JBC Focus on PI3-Kinase with Echelon

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Originally published In Press as doi:10.1074/jbc.M010450200 on February 26, 2001

J. Biol. Chem., Vol. 276, Issue 20, 17301-17306, May 18, 2001
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow All Versions of this Article:
276/20/17301    most recent
M010450200v1
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrow reprints & permissions
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Tong, L.
Right arrow Articles by Cotman, C. W.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Tong, L.
Right arrow Articles by Cotman, C. W.
Social Bookmarking
Add to CiteULike   Add to Complore   Add to Connotea   Add to Del.icio.us   Add to Digg   Add to Reddit   Add to Technorati  
What's this?

beta -Amyloid-(1-42) Impairs Activity-dependent cAMP-response Element-binding Protein Signaling in Neurons at Concentrations in Which Cell Survival Is Not Compromised*

Liqi TongDagger , Phillip L. Thornton, Robert Balazs, and Carl W. Cotman

From the University of California, Irvine Institute for Brain Aging and Dementia, Irvine, California 92697-4540

Cognitive impairment is a major feature of Alzheimer's disease and is accompanied by beta -amyloid (Abeta ) deposition. Transgenic animal models that overexpress Abeta exhibit learning and memory impairments, but neuronal degeneration is not a consistent characteristic. We report that levels of Abeta -(1-42), which do not compromise the survival of cortical neurons, may indeed interfere with functions critical for neuronal plasticity. Pretreatment with Abeta -(1-42), at sublethal concentrations, resulted in a suppression of cAMP-response element-binding protein (CREB) phosphorylation, induced by exposure to either 30 mM KCl or 10 µM N-methyl-D-aspartate. The effects of Abeta -(1-42) seem to involve mechanisms unrelated to degenerative changes, since Abeta -(25-35), a toxic fragment of Abeta , at sublethal concentrations did not interfere with activity-dependent CREB phosphorylation. Furthermore, caspase inhibitors failed to counteract the Abeta -(1-42)-evoked suppression of CREB activation. Abeta -(1-42) also interfered with events downstream of activated CREB. The Abeta -(1-42) treatment suppressed the activation of the cAMP response element-containing brain-derived neurotrophic factor (BDNF) exon III promoter and the expression of BDNF exon IIII mRNA induced by neuronal depolarization. In view of the critical role of CREB and BDNF in neuronal plasticity, including learning and memory, the observations indicate a novel pathway through which Abeta may interfere with neuronal functions and contribute to cognitive deficit in Alzheimer's disease before the stage of massive neuronal degeneration.

* This work was supported by National Institutes of Health Grant RO1-NS-40953.The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

Dagger To whom correspondence should be addressed: Institute for Brain Aging and Dementia, University of California, Irvine, CA 92697-4540. Tel.: 949-824-6071; Fax: 949-824-2071; E-mail: tongl@uci.edu.

Copyright © 2001 by The American Society for Biochemistry and Molecular Biology, Inc.
Add to CiteULike CiteULike   Add to Complore Complore   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us   Add to Digg Digg   Add to Reddit Reddit   Add to Technorati Technorati    What's this?


This article has been cited by other articles:


Home page
 J. Biol. Chem.Home page
V. Buggia-Prevot, J. Sevalle, S. Rossner, and F. Checler
NF{kappa}B-dependent Control of BACE1 Promoter Transactivation by A{beta}42
J. Biol. Chem., April 11, 2008; 283(15): 10037 - 10047.
[Abstract] [Full Text] [PDF]

Home page
 BrainHome page
S. Petratos, Q.-X. Li, A. J. George, X. Hou, M. L. Kerr, S. E. Unabia, I. Hatzinisiriou, D. Maksel, M.-I. Aguilar, and D. H. Small
The -amyloid protein of Alzheimer's disease increases neuronal CRMP-2 phosphorylation by a Rho-GTP mechanism
Brain, January 1, 2008; 131(1): 90 - 108.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
D. J. Garzon and M. Fahnestock
Oligomeric Amyloid Decreases Basal Levels of Brain-Derived Neurotrophic factor (BDNF) mRNA via Specific Downregulation of BDNF Transcripts IV and V in Differentiated Human Neuroblastoma Cells
J. Neurosci., March 7, 2007; 27(10): 2628 - 2635.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
P. N. Lacor, M. C. Buniel, P. W. Furlow, A. Sanz Clemente, P. T. Velasco, M. Wood, K. L. Viola, and W. L. Klein
A{beta} Oligomer-Induced Aberrations in Synapse Composition, Shape, and Density Provide a Molecular Basis for Loss of Connectivity in Alzheimer's Disease
J. Neurosci., January 24, 2007; 27(4): 796 - 807.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
J. Shen and R. J. Kelleher III
The presenilin hypothesis of Alzheimer's disease: Evidence for a loss-of-function pathogenic mechanism
PNAS, January 9, 2007; 104(2): 403 - 409.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
D. Puzzo, O. Vitolo, F. Trinchese, J. P. Jacob, A. Palmeri, and O. Arancio
Amyloid-{beta} Peptide Inhibits Activation of the Nitric Oxide/cGMP/cAMP-Responsive Element-Binding Protein Pathway during Hippocampal Synaptic Plasticity
J. Neurosci., July 20, 2005; 25(29): 6887 - 6897.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Pharmacol.Home page
S. Rakhit, C. J. Clark, C. T. O'Shaughnessy, and B. J. Morris
N-Methyl-D-aspartate and Brain-Derived Neurotrophic Factor Induce Distinct Profiles of Extracellular Signal-Regulated Kinase, Mitogen- and Stress-Activated Kinase, and Ribosomal S6 Kinase Phosphorylation in Cortical Neurons
Mol. Pharmacol., April 1, 2005; 67(4): 1158 - 1165.
[Abstract] [Full Text] [PDF]

