Correction: Neural stem cells genetically-modified to express neprilysin reduce pathology in Alzheimer transgenic models
Mathew Blurton-Jones, Brian Spencer, Sara Michael, Nicholas A. Castello, Andranik A. Agazaryan, Joy L. Davis, Franz-Josef Müller, Jeanne F. Loring, Eliezer Masliah, Frank M. LaFerla
Abstract
Genes, proteins, chemicals, diseases, species, mutations and cell lines named across the full text — each resolved to its canonical identifier and authoritative record.
Click any figure to enlarge with its caption.
Figure 6Peer Reviews
No public reviews on file for this paper yet. If you reviewed it on a platform where reviews are public (OpenReview, ICLR, NeurIPS, ICML), you can paste yours below so the community can read it here.
Videos
No videos yet. Explain this paper in a talk, walkthrough, or lecture? Add one.
Taxonomy
TopicsAnesthesia and Neurotoxicity Research · Pluripotent Stem Cells Research · Biomedical Ethics and Regulation
**Correction: Stem Cell Research & Therapy 2014, 5:46 ** 10.1186/scrt440
The original article contains an artifact in Fig. 6H that obscures the view of the lower-middle portion of the image. The correct original image for Fig. 6H can be viewed in this Correction article.
Fig. 6sNEP-NSCs reduce plaque pathology and resist degeneration in a second transgenic AD model. Neprilysin immunoreactivity in the contralateral (A) and ipsilateral (B) hippocampus of sNEP-NSC transplanted transgenic mice reveals high levels of NSC neprilysin expression in vivo. (C-D) Control NSCs, in contrast, produce little to no neprilysin following transplantation, quantified in (E). At 10 months of age, Thy1-APP mice exhibit considerable amyloidosis (6E10 labelling, green) within the hippocampus (F). However, transplantation of sNEP-NSCs significantly reduced Aβ pathology within the ipsilateral hippocampus (G). Control NSCs by comparison have no effect on Aβ levels (H-I), quantified in (J). GFP labelling (green) reveals examples of NSCs engrafted into the ipsilateral hippocampus (L, N), but not within the contralateral vehicle-injected side of the brain (K, M). In line with in vitro findings, caspase activation is reduced by expression of neprilysin (O). Little active caspase-3 immunoreactivity (red) is detected within the ipsilateral hippocampi of transgenic mice (P, R). However, caspase-3 activation (red) within sNEP-NSCs (Q) is significantly reduced versus control NSCs (S). Furthermore, levels of the presynaptic terminal marker synaptophysin (T-X) are significantly increased by sNEP-NSC transplantation (U), suggesting that neprilysin expression can reduce Aβ-induced synaptotoxicity. N = 6/group, error bars represent standard error of the mean (SEM). Scale Bar = 30 μm in A-D, 350 μm in F-I, 14 μm in K-S, 45 μm in T-W. Aβ, beta-amyloid; AD, Alzheimer’s disease; NSCs, neural stem cells; sNEP, secreted neprilysin.