Fig. 1
From: TDP-43 pathology is associated with increased tau burdens and seeding
Pathological tau expression is increased in AD cases with comorbid LATE-NC. Immunohistological quantification of the percentage of p-tau202/205 positive neurons (tangles and pretangles) shows that p-tau pathology is significantly increased in AD(LATE-NC+), n = 55 compared to controls (n = 26) and AD(LATE-NC-) cases (n = 12) in the (a) CA1 subfield of the posterior hippocampus and compared to controls in (b) frontal cortex. Multiple linear regressions controlled for age and sex were used to compare the three neuropathological subgroups. Simple linear regressions in the whole cohort show that hippocampal pTDP-43 pathology is significantly associated with (c) hippocampal and (d) cortical p-tau pathology. Overview of p-tau202/205 immunostainings in the hippocampus and frontal cortex of a control, AD(LATE-NC-) and AD(LATE-NC+) case is shown in (e), 200 × magnification pictures and scale bars = 50µm. p-tau199 levels in sarkosyl-insoluble homogenates of the (f) entorhinal cortex or (g) frontal cortex of 10 controls, 8 AD(LATE-NC-), 11 AD(LATE-NC+) and 5 FTLD-TDP show that AD(LATE-NC +) cases have increased p-tau199 in both regions compared to controls, AD(LATE-NC-) and FTLD-TDP cases. Physiological TDP-43 levels are significantly decreased in the entorhinal cortex of FTLD-TDP cases, compared to the AD groups (h). Levels of total TDP-43 are similar among groups in the frontal cortex (i). Multiple linear regressions were used to compare the three neuropathological subgroups. Spearman correlation analyses in the whole cohort including all variables analyzed is depicted in (j), coefficient values are displayed; blank cells mean coefficient value < 0.01