Home page
 Mol. Pharmacol.Home page
K. Watson and G.-H. Fan
Macrophage Inflammatory Protein 2 Inhibits {beta}-Amyloid Peptide (1-42)-Mediated Hippocampal Neuronal Apoptosis through Activation of Mitogen-Activated Protein Kinase and Phosphatidylinositol 3-Kinase Signaling Pathways
Mol. Pharmacol., March 1, 2005; 67(3): 757 - 765.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
P. N. Lacor, M. C. Buniel, L. Chang, S. J. Fernandez, Y. Gong, K. L. Viola, M. P. Lambert, P. T. Velasco, E. H. Bigio, C. E. Finch, et al.
Synaptic Targeting by Alzheimer's-Related Amyloid {beta} Oligomers
J. Neurosci., November 10, 2004; 24(45): 10191 - 10200.
[Abstract] [Full Text] [PDF]

Home page
 J. Neurosci.Home page
L. Tong, R. Balazs, P. L. Thornton, and C. W. Cotman
{beta}-Amyloid Peptide at Sublethal Concentrations Downregulates Brain-Derived Neurotrophic Factor Functions in Cultured Cortical Neurons
J. Neurosci., July 28, 2004; 24(30): 6799 - 6809.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
G. Bitan, S. S. Vollers, and D. B. Teplow
Elucidation of Primary Structure Elements Controlling Early Amyloid {beta}-Protein Oligomerization
J. Biol. Chem., September 12, 2003; 278(37): 34882 - 34889.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
Y. Gong, L. Chang, K. L. Viola, P. N. Lacor, M. P Lambert, C. E. Finch, G. A. Krafft, and W. L. Klein
Alzheimer's disease-affected brain: Presence of oligomeric A{beta} ligands (ADDLs) suggests a molecular basis for reversible memory loss
PNAS, September 2, 2003; 100(18): 10417 - 10422.
[Abstract] [Full Text] [PDF]

Home page
 NeurologyHome page
G. S. Watson, E. R. Peskind, S. Asthana, K. Purganan, C. Wait, D. Chapman, M. W. Schwartz, S. Plymate, and S. Craft
Insulin increases CSF A{beta}42 levels in normal older adults
Neurology, June 24, 2003; 60(12): 1899 - 1903.
[Abstract] [Full Text] [PDF]

Home page
 Proc. Natl. Acad. Sci. USAHome page
O. V. Vitolo, A. Sant'Angelo, V. Costanzo, F. Battaglia, O. Arancio, and M. Shelanski
Amyloid beta -peptide inhibition of the PKA/CREB pathway and long-term potentiation: Reversibility by drugs that enhance cAMP signaling
PNAS, October 1, 2002; 99(20): 13217 - 13221.
[Abstract] [Full Text] [PDF]

Home page
 J. Biol. Chem.Home page
N. G. Bazan and W. J. Lukiw
Cyclooxygenase-2 and Presenilin-1 Gene Expression Induced by Interleukin-1beta and Amyloid beta 42 Peptide Is Potentiated by Hypoxia in Primary Human Neural Cells
J. Biol. Chem., August 9, 2002; 277(33): 30359 - 30367.
[Abstract] [Full Text] [PDF]

Home page
 IOVSHome page
S. J. McKinnon, D. M. Lehman, L. A. Kerrigan-Baumrind, C. A. Merges, M. E. Pease, D. F. Kerrigan, N. L. Ransom, N. G. Tahzib, H. A. Reitsamer, H. Levkovitch-Verbin, et al.
Caspase Activation and Amyloid Precursor Protein Cleavage in Rat Ocular Hypertension
Invest. Ophthalmol. Vis. Sci., April 1, 2002; 43(4): 1077 - 1087.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 All ASBMB Journals   Molecular and Cellular Proteomics 
 Journal of Lipid Research   ASBMB Today 
Copyright © 2001 by the American Society for Biochemistry and Molecular Biology.