Figure 3.
Increased deposition of amyloid peptides Aβ1–42 and Aβ1–40 in NA-depleted APP23 mice. A, Sections of the frontal cortex (FC), hippocampus (HC), and paraventricular thalamus (THL) from saline-injected (tg-con) and NA-depleted APP23 (tg-dsp4) mice were stained with antibodies directed against Aβ1–42 or with thioflavine S. Labeling of both LC projection areas (FC, HC) revealed a marked increase of amyloid deposits. In contrast, no differences of Aβ deposition were observed in the THL. Scale bar, 250 μm. B, Quantification of plaque load (Aβ1–42 or thioflavine S-stained plaque area as a percentage of total region) and plaque staining intensity revealed statistically significant increases in amyloid deposition in response to LC degeneration in the FC and HC, but not within the THL (mean ± SEM; n = 20 animals per group; ANOVA, followed by a Tukey’s test; *p < 0.05, **p < 0.01). C, Western blot detection and subsequent densitometric analysis of Aβ1–40 and Aβ1–42 in lysates of the HC, a LC projection area, confirmed the immunohistochemical results (mean ± SEM; n = 8; ANOVA, followed by a Tukey’s test; *p < 0.05).