Fig. 3
From: P-tau subgroups in AD relate to distinct amyloid production and synaptic integrity profiles
Associations of p-tau subgroups with protein levels were independent of clinical stage. Protein level differences are shown stratified for clinical stage: preclinical AD, prodromal AD, and AD dementia. Controls were cognitively normal individuals with normal CSF amyloid, t-tau, and p-tau. Protein levels were Z-scored relative to controls. The box of the boxplot indicates the 25th percentile, median, and 75th percentile, and whiskers indicate the 1.5× interquartile range. Arrows indicate the protein measurements outside of the y-axis. Differences between p-tau subgroups in the protein levels were calculated with linear models adjusted for age, sex, diagnostic group (controls, preclinical AD, prodromal AD, and AD dementia), and the interaction between protein level and diagnostic group. p-values were adjusted for the multiple comparisons between p-tau subgroups with the Sidak method. BACE1, beta-site amyloid precursor protein cleaving enzyme 1; Aβ40, amyloid-beta 1–40; NfL, neurofilament light; VAMP2, vesicle-associated membrane protein 2; NRGN, neurogranin. *p-value < 0.05; **p-value < 0.01; ***p-value < 0.001; n.s., not significant