Li, Shaomin

Selkoe, Dennis J.

Shankar, Ganesh M.

English

PubMed

Shaomin Li

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Frontiers in Cellular Neuroscience

How do soluble oligomers of amyloid &beta;-protein impair hippocampal synaptic plasticity?

Li, 

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How do soluble oligomers of amyloid β-protein impair hippocampal synaptic plasticity?

4:5. doi: 10.3389/fncel.2010.00005 Copyright ©

Aberrant excitatory neuronal activity and compensatory remodeling of inhibitory hippocampal circuits in mouse models of Alzheimer’s disease.

Aberrant expression of the glutamate transporter excitatory amino acid transporter 1 (EAAT1) in Alzheimer’s disease.

Alterations in expression of glutamatergic transporters and receptors in sporadic Alzheimer’s disease.

Altered expression of the glutamate transporter EAAT2b in neurological disease.

Amyloid beta peptide (25-35) inhibits Na+-dependent glutamate uptake in rat hippocampal astrocyte cultures.

Amyloid beta-protein fragments 25-35 and 31-35 potentiate long-term depression in hippocampal CA1 region of rats in vivo.

Beta-amyloid 25-35 inhibits glutamate uptake in cultured neurons and astrocytes: modulation of uptake as a survival mechanism.

beta-amyloid neurotoxicity is mediated by a glutamate-triggered excitotoxic cascade in rat nucleus basalis.

Beta-amyloid peptides destabilize calcium homeostasis and render human cortical neurons vulnerable to excitotoxicity.

Betaamyloid-mediated inhibition of NMDA receptordependent long-term potentiation induction involves activation of microglia and stimulation of inducible nitric oxide synthase and superoxide.

Bidirectional activitydependent morphological plasticity in hippocampal neurons.

Deﬁ cient glutamate transport is associated with neurodegeneration in Alzheimer’s disease.

Dendritic spine loss and synaptic alterations in Alzheimer’s disease.

Detergent-insoluble EAAC1/ EAAT3 aberrantly accumulates in hippocampal neurons of Alzheimer’s disease patients.

Effects of secreted oligomers of amyloid beta-protein on hippocampal synaptic plasticity: a potent role for trimers.

Excitatory amino acids and Alzheimer’s disease.

Glutamate and other CSF amino acids in Alzheimer’s disease.

Glutamate transporters regulate excitability in local networks in rat neocortex.

Glutamate-mediated excitotoxicity and neurodegeneration in Alzheimer’s disease.

Intracerebroventricular administration of amyloid b-protein oligomers selectively increases dorsal hippocampal dialysate glutamate levels in the awake rat.

Modulation of Na(+),K(+) pumping and neurotransmitter uptake by beta-amyloid.

NMDA receptor regulation by amyloid-beta does not account for its inhibition of LTP in rat hippocampus.

Physical basis of cognitive alterations in Alzheimer’s disease: synapse loss is the major correlate of cognitive impairment.

Shrinkage of dendritic spines associated with long-term depression of hippocampal synapses.

Soluble amyloid beta peptide concentration as a predictor of synaptic change in Alzheimer’s disease.

Soluble amyloid β-protein dimers isolated directly from Alzheimer disease patients potently impair synaptic plasticity and memory.

Soluble oligomers of amyloid beta protein facilitate hippocampal longterm depression by disrupting neuronal glutamate uptake.

Soluble oligomers of beta amyloid (1-42) inhibit long-term potentiation but not long-term depression in rat dentate gyrus. Brain Res.

Soluble pool of Abeta amyloid as a determinant of severity of neurodegeneration in Alzheimer’s disease.

Structural basis of long-term potentiation in single dendritic spines.

Use-dependent effects of amyloidogenic fragments of (beta)-amyloid precursor protein on synaptic plasticity in rat hippocampus in vivo.

http://www.pubmedcentral.nih.gov/articlerender.fcgi?artid=2859875

How do Soluble Oligomers of Amyloid β-protein Impair Hippocampal Synaptic Plasticity?

How do Soluble Oligomers of Amyloid β-protein Impair Hippocampal Synaptic Plasticity?

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