Regulation of NMDA receptor trafficking by amyloid-β

By E. Snyder, Yi Nong, C. Almeida, Surojit Paul, T. Moran, E. Choi, A. Nairn, Michael W. Salter, P. Lombroso, G. Gouras and 1 more. Nature Neuroscience, 2005

1,634 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/ffafcce312bfdb102e3e5b15440a679150e70ec0

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

In Cellular and Molecular Neuroscience

1. D. Selkoe
2. L. Mucke
3. D. Holtzman
4. J. Palop
5. G. Bu
6. G. Shankar
7. Nina E. Shepardson
8. Shaomin Li

In Molecular Biology

1. D. Selkoe
2. Berislav Zlokovic
3. D. Holtzman
4. L. Mucke
5. A. Sagare
6. J. Palop
7. G. Bu
8. R. Deane

In Physiology

1. D. Selkoe
2. D. Holtzman
3. L. Mucke
4. Berislav Zlokovic
5. J. Palop
6. G. Bu
7. J. Herz
8. Bradley T. Hyman

Citations in the corpus

• Alzheimer Amyloid-β Oligomer Bound to Post-Synaptic Prion Protein Activates Fyn to Impair Neurons (2012, neutral): “To prepare capture plates, 20 ml per well of 0 or 100 nM human recombinant PrP(23-111) in 30 mM Na2CO3 and 80 mM NaHCO3 (pH 9.”
• Trafficking and proteolytic processing of APP. (2012, neutral): “…application of synthetic Ab reduces the levels of surface NMDA and GluR1 receptors in dissociated cultured hippocampal neurons (Almeida et al. 2005; Snyder et al. 2005), Hsieh et al. (2006) confirmed that Ab generated in situ also leads to decreases in surface and synaptic AMPA receptors on both…”
• Glutamate Receptor Ion Channels: Structure, Regