Cerebral amyloid angiopathy (CAA) of
amyloid β-
protein (Aβ) type is common in
Alzheimer's disease (AD). Aβ
immunotherapies have been reported to induce CAA-related
intracerebral hemorrhages (ICH) or vasogenic
edema. For the purpose of developing a method to predict CAA-related ICH and other
cerebrovascular disorders in AD, the
biomarkers, and risk factors are reviewed. The
biomarkers include (1) greater occipital uptake on
amyloid positron emission tomography imaging and a decrease of cerebrospinal fluid Aβ40 levels as markers suggestive of CAA, and (2) symptomatic lobar ICH, lobar microhemorrhages, focal subarachnoidal
hemorrhages/superficial
siderosis, cortical microinfarcts, and subacute
encephalopathy (caused by CAA-related
inflammation or
angiitis) as imaging findings of CAA-related ICH and other disorders. The risk factors include (1) old age and AD, (2) CAA-related gene mutations and
apolipoprotein E genotype as genetic factors, (3) thrombolytic, anti-coagulation, and anti-platelet
therapies,
hypertension, and minor
head trauma as
hemorrhage-inducing factors, and (4) anti-
amyloid therapies. Positive findings for one or more
biomarkers plus one or more risk factors would be associated with a significant risk of CAA-related ICH and other
cerebrovascular disorders. To establish a method to predict future occurrence of CAA-related ICH and other
cerebrovascular disorders in AD, prospective studies with a large number of AD patients are necessary, which will allow us to statistically evaluate to what extent each
biomarker or risk factor would increase the risk. In addition, further studies with progress of technologies are necessary to more precisely detect CAA and CAA-related
cerebrovascular disorders.