cerebral amyloid angiopathy (CAA) is a disorder characterized by the deposition of amyloid in the arterial media and adventitia, leading to intracerebral hemorrhage (ICH). The Boston Criteria, developed in 1995 and 1996, provide a standardized set of diagnostic criteria for CAA-related ICH in living patients. These criteria combine clinical, radiologic, and pathologic data to categorize lobar intracerebral hemorrhage as possible, probable, or definite based on the likelihood of underlying CAA. The criteria are crucial for disease classification in future clinical studies. The incidence of CAA-related ICH is increasing due to the aging population and the use of anticoagulants. CAA is caused by the deposition of β-amyloid (Aβ) within small cortical and leptomeningeal arteries, leading to vessel fragility and rupture. Aβ is also found in Alzheimer's disease, and patients with CAA often have co-existing Alzheimer's disease. The strongest risk factor for CAA is age, and the apolipoprotein E genotype plays a role in the occurrence of CAA-related ICH. Cerebral amyloid angiopathy should be considered in elderly patients over 55 years old who present with lobar ICH, even if they have hypertension. Recurrent ICH is common, and survivors often face chronic disability. CAA can also cause other neurological symptoms, such as transient neurologic symptoms, small cortical infarctions, and dementia. Definitive diagnosis of CAA is confirmed through microscopic examination of brain or leptomeningeal tissue, which reveals hyaline eosinophilic material consistent with Aβ.Cerebral amyloid angiopathy (CAA) is a disorder characterized by the deposition of amyloid in the arterial media and adventitia, leading to intracerebral hemorrhage (ICH). The Boston Criteria, developed in 1995 and 1996, provide a standardized set of diagnostic criteria for CAA-related ICH in living patients. These criteria combine clinical, radiologic, and pathologic data to categorize lobar intracerebral hemorrhage as possible, probable, or definite based on the likelihood of underlying CAA. The criteria are crucial for disease classification in future clinical studies. The incidence of CAA-related ICH is increasing due to the aging population and the use of anticoagulants. CAA is caused by the deposition of β-amyloid (Aβ) within small cortical and leptomeningeal arteries, leading to vessel fragility and rupture. Aβ is also found in Alzheimer's disease, and patients with CAA often have co-existing Alzheimer's disease. The strongest risk factor for CAA is age, and the apolipoprotein E genotype plays a role in the occurrence of CAA-related ICH. Cerebral amyloid angiopathy should be considered in elderly patients over 55 years old who present with lobar ICH, even if they have hypertension. Recurrent ICH is common, and survivors often face chronic disability. CAA can also cause other neurological symptoms, such as transient neurologic symptoms, small cortical infarctions, and dementia. Definitive diagnosis of CAA is confirmed through microscopic examination of brain or leptomeningeal tissue, which reveals hyaline eosinophilic material consistent with Aβ.