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Publication : Tau-knockout mice show reduced GSK3-induced hippocampal degeneration and learning deficits.

First Author  Gómez de Barreda E Year  2010
Journal  Neurobiol Dis Volume  37
Issue  3 Pages  622-9
PubMed ID  20004245 Mgi Jnum  J:158536
Mgi Id  MGI:4439004 Doi  10.1016/j.nbd.2009.11.017
Citation  Gomez de Barreda E, et al. (2010) Tau-knockout mice show reduced GSK3-induced hippocampal degeneration and learning deficits. Neurobiol Dis 37(3):622-9
abstractText  It has been proposed that deregulation of neuronal glycogen synthase kinase 3 (GSK3) activity may be a key feature in Alzheimer disease pathogenesis. We have previously generated transgenic mice that overexpress GSK3beta in forebrain regions including dentate gyrus (DG), a region involved in learning and memory acquisition. We have found that GSK3 overexpression results in DG degeneration. To test whether tau protein modified by GSK3 plays a role in that neurodegeneration, we have brought GSK3 overexpressing mice to a tau knockout background. Our results indicate that the toxic effect of GSK3 overexpression is milder and slower in the absence of tau. Thus, we suggest that the hyperphosphorylated tau mediates, at least in part, the pathology observed in the brain of GSK3 overexpressing mice.
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