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Publication : Amyloid β Is Not the Major Factor Accounting for Impaired Adult Hippocampal Neurogenesis in Mice Overexpressing Amyloid Precursor Protein.

First Author  Pan H Year  2016
Journal  Stem Cell Reports Volume  7
Issue  4 Pages  707-718
PubMed ID  27693425 Mgi Jnum  J:244954
Mgi Id  MGI:5913733 Doi  10.1016/j.stemcr.2016.08.019
Citation  Pan H, et al. (2016) Amyloid beta Is Not the Major Factor Accounting for Impaired Adult Hippocampal Neurogenesis in Mice Overexpressing Amyloid Precursor Protein. Stem Cell Reports 7(4):707-718
abstractText  Adult hippocampal neurogenesis was impaired in several Alzheimer's disease models overexpressing mutant human amyloid precursor protein (hAPP). However, the effects of wild-type hAPP on adult neurogenesis and whether the impaired adult hippocampal neurogenesis was caused by amyloid beta (Abeta) or APP remained unclear. Here, we found that neurogenesis was impaired in the dentate gyrus (DG) of adult mice overexpressing wild-type hAPP (hAPP-I5) compared with controls. However, the adult hippocampal neurogenesis was more severely impaired in hAPP-I5 than that in hAPP-J20 mice, which express similar levels of hAPP mRNA but much higher levels of Abeta. Furthermore, reducing Abeta levels did not affect the number of doublecortin-positive cells in the DG of hAPP-J20 mice. Our results suggested that hAPP was more likely an important factor inhibiting adult neurogenesis, and Abeta was not the major factor affecting neurogenesis in the adult hippocampus of hAPP mice.
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