Abstract
Arising from C. J. Phiel, C. A. Wilson, V. M.-Y. Lee & P. S. Klein Nature 423, 435–439 (2003)10.1038/nature01640
A major unresolved issue in Alzheimer’s disease is identifying the mechanisms that regulate proteolytic processing of amyloid precursor protein (APP)—glycogen synthase kinase-3 (GSK-3) isozymes are thought to be important in this regulation. Phiel et al.1 proposed that GSK-3α, but not GSK-3β, controls production of amyloid1. We analysed the proteolytic processing of mouse and human APP in mouse brain in vivo in five different genetic and viral models. Our data do not yield evidence for either GSK-3α-mediated or GSK-3β-mediated control of APP processing in brain in vivo.
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References
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Generation of transgenic and knockout mice, B.L., D.D., H.D., S.P. and J.R.W.; generation of AAV vectors and intracerebral injections, T.J., D.D. and S.K.; brain analysis, T.J., I.D., B.L., M.G., A.K. and P.B.; design of experiments, data analysis and figures, T.J., I.D., P.B. and F.V.L.; writing of manuscript, T.J. and F.V.L. T.J., I.D. and B.L. contributed equally to this work.
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Jaworski, T., Dewachter, I., Lechat, B. et al. GSK-3α/β kinases and amyloid production in vivo. Nature 480, E4–E5 (2011). https://doi.org/10.1038/nature10615
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DOI: https://doi.org/10.1038/nature10615
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