Histological analysis of brain sections indicates the spread of ZIP did not extend into subcortical regions (Fig. 3A), but encompasses several areas involved in skilled reaching including M1, M2, and S1 limb regions [14], [15] (Fig. 3B).
Following injection of fluorescent RVG-9r LSPCs into mice, examination of brain sections indicated widespread presence of siRNA in the CNS.
In situ hybridization of Amfutsch and Amtau using developing pupal brain sections indicated that, although both genes were expressed in the pupal brains, they were differentially expressed in the pupal brains, suggesting that these genes function in a brain-region dependent manner during pupal stages (Supporting Information S1, Fig. S5 and S6).
Images taken from eight selected areas in the cortex and from nine selected areas in the hippocampus of each brain section (indicated in Figure 1b, c) were used for quantifying β-amyloid plaques and GFP+/Iba-1+ cells.
The binding of FITC-Tf is inhibited competitively by pre-incubation of brain sections with unlabeled apo-Tf, indicating the specificity of the reaction (Figure 2A, panels 3 and 4, white arrow-head).
18F-7B demonstrated labeling of Aβ plaques in cortex of AD brain sections and the binding to Aβ was inhibited in the presence of its unlabeled counterpart (7A) indicating specificity of the probe.
The evolution of APP accumulations in brain sections depicted the detailed progression of axonal pathology.
Brain sections without the primary antibodies served as negative controls.
The VLa, Vapc, and VM are likely to be also primary targets of the ft in the human brain, as indicated by the course of the tract, particularly on sagittal sections (e.g. Fig. 5).
Normal human brain sections did not show any immunolabeling with the plasma from pABri vaccinated mice indicating a specificity for pathology associated protein conformers.
