Fig. 3: AD and related tauopathies present with distinct tau acetylation profiles.

a Immunoblotting of control and AD brains homogenates using antibodies to detect ac-K311, total tau (TAU-5), and GAPDH. b Immunoblots from a were quantified and normalized to control (soluble) or AD (insoluble) samples. c Immunohistochemistry (IHC) analysis using ac-K311 (#5089) in a panel of 3R and 4R tauopathies: Alzheimer’s disease (AD), Pick’s disease (PiD), corticobasal degeneration (CBD), and progressive supranuclear palsy (PSP). Only 3R-tauopathies (AD and PiD) demonstrated ac-K311-immunoreactive pathological lesions. Scale bar = 50 μm. d Double-labeling IF to mark ac-K311 (red) in combination with tau-isoform specific antibodies. The green channel represents 4R-tau (RD4) in AD, CBD, and PSP or 3R-tau (RD3) in AD and PiD. Ac-K311 colocalized strongly to 3R-tau pathology in AD and PiD. Scale bar = 50 μm. e Immunoblotting of isolated PHF-tau from the indicated tauopathies probed with ac-K311, 3R-tau (RD3), 4R-tau (RD4), and total tau (K9JA) antibodies. The arrows highlighting tau bands 1–5 represent distinctly migrating tau bands that are resolved by immunoblotting. Statistical tests: p value determined by unpaired t-test with Welch’s correction from n = 5 independent samples (b). Representative images are shown from n = 10 (c, d) and n = 2 (e) independent samples. Error bars represent means ± SEM. *p < 0.05 and **p < 0.01. Source data are provided as a Source Data file.