From the Guidelines
Cerebral amyloid angiopathy (CAA) is a condition where amyloid protein deposits build up in the walls of blood vessels in the brain, primarily affecting small to medium-sized arteries, and is a common cause of lobar hemorrhages, particularly in older adults with increasing prevalence after age 65. This condition is characterized by the deposition of beta-amyloid peptides in the walls of arterioles and capillaries in the leptomeninges, cerebral cortex, and cerebellar hemispheres, leading to weakened blood vessel walls that are prone to leaking or rupturing 1. The primary risk factors for CAA are age and apolipoprotein E genotypes containing the ε2 or ε4 alleles. Key features of CAA include:
- Recurrent brain bleeds
- Cognitive impairment
- Transient neurological symptoms
- Diagnosis typically involves brain imaging such as MRI, which may show microbleeds or white matter changes
- Management focuses on preventing complications through blood pressure control, avoiding anticoagulant medications when possible, and treating symptoms
- The condition is progressive, and understanding it is important for managing stroke risk in elderly patients and those with cognitive decline. It is essential to note that CAA often coexists with Alzheimer's disease, as both conditions involve the accumulation of beta-amyloid protein 1. Recent guidelines emphasize the importance of blood pressure control in preventing recurrent intracerebral hemorrhage (ICH), with a target blood pressure of less than 140/90 mmHg, and highlight the need for careful consideration of anticoagulation therapy in patients with a history of ICH 1.
From the Research
Definition and Characteristics of Cerebral Amyloid Angiopathy (CAA)
- Cerebral amyloid angiopathy (CAA) is characterized by the deposition of amyloid β-protein (Aβ) in the leptomeningeal and cortical blood vessels 2, 3, 4, 5, 6.
- This condition is an age-dependent risk factor for intracerebral hemorrhage (ICH), ischemic stroke, and contributes to cerebrovascular dysfunction leading to cognitive impairment 2, 4, 5.
- CAA is defined as the deposition of amyloid ß peptide within leptomeningial and cortical vessels, likely reflecting an imbalance between Aβ production and clearance 4.
Pathogenesis and Clinical Presentation
- The pathogenesis of CAA involves the accumulation of amyloid beta (Aβ) peptides in cerebral vessels, leading to vessel damage, impaired blood flow, and subsequent cognitive decline 5.
- CAA can cause a spectrum of neurological events including lobar intracerebral hemorrhage, brain ischemia, and cognitive decline 4.
- The condition poses significant challenges in terms of understanding its underlying mechanisms, accurate diagnosis, and effective treatment strategies 5.
Diagnosis and Treatment
- Accurate diagnosis of CAA often requires advanced imaging techniques, such as magnetic resonance imaging (MRI) or positron emission tomography (PET) scans, to detect characteristic amyloid deposits in the brain 5, 6.
- Treatment of CAA focuses on preventing further deposition of amyloid plaques, managing associated symptoms, and reducing the risk of complications such as cerebral hemorrhage 5, 6.
- Currently, there are no disease-modifying therapies specifically approved for CAA, but several experimental treatments targeting Aβ clearance and anti-inflammatory approaches are being investigated in clinical trials 5, 6.