Fig. 1

Upregulation of MIF in AD patients and AD model mice. a Human brain tissues obtained from Columbia University were lysed in RIPA-DOC buffer, and an equal amount of protein was resolved on a 12% tris-tricine gel. MIF was detected by anti-MIF antibody, and β-actin was detected by the β-actin antibody. b Quantification of (A). Values were expressed as mean ± SEM, n = 5. *p < 0.05 by Student’s t test. c Concentrations of MIF in CSF collected from patients with MCI, AD, and VD, and control subjects were measured by ELISA. Values were expressed as mean ± SEM, n = 30 for control, 28 for AD, 10 for MCI, and 17 for VD. *p < 0.05 by one-way ANOVA with Newman-Keuls post hoc tests compared to control. #p < 0.05 by one-way ANOVA with Newman-Keuls post hoc tests compared to AD. d APP23/PS45 double transgenic mice and the wildtype controls were euthanized at the ages of 2 and 3 months. Half of the brain was fixed and sectioned for plaque assessment, and the other half was used for MIF expression evaluation. Thioflavin S (a, b) and 4G8 (c, d) were used to stained representative brain sections for plaque detection. Arrows point to neuritic plaques. e Brain tissues were lysed in RIPA-DOC buffer, and an equal amount of protein was resolved on a 12% tris-tricine gel. MIF was detected by anti-MIF antibody, and β-actin was detected by β-actin antibody serving as the loading control. The ratio of MIF to β-actin was normalized to wildtype mice. Values were expressed as mean ± SEM, n = 4~8 for wildtype mice and 4~10 for APP23/PS45 mice. p > 0.05 by Student’s t tests. (I) *p < 0.05 by Student’s t tests