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Papers In Press, published online ahead of print May 7, 2003
J. Biol. Chem, 10.1074/jbc.M302530200
Submitted on March 12, 2003
Revised on April 30, 2003
Accepted on May 7, 2003

Activation of the JNK signalling cascade mediates the effect of Abeta on LTP and cell death in hippocampus: A role for IL-1beta

Aedín M. Minogue, Adrian W. Schmid, Marie P. Fogarty, Alison C. Moore, Veronica A. Campbell, Caroline E. Herron, and Marina A. Lynch

Department of Physiology, Trinity College Institute of Neuroscience, Dublin 2

Corresponding Author: lynchma{at}tcd.ie

Amyloid-beta (Abeta )is a major constituent of the neuritic plaque found in the brain of Alzheimer’s Disease patients and a great deal of evidence suggests that the neuronal loss which is associated with the disease is a consequence of the actions of Abeta . In the past few years, it has become apparent that activation of c-Jun N-terminal kinase (JNK) mediates some of the effects of Abeta on cultured cells; in particular, the evidence suggests that Abeta -triggered JNK activation leads to cell death. In this study, we investigated the effect of intracerebroventricular injection of Abeta (1-40) on signalling events in the hippocampus and on long-term potentiation in Schaffer collateral-CA1 pyramidal cell synapses in vivo. We report that Abeta (1-40) induced activation of JNK in CA1 and that this was coupled with expression of the proapoptotic protein, Bax, cytosolic cytochrome c expression, poly-(ADP-ribose) polymerase cleavage and Fas ligand expression in the hippocampus. These data indicate that Abeta (1-40) inhibited expression of LTP and this effect was abrogated by administration of the JNK inhibitor peptide, D-JNKI1. In parallel with these findings, we observed that Abeta -induced changes in caspase-3 activation and TUNEL staining in neuronal cultured cells were inhibited by D-JNKI1. We present evidence which suggests that IL-1beta plays a significant role in mediating the effects of Abeta (1-40) since Abeta (1-40) increased hippocampal IL-1beta and since several effects of Abeta (1-40) were inhibited by the caspase-1 inhibitor, Ac-YVAD-CMK. On the basis of our findings we propose that Abeta -induced changes in hippocampal plasticity are likely to be dependent upon IL-1beta -triggered activation of JNK.


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