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. 2021 Dec 9;5(1):855–869. doi: 10.3233/ADR-210050

Fig. 3.

Fig. 3

Detection of eIF2α phosphorylation in tauopathies and age-matched controls. p-eIF2α and GAPDH immunoreactivity for (A) AD, (B) PiD, and (C) PSP together with relative age-matched non-demented controls. Quantification of p-eIF2α immunoreactivity from individual samples was normalized to the immunoreactivity of a loading control, GAPDH. Data were analyzed using a two-tailed unpaired t-test revealing no significant differences (p = 0.4892, t = 0.6983; p = 0.3604, t = 0.9362; p = 0.8813, t = 0.1514 for AD, PiD, and PSP, respectively). (B, C) p-eIF2α, eIF2α, and actin immunoreactivity for (B) PiD and (C) PSP. Quantification revealed no significant difference when normalizing p-eIF2α over eIF2α (p = 0.3653, U = 46; p = 0.5288, U = 41 for PiD, PSP), p-eIF2α over actin (p = 0.8977, U = 58; p = 0.5607, t = 0.5927 for PiD, PSP) or eIF2α over actin (p = 0.6522, U = 53 p = 0.9705, U = 49 for PiD, PSP). Shown are means, error bars show SEM. ns, not significant. Number of cases: ND = 20, AD = 20, nPiD = 11, PiD = 11, nPSP = 10, PSP = 10. Each lane corresponds to one individual case. Colored symbols in (A) correspond to individuals with LBD co-morbidity (red), APOE 4.4 genotype (blue), and CVD co-morbidity (magenta).