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Introduction We aimed to investigate if cerebral amyloid angiopathy (CAA) is more frequent in genetically determined than in sporadic early-onset forms of Alzheimer's disease (AD) (early-onset AD [EOAD]). Methods Neuroimaging features of CAA, apolipoprotein ( APOE ), and cerebrospinal fluid amyloid β (Aβ) 40 levels were studied in subjects with Down syndrome (DS, n = 117), autosomal-dominant AD (ADAD, n = 29), sporadic EOAD ( n = 42), and healthy controls ( n = 68). Results CAA was present in 31%, 38%, and 12% of cognitively impaired DS, symptomatic ADAD, and sporadic EOAD subjects and in 13% and 4% of cognitively unimpaired DS individuals and healthy controls, respectively. APOE e4 genotype was borderline significantly associated with CAA in sporadic EOAD ( P = .06) but not with DS or ADAD. There were no differences in Aβ040 levels between groups or between subjects with and without CAA. Discussion CAA is more frequently found in genetically determined AD than in sporadic EOAD. Cerebrospinal fluid Aβ40 levels are not a useful biomarker for CAA in AD.

clinical characteristics of probable CAA based on Boston’s criteria and also investigated predictive factors associated with certain features of CAA. Methods: We retrospectively reviewed patients diagnosed as probable CAA based on the Boston’s criteria who underwent MRI, including gradient echo (GRE) andfluid attenuated inversion recovery (FLAIR) images and clinical assessment fromAugust 2006 toMay 2013.AllGRE images of each subject were reviewed by 1 rater to describe the location and numbers of intracranial hemorrhages. The white matter hyperintensity was rated based on rating scales proposed by Clinical Research Center for Dementia of South Korea (CREDOS). Statistical analyses were performed using SPSS version 21.0 and SAS 6.0.Results: A total of 92 patients were included in this study. Themean age of onsetwas 68.669.9years (M:F1⁄461:31). Sixty-three patients (68%) had hypertension. The initial diagnoses included cognitive impairment (48 patients, 52%), lobar ICH (14 patients, 15.2%), and lacunar infarction (10 patients, 10.9%). Thirty-nine patients had deep microbleeds. Fifty-three patients (57%) showed posterior dominant distribution (parietal and occipital lobe) of hemorrhages. Themedian number of microbleeds was 15 [interquartile range (IQR): 7-41.33]. Patients with posterior dominant location were older (p 1⁄40.028) and complained of cognitive decline more often (p 1⁄40.034). This group had more microbleeds (p1⁄40.006) and showed more severewhitematter hyperintensities (p1⁄40.008). They also tended to have lower recall score of MMSE than the other group. Patients with deep microbleeds showed more severe white matter hyperintensities (p 1⁄40.002). Twenty-four patients performed follow-up MR imaging. The mean interval time was 28.6624.2 months. Large number of microbleeds at baseline was associated with increasing rate of newmicrobleeds at follow-up scan.Conclusions:We found the impact of location of intracranial hemorrhages on cognitive impairment andwhitematter hyperintensities in patientswithCAA.Thedistribution and the number of microbleeds at baseline were factors associated with disease progression. These data indicate that early evaluation of the location and number of microbleeds can be helpful to assess clinical characteristics and prognosis in patients with probable CAA.