The role of amyloid beta clearance in cerebral amyloid angiopathy: more potential therapeutic targets

Cerebral amyloid angiopathy (CAA) is characterized by the deposition of amyloid β-protein (Aβ) in the leptomeningeal and cortical blood vessels, which is an age-dependent risk factor for intracerebral hemorrhage (ICH), ischemic stroke and contributes to cerebrovascular dysfunction leading to cognitive impairment. However clinical prevention and treatment of the disease is very difficult because of its occult onset and severity of the symptoms. In recent years, many anti-amyloid β immunotherapies have not demonstrated clinical efficacy in subjects with Alzheimer’s disease (AD), and the failure may be due to the deposition of Aβ in the cerebrovascular export pathway resulting in further damage to blood vessels and aggravating CAA. So decreased clearance of Aβ in blood vessels plays a crucial role in the development of CAA and AD, and identification of the molecular pathways involved will provide new targets for treatment. In this review, we mainly describe the mechanisms of Aβ clearance through vessels, especially in terms of some proteins and receptors involved in this process.