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Title: Coexpression of GSK-3beta corrects phenotypic aberrations of dorsal root ganglion cells, cultured from adult transgenic mice overexpressing human protein tau
Authors: Nuydens, R ×
Van Den Kieboom, G
Nolten, C
Verhulst, C
Van Osta, P
Spittaels, K
Van Den Haute, Chris
De Feyter, E
Geerts, H
Van Leuven, Freddy #
Issue Date: Feb-2002
Publisher: Blackwell Science
Series Title: Neurobiology of Disease vol:9 issue:1 pages:38-48
Abstract: Coexpression of constitutively active GSK-3beta[S9A] rescued the axonal pathology induced by overexpression of human tau in transgenic mice (Spittaels et al., (2000) J. Biol. Chem. 275, 41340-41349). We isolated dorsal root ganglion (DRG) neuronal cultures from adult tau4R- and tau4R x GSK-3beta-transgenic mice to define the mechanisms at the cellular and subcellular level. DRG from tau4R-transgenics showed a reduced sprouting capacity while density and stability of microtubules in the axonal processes were significantly increased. Video-enhanced contrast microscopy demonstrated a dramatic inhibition of fast axonal transport. Coexpression of GSK-3beta increased tau phosphorylation and reversed the effects on microtubule stability and saltatory motion. In DRG from GSK-3beta single transgenics, increased tau phosphorylation was evident without any major effects on microtubule stability or axonal transport. These observations support the hypothesis that excess tau competed with motor-proteins for binding to microtubules and/or that a rigid microtubular system inhibits axonal transport.
ISSN: 0969-9961
Publication status: published
KU Leuven publication type: IT
Appears in Collections:Research Group for Neurobiology and Gene Therapy
Associated Laboratories - miscellaneous (-)
Department of Human Genetics - miscellaneous
× corresponding author
# (joint) last author

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