Fig. 3 |. Rate of change per year in serum NfL in mutation carriers mirrors rate of change in cortical thinning.

a, Relationship between estimated annual rate of change in serum NfL and estimated annual rate of change in precuneus cortical thickness for non-carriers, presymptomatic (Presym) mutation carriers, and symptomatic (Sym) mutation carriers (including converters to the symptomatic phase, see Fig. 2c). Results from LMEMs revealed a significant association in symptomatic mutation carriers (n = 60; B(s.e.m.) = −0.914(0.367), P = 0.018) and a close to significant association in presymptomatic mutation carriers (n = 65; B(s.e.m.) = −0.325(0.166), P = 0.054) but not in non-carriers (n = 59; B(s.e.m.) = −0.210(0.149), P = 0.886). Between-group comparison indicated that the rate of change in serum NfL was slightly more associated in symptomatic than in asymptomatic mutation carriers (B(s.e.m.) = −0.573(0.305), P = 0.063). b, Relationship between rate of change in serum NfL and rate of change in precuneus 18F-FDG PET. Using LMEMs, a positive association was only found in symptomatic mutation carriers (n = 55; B(s.e.m.) = −1.149(0.501), P = 0.031) but not in presymptomatic mutation carriers (n = 64; B(s.e.m.) = −0.227(0.456), P = 0.620) or non-carriers (n = 55; B(s.e.m.) = 0.161(0.347), P = 0.465). c, Relationship between rate of change in serum NfL and rate of change in precuneus amyloid-β-PET. Using LMEMs, no significant association in any of the three groups was found (non-carriers: n = 57; B(s.e.m.) = −0.468(0.547), P = 0.403; presymptomatic mutation carriers: n = 64; B(s.e.m.) = 1.248(1.000), P = 0.216; symptomatic mutation carriers: n = 51; B(s.e.m.) = 1.805(1.556), P = 0.266). The shaded area around each linear fit line represents one s.e.m. Note that not all participants with longitudinal NfL measurements had imaging parameters available, thus sample sizes (n) are slightly lower compared to those in Fig. 2c.