Cerebral amyloid angiopathy (CAA) is one of the most common small vessel diseases. With the deposition of amyloid beta within the walls of cerebral blood vessels, CAA can result in damage to blood vessels over time and ultimately intracerebral haemorrhage (ICH). Not only is CAA a leading cause of ICH but CAA is commonly observed in Alzheimer's disease (AD), yet there are still no effective treatments for CAA. The pathophysiology of CAA has yet to be fully elucidated but we know the perivascular environment is heavily impacted by the deposition of amyloid within blood vessels. In recent years, there has been an increased interest in the role that perivascular clearance may play in the development of the disease. Additionally, the role of the immune system has also come into question, especially regarding CAA-related inflammation. In this review, we aim to discuss the immune impacts of CAA within the perivascular environment, and probe how specific cells within this environment may be involved in the pathogenesis of CAA. Importantly, we also consider how some of these immune cells may be key treatment avenues to explore.
Eyre et al. (Mon,) studied this question.