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The immunosuppressant rapamycin exacerbates neurotoxicity of Aβ peptide by Claire Lafay-Chebassier; Marie Christine Pérault-Pochat; Guylène Page; Agnès Rioux Bilan; Milena Damjanac; Stéphanie Pain; Jean-Luc Houeto; Roger Gil; Jacques Hugon is a Neuroscience article available to read on EtoBox.

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## Abstract Alzheimer's disease (AD) is a neurodegenerative disease of the central nervous system characterized by two major lesions: extracellular senile plaques and intraneuronal neurofibrillary tangles. β‐Amyloid (Aβ) is known to play a major role in the pathogenesis of AD. Protein synthesis and especially translation initiation are modulated by different factors, including the PKR/eIF2 and the mTOR/p70S6K pathways. mRNA translation is altered in the brain of AD patients. Very little is known about the translation control mediated by mTOR in AD, although mTOR is a central regulator of translation initiation and also ribosome biogenesis and cell growth and proliferation. In this study, by using Western blotting, we show that mTOR pathway is down‐regulated by Aβ treatment in human neuroblastoma cells, and the underlying mechanism explaining a transient activation of p70S6K is linked to cross‐talk between mTOR and ERK1/2 at this kinase level. This phenomenon is associated with caspase‐3 activation, and inhibition of mTOR by the inhibitor rapamycin enhances Aβ‐induced cell death. Moreover, in our cell model, insulin‐like growth factor‐1 is able to increase markedly the p70S6K phosph

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Author

Claire Lafay-Chebassier; Marie Christine Pérault-Pochat; Guylène Page; Agnès Rioux Bilan; Milena Damjanac; Stéphanie Pain; Jean-Luc Houeto; Roger Gil; Jacques Hugon

Publisher

John Wiley and Sons; Wiley (John Wiley & Sons); John Wiley & Sons Inc.; Wiley (ISSN 0360-4012)

Published

2006

Language

EN

Field

Neuroscience (Life Sciences)