Artículo de revista
Aβ1-42 stimulates actin polymerization in hippocampal neurons through Rac1 and Cdc42 Rho GTPases
Fecha
2007Registro en:
Journal of Cell Science, Volumen 120, Issue 2, 2018, Pages 279-288
00219533
10.1242/jcs.03323
Autor
Mendoza Naranjo, Ariadna
González Billault, Christian
Maccioni Baraona, Ricardo
Institución
Resumen
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 (Aβ) is associated with increased activity of Rac1/Cdc42 Rho GTPases. Rac1 upregulation involves the participation of Tiam1, a Rac guanine-nucleotide exchange factor, where Aβ exposure leads to Tiam1 activation by a Ca2+ -dependent mechanism. These results point to Rho GTPases as one of the targets in Aβ-induced neurodegeneration in Alzheimer's disease pathology, with a role in mediating changes in the actin cytoskeletal dynamics.