Fig. 3
a Plots for the concentrations of plasma p-tau181 in the control patients (n = 22) and the clinically diagnosed patients with DS (n = 20) of Cohort 2. The solid lines represent the mean value ± standard errors (SE) of the concentrations of each group. The concentration of plasma p-tau181 in the DS group was significantly higher than that in the age-matched controls (p = 0.0313, Mann–Whitney U test). The dashed line corresponds to the cut-off value of the plasma p-tau181 to discriminate AD from control (0.0921 pg/ml) derived from the ROC analysis of AD and control groups in Cohort 1 (Fig. 2a). b A scatter plot of the levels of plasma p-tau181 versus the patient age of the DS patients (n = 20) and a linear regression line for the correlation of those two parameters. There is a significant correlation between the levels of plasma p-tau181 and the age of the DS patients (R2 = 0.4451, p = 0.0013, Pearson correlation). c A scatter plot of the levels of plasma p-tau181 versus the social ages of the DS patients (n = 18) indexed by social maturity scale developed for the Japanese (S-M) [18] that represents the intellectual ability of each DS patient. The solid lines represent the linear regression line between those two parameters. The levels of plasma p-tau181 were weakly correlated negatively with the social ages of DS patients, but the correlation was not significant (p = 0.0563, n = 18). d A scatter plot of the levels of plasma p-tau181 versus the Δsocial ages of the DS patients (n = 6), which indicates the changes of the social ages of the patient during the ~1-year follow-up period. The larger negative values of Δsocial ages means the more cognitive decline the patient had. e A scatter plot of the levels of plasma p-tau181 versus the mean cortical SUVR in PiB-PET study of the DS patients (n = 6), which represents the severity of cerebral Aβ-amyloid burden