Fig. 1

Plasma Aβ38, Aβ40, and Aβ42 levels in patients with D-CAA and controls for discovery, and patients with D-CAA and controls for validation. Scatterplots in all panels (depicting median and interquartile range). p-values are adjusted for age and sex. A Patients and controls for discovery. Plasma Aβ38 levels were significantly decreased in presymptomatic and symptomatic D-CAA patients versus their respective age-matched controls (both p < 0.001), but not in patients with symptomatic D-CAA versus patients with presymptomatic D-CAA (p = 0.96). B Patients and controls for discovery. Plasma Aβ40 levels were significantly decreased in patients with presymptomatic (p = 0.009) and symptomatic D-CAA (p = 0.01) versus their respective age-matched controls, but not in patients with symptomatic D-CAA versus patients with presymptomatic D-CAA (p = 0.98). C Patients and controls for discovery. Plasma Aβ42 levels were significantly decreased in patients with presymptomatic and symptomatic D-CAA versus their respective age-matched controls (both < 0.001), but levels in patients with presymptomatic D-CAA and symptomatic D-CAA were similar (p = 0.38). D Patients with D-CAA and controls for validation. Plasma Aβ38 levels were similar in presymptomatic (p = 0.18) and symptomatic D-CAA patients (p = 0.14) versus their respective age-matched controls. Levels were decreased in patients with presymptomatic D-CAA versus patients with symptomatic D-CAA (p = 0.002). E Patients with D-CAA and controls for validation. Plasma Aβ40 levels were similar in patients with presymptomatic (p = 0.28) and patients with symptomatic D-CAA (p = 0.38) versus their respective age-matched controls. Levels were decreased in patients with presymptomatic D-CAA compared to symptomatic D-CAA (p < 0.001). F Patients with D-CAA and controls for validation. Plasma Aβ42 levels were similar in patients with presymptomatic D-CAA and controls (p = 0.63) but decreased in symptomatic D-CAA patients (p = 0.033) versus controls. Levels in patients with presymptomatic D-CAA were similar to symptomatic D-CAA (p = 0.10). G ROC analysis of plasma Aβ38 yielded an AUC of 0.87 (95% CI 0.73–1.00; p = 0.001) to discriminate patients with presymptomatic D-CAA from controls and an AUC of 0.86 (95% CI 0.76–0.97; p < 0.001) to discriminate patients with symptomatic D-CAA from controls, in the discovery cohort. H ROC analysis of plasma Aβ40 yielded an AUC of 0.77 (95% CI 0.59–0.96; p = 0.018) to discriminate patients with presymptomatic D-CAA from controls and an AUC of 0.73 (95% CI 0.59–0.87; p = 0.006) to discriminate patients with symptomatic D-CAA from controls, in the discovery cohort. I ROC analysis of plasma Aβ42 yielded an AUC of 0.89 (95% CI 0.77–1.00; p = 0.001) to discriminate patients with presymptomatic D-CAA from controls and an AUC of 0.85 (95% CI 0.74–0.96; p < 0.0001) to discriminate patients with symptomatic D-CAA from controls, in the discovery cohort. In the validation cohort, ROC analysis of plasma Aβ42 yielded an AUC of 0.65 (95% CI 0.52–0.77; p = 0.036) to discriminate patients with symptomatic D-CAA from controls. *p < 0.05, **p < 0.01, ***p < 0.001. Abbreviations: AUC, area under the curve; D-CAA, Dutch-type cerebral amyloid angiopathy; Presymp D-CAA, presymptomatic D-CAA patients; Symp D-CAA, symptomatic D-CAA patients; OC, older controls; sCAA, sporadic CAA patients; ROC, receiver operator curve; YC, young controls