Fig. 4: Neurophysiological impacts of AD proteinopathy are associated with longitudinal cognitive declines.
a, Box plots show the median, quartiles, minima and maxima, while violin plots show the density distribution of the annual rate of change calculated for the RBANS attention–memory composite score (attention, immediate and delayed memory) of the participants, separated according to Aβ and tau positivity. The two-sided, one-factor ANCOVA analysis (F(2, 93) = 8.81, PFDR = 0.001) revealed that individuals expressing both Aβ and tau pathology (Aβ+/Tau+, n = 11) showed steeper cognitive decline compared to individuals with no pathology (Aβ−/Tau−, n = 49) and individuals with Aβ but no entorhinal cortex tau load (Aβ+/Tau−, n = 42). Tukey HSD P values adjusted for multiple comparisons are shown for the difference between the Aβ+/Tau+ and the Aβ−/Tau− and Aβ+/Tau− groups. b, Linear regression models demonstrated an interaction effect (t(92) = 3.37, PFDR = 0.002), where a more pronounced shift in the Aβ–alpha-band activity relationship for individuals with higher entorhinal tau was associated with longitudinal decline in attention–memory composite scores. The thick colored lines represent the line of best fit across participants in the Aβ−/Tau− (blue, n = 49), Aβ+/Tau− (green, n = 42) and Aβ+/Tau+ (red, n = 11) groups. The shaded area represents the 95% confidence intervals. Note that whole-brain Aβ and entorhinal tau SUVR values were treated as continuous variables for this analysis, and that participants were divided according to Aβ/Tau +/− groups only for visualization purposes. Corresponding t statistic and one-sided, FDR corrected P values are overlaid on the scatter plot.
