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First published online 2 January 2007
doi: 10.1242/jcs.03323

Journal of Cell Science 120, 279-288 (2007)
Published by The Company of Biologists 2007
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Research Article

Abeta1-42 stimulates actin polymerization in hippocampal neurons through Rac1 and Cdc42 Rho GTPases

Ariadna Mendoza-Naranjo1,*, Christian Gonzalez-Billault1 and Ricardo B. Maccioni1,2

1 Laboratory of Cellular, Molecular Biology and Neuroscience, Department of Biology, Faculty of Sciences and
2 Department of Neurological Sciences, Universidad de Chile, Las Palmeras 3425, Nunoa, Santiago, Chile

* Author for correspondence (e-mail: amendoza{at}med.uchile.cl)

Accepted 30 October 2006

A number of psychiatric and neurodegenerative disorders, such as Alzheimer's disease, are characterized by abnormalities in the neuronal cytoskeleton. Here, we find that the enhancement in actin polymerization induced by fibrillar amyloid-beta peptide (Abeta) is associated with increased activity of Rac1/Cdc42 Rho GTPases. Rac1 upregulation involves the participation of Tiam1, a Rac guanine-nucleotide exchange factor, where Abeta exposure leads to Tiam1 activation by a Ca2+-dependent mechanism. These results point to Rho GTPases as one of the targets in Abeta-induced neurodegeneration in Alzheimer's disease pathology, with a role in mediating changes in the actin cytoskeletal dynamics.

Key words: Alzheimer's disease, Amyloid beta, Rac1 Cdc42 Rho GTPases, Actin polymerization, Tiam1


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