Figure 8.

TNEA treatment restored the defective recognition and degradation of autophagy substrates in 5XFAD mice brains. (A, B) Representative fluorescent images of LC3B (green) and Aβ₄₂ (red) in prefrontal cortex (PFC) (A) and hippocampal (HI) CA1 (B) of mice from 5XFAD and 5XFAD+TNEA groups. Original magnification: 60×, scale bar: 50 μm. Corresponding zoom-in images (scale bar: 25 μm) were processed using ImageJ to demonstrate the colocalization. The area of LC3B and Aβ42 colocalization was quantified as mean ± SEM (male, n = 6) and analyzed by unpaired t test. **p < 0 .01 vs. 5XFAD group. (C, D) Representative fluorescence images of SQSTM1 (green) and APP/Aβ (6E10, red) in PFC (C) and CA1 (D) of mice from 5XFAD and 5XFAD+TNEA groups. Original magnification: 20×, scale bar: 200 μm. Corresponding zoom-in images (scale bar: 100 μm) were processed using ImageJ to demonstrate the colocalization. The area of plaque-associated SQSTM1 was quantified as mean ± SEM (male, n = 5 to 6) and analyzed by unpaired t test. *p < 0 .05 vs. 5XFAD group