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Neuron. 2006 Dec 7;52(5):831-43.

AMPAR removal underlies Abeta-induced synaptic depression and dendritic spine loss.

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1
Cold Spring Harbor Laboratory, Cold Spring Harbor, New York 11724, USA.

Abstract

Beta amyloid (Abeta), a peptide generated from the amyloid precursor protein (APP) by neurons, is widely believed to underlie the pathophysiology of Alzheimer's disease. Recent studies indicate that this peptide can drive loss of surface AMPA and NMDA type glutamate receptors. We now show that Abeta employs signaling pathways of long-term depression (LTD) to drive endocytosis of synaptic AMPA receptors. Synaptic removal of AMPA receptors is necessary and sufficient to produce loss of dendritic spines and synaptic NMDA responses. Our studies indicate the central role played by AMPA receptor trafficking in Abeta-induced modification of synaptic structure and function.

PMID:
17145504
PMCID:
PMC1850952
DOI:
10.1016/j.neuron.2006.10.035
[Indexed for MEDLINE]
Free PMC Article

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