Disruption of glutamate receptors at Shank-postsynaptic platform in Alzheimer's disease
- 25 July 2009
- journal article
- Published by Elsevier in Brain Research
- Vol. 1292, 191-198
- https://doi.org/10.1016/j.brainres.2009.07.056
Abstract
No abstract availableKeywords
This publication has 36 references indexed in Scilit:
- Oligomeric amyloid β associates with postsynaptic densities and correlates with excitatory synapse loss near senile plaquesProceedings of the National Academy of Sciences, 2009
- Smaller Dendritic Spines, Weaker Synaptic Transmission, but Enhanced Spatial Learning in Mice Lacking Shank1Journal of Neuroscience, 2008
- Properties of glutamate receptors of Alzheimer's disease brain transplanted to frog oocytesProceedings of the National Academy of Sciences, 2007
- Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid β-peptideNature Reviews Molecular Cell Biology, 2007
- Proteomics Analysis and Protein Expression during Sporozoite Excystation of Cryptosporidium parvum (Coccidia, Apicomplexa)Molecular & Cellular Proteomics, 2007
- Absence of synaptophysin near cortical neurons containing oligomer Aβ in Alzheimer's disease brainJournal of Neuroscience Research, 2006
- Non‐fibrillar β‐amyloid abates spike‐timing‐dependent synaptic potentiation at excitatory synapses in layer 2/3 of the neocortex by targeting postsynaptic AMPA receptorsEuropean Journal of Neuroscience, 2006
- α3Na+/K+-ATPase Is a Neuronal Receptor for AgrinCell, 2006
- MemantineDrugs, 2006
- Alzheimer's Disease Is a Synaptic FailureScience, 2002