Cerebral Amyloid Angiopathies (CAA) refer to a group of neurological disorders characterized by the accumulation of abnormal amyloid protein deposits within the walls of cerebral blood vessels. These deposits predominantly contain a specific protein known as amyloid-beta, which is typically associated with Alzheimer's disease.
In CAA, the amyloid-beta protein tends to build up in the small to medium-sized arteries and capillaries of the brain. Over time, these protein deposits lead to structural changes and degeneration of the blood vessels, impairing their ability to effectively deliver oxygen and nutrients to brain tissue. As a result, the affected vessels become weak, prone to bleeding, and may lead to hemorrhages or microbleeds within the brain.
Symptoms of CAA can vary depending on the location, extent, and severity of the blood vessel damage. Common clinical manifestations may include recurrent, often spontaneous, lobar intracerebral hemorrhages (bleeding within the brain tissue), cognitive decline, stroke-like symptoms, and small vessel ischemic disease (caused by impaired blood flow in the brain's small vessels).
CAA can be classified as sporadic or hereditary, with sporadic cases occurring without a known genetic cause and commonly associated with aging. Hereditary forms, on the other hand, are typically linked to specific mutations in genes involved in amyloid protein production. Diagnosing CAA often involves neuroimaging techniques such as magnetic resonance imaging (MRI) to detect characteristic signs of amyloid deposition in the brain.
While there is no cure for CAA, management primarily focuses on controlling symptoms and preventing further complications. Treatment measures may include blood pressure control, anticoagulants or antiplatelet medications to reduce the risk of bleeding, and management of associated conditions such as Alzheimer's disease.
