Activation of the neuronal c-Abl tyrosine kinase by amyloid-beta-peptide and reactive oxygen species.

Abstract:

:The deposition and accumulation of amyloid-beta-peptide (Abeta) in the brain are considered a sine qua non for Alzheimer's disease. The experimental delivery of fibrilized Abeta serves as a cellular model for several facets of the disease including the induction of synaptic dysfunction and apoptosis. c-Abl kinase is involved in the regulation of apoptosis and its pro-apoptotic function is in part mediated by its interaction with p73, a p53 homologue. We found that c-Abl activation is involved in cell signals that regulate neuronal death response to Abeta fibrils. Abeta peptide fibrils induced an increase of the c-Abl activity in rat hippocampal neurons as well as an increase in nuclear p73 protein levels and the p73-c-Abl complex. The neuronal cell death induced by Abeta fibrils was prevented by the inhibition of c-Abl with imatinib mesylate (Gleevec or STI571) and by the inhibition c-Abl expression by RNAi. These results directly point to a therapeutic strategy for the treatment of Alzheimer's disease.

journal_name

Neurobiol Dis

journal_title

Neurobiology of disease

authors

Alvarez AR,Sandoval PC,Leal NR,Castro PU,Kosik KS

doi

10.1016/j.nbd.2004.06.007

keywords:

subject

Has Abstract

pub_date

2004-11-01 00:00:00

pages

326-36

issue

2

eissn

0969-9961

issn

1095-953X

pii

S0969-9961(04)00135-4

journal_volume

17

pub_type

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