Cerebral amyloid angiopathies (CAA) are defined by the deposition of amyloid proteins in the wall of the cerebral vessels. The clinical presentation ranges from asymptomatic deposition in normal vessels, to a severe involvement of the wall of cerebral vessels leading to intracerebral hemorrhages (ICHs) or brain ischemia. Aβ CAA is responsible for the most frequent type of CAA. It usually consists of multiple, nonhemorrhagic, small, cortical infarcts, that are sometimes silent or revealed by transient neurological deficits. This chapter also highlights amyloid angiopathies of undetermined biochemical nature without and with mutation of the gene BRI. CAA can only be diagnosed by means of histological investigation. Therefore, attempts should be made to improve the diagnostic possibilities in vivo, for example, by means of new magnetic resonance imaging (MRI) techniques or radioactive labeled compounds. More success is to be expected from therapies such as amyloid breaker peptides or antibodies against amyloid.