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Central Nervous System

Synaptic memory mechanisms: Alzheimer's disease amyloid β-peptide-induced dysfunction

M.J. Rowan, I. Klyubin, Q. Wang, N.W. Hu, R. Anwyl
Biochemical Society Transactions Nov 01, 2007, 35 (5) 1219-1223; DOI: 10.1042/BST0351219
M.J. Rowan
Trinity College Institute of Neuroscience, Trinity College, Dublin 2, IrelandDepartment of Pharmacology and Therapeutics, Trinity College, Dublin 2, Ireland
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  • For correspondence: mrowan@tcd.ie
I. Klyubin
Department of Pharmacology and Therapeutics, Trinity College, Dublin 2, Ireland
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Q. Wang
Department of Physiology, Trinity College, Dublin 2, Ireland
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N.W. Hu
Department of Pharmacology and Therapeutics, Trinity College, Dublin 2, Ireland
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R. Anwyl
Trinity College Institute of Neuroscience, Trinity College, Dublin 2, IrelandDepartment of Physiology, Trinity College, Dublin 2, Ireland
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Abstract

There is growing evidence that mild cognitive impairment in early AD (Alzheimer's disease) may be due to synaptic dysfunction caused by the accumulation of non-fibrillar, oligomeric Aβ (amyloid β-peptide), long before widespread synaptic loss and neurodegeneration occurs. Soluble Aβ oligomers can rapidly disrupt synaptic memory mechanisms at extremely low concentrations via stress-activated kinases and oxidative/nitrosative stress mediators. Here, we summarize experiments that investigated whether certain putative receptors for Aβ, the αv integrin extracellular cell matrix-binding protein and the cytokine TNFα (tumour necrosis factor α) type-1 death receptor mediate Aβ oligomer-induced inhibition of LTP (long-term potentiation). Ligands that neutralize TNFα or genetic knockout of TNF-R1s (type-1 TNFα receptors) prevented Aβ-triggered inhibition of LTP in hippocampal slices. Similarly, antibodies to αv-containing integrins abrogated LTP block by Aβ. Protection against the synaptic plasticity-disruptive effects of soluble Aβ was also achieved using systemically administered small molecules targeting these mechanisms in vivo. Taken together, this research lends support to therapeutic trials of drugs antagonizing synaptic plasticity-disrupting actions of Aβ oligomers in preclinical AD.

  • Alzheimer's disease
  • amyloid β-peptide (Aβ)
  • glutamatergic transmission
  • hippocampus
  • integrin
  • long-term potentiation (LTP)
  • synaptic memory
  • tumour necrosis factor α (TNFα)

Footnotes

  • Central Nervous System: A Focus Topic at Life Sciences 2007, held at SECC Glasgow, U.K., 9–12 July 2007. Edited by C. Dart (Liverpool, U.K.), M. Houslay (Glasgow, U.K.), M. Ludwig (Edinburgh, U.K.), R. Porter (Trinity College Dublin, Ireland) and J. Potts (Misouri-Columbia, U.S.A.).

Abbreviations: Aβ, amyloid β-peptide; AD, Alzheimer's disease; APP, amyloid precursor protein; CSF, cerebrospinal fluid; HFS, high-frequency conditioning stimulation; LTD, long-term depression; LTP, long-term potentiation; mGluR, metabotropic glutamate receptor; NMDA, N-methyl-D-aspartate; NMDAR, NMDA receptor; TNFα, tumour necrosis factor α; TNF-R1, type-1 TNFα receptor

  • © The Authors Journal compilation © 2007 Biochemical Society
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November 2007

Volume: 35 Issue: 5

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Synaptic memory mechanisms: Alzheimer's disease amyloid β-peptide-induced dysfunction
M.J. Rowan, I. Klyubin, Q. Wang, N.W. Hu, R. Anwyl
Biochemical Society Transactions Nov 2007, 35 (5) 1219-1223; DOI: 10.1042/BST0351219
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Synaptic memory mechanisms: Alzheimer's disease amyloid β-peptide-induced dysfunction
M.J. Rowan, I. Klyubin, Q. Wang, N.W. Hu, R. Anwyl
Biochemical Society Transactions Nov 2007, 35 (5) 1219-1223; DOI: 10.1042/BST0351219

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  • Article
    • Abstract
    • Introduction
    • The pro-inflammatory cytokine TNFα mediates the disruption of LTP by Aβ
    • The cell adhesion molecule αv integrin mediates the disruption of LTP by Aβ
    • Conclusion
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Keywords

Alzheimer's disease
amyloid β-peptide (Aβ)
glutamatergic transmission
hippocampus
integrin
long-term potentiation (LTP)
synaptic memory
tumour necrosis factor α (TNFα)

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