Fig. 6: Alzheimer’s disease-specific and non-specific biomarkers in soluble tau.

Soluble tau PTMs specific to AD (a) and those not allowing to distinguish between AD and non-AD tauopathies (b)  are numbered according to full-length (2N4R) tau protein. Each box represents a different condition. The line inside the box denotes the median value (50th percentile), while the box contains the 25th to 75th percentiles of PTM abundances (AUC of XIC). The whiskers mark the 5th and 95th percentiles, and values beyond these upper and lower bounds are considered outliers. a Soluble tau Ub-K267 (when associated with P-S262), Ub-K317, and Ub-K311 were exclusively identified in AD, not in CTL or other tauopathies. b Soluble tau P-T217 (when associated to P-T212), P-T231 (when associated to P-S238 with or without P-S237) and P-S396 (when associated to P-S400 with or without P-S404) were significantly different from controls in all tauopathies but were not able to distinguish between AD and non-AD tauopathies. Data were analysed using an unpaired Wilcoxon test (*P < 0.05, **P < 0.005, ***P < 0.0005). All statistical tests were two-tailed. S serine, T threonine, K lysine, Ub- ubiquitination, P- phosphorylation. AD Alzheimer’s disease (n = 15 biologically independent samples), CBD corticobasal degeneration (n = 5 biologically independent samples), PiD Pick’s disease (n = 5 biologically independent samples); FTLD, frontotemporal lobe degeneration (n = 10 biologically independent samples, including FTLD-4R, n = 4 and FTLD-3R, n = 6); control individuals, CTL (n = 5 biologically independent samples). Source data are provided as a Source Data file (see sheet 3 for the abundances values and sheet 5 for the Wilcoxon test’s exact p values).