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Amyloid-β protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory
TLDR
It is concluded that soluble Aβ oligomers extracted from Alzheimer's disease brains potently impair synapse structure and function and that dimers are the smallest synaptotoxic species. Expand
Natural Oligomers of the Alzheimer Amyloid-β Protein Induce Reversible Synapse Loss by Modulating an NMDA-Type Glutamate Receptor-Dependent Signaling Pathway
TLDR
It is concluded that soluble, low-n oligomers of human Aβ trigger synapse loss that can be reversed by therapeutic agents and provides a quantitative cellular model for elucidating the molecular basis of Aβ-induced neuronal dysfunction. Expand
Soluble Aβ Oligomers Inhibit Long-Term Potentiation through a Mechanism Involving Excessive Activation of Extrasynaptic NR2B-Containing NMDA Receptors
TLDR
Soluble Aβ oligomers at low nanomolar levels present in AD brain increase activation of extrasynaptic NR2B-containing receptors, thereby impairing synaptic plasticity. Expand
Soluble Oligomers of Amyloid β Protein Facilitate Hippocampal Long-Term Depression by Disrupting Neuronal Glutamate Uptake
TLDR
It is concluded that soluble Abeta oligomers perturb synaptic plasticity by altering glutamate recycling at the synapse and promoting synapse depression. Expand
Natural oligomers of the amyloid-β protein specifically disrupt cognitive function
TLDR
The biochemical isolation of discrete amyloid-β moieties with pathophysiological properties sets the stage for a new approach to studying the molecular mechanisms of cognitive impairment in Alzheimer disease and related neurodegenerative disorders. Expand
Effects of secreted oligomers of amyloid β‐protein on hippocampal synaptic plasticity: a potent role for trimers
TLDR
The hypothesis that diffusible oligomers of Aβ initiate a synaptic dysfunction that may be an early event in AD is supported and specific assemblies, particularly timers of naturally secreted Aβ oligomers are potent and selective inhibitors of certain forms of hippocampal LTP. Expand
Protein Aggregation in the Brain: The Molecular Basis for Alzheimer’s and Parkinson’s Diseases
TLDR
This theme of protein aggregation as it relates to the two most common neurodegenerative conditions—Alzheimer's and Parkinson’s diseases is discussed. Expand
Amyloid beta protein immunotherapy neutralizes Abeta oligomers that disrupt synaptic plasticity in vivo.
TLDR
The ability of exogenous and endogenous antibodies to rapidly neutralize soluble Abeta oligomers that disrupt synaptic plasticity in vivo suggests that treatment with such antibodies might show reversible cognitive deficits in early Alzheimer disease. Expand
Amyloid β protein immunotherapy neutralizes Aβ oligomers that disrupt synaptic plasticity in vivo
TLDR
The ability of exogenous and endogenous antibodies to rapidly neutralize soluble Aβ oligomers that disrupt synaptic plasticity in vivo suggests that treatment with such antibodies might show reversible cognitive deficits in early Alzheimer disease. Expand
Certain Inhibitors of Synthetic Amyloid β-Peptide (Aβ) Fibrillogenesis Block Oligomerization of Natural Aβ and Thereby Rescue Long-Term Potentiation
Recent studies support the hypothesis that soluble oligomers of amyloid β-peptide (Aβ) rather than mature amyloid fibrils are the earliest effectors of synaptic compromise in Alzheimer's disease. WeExpand
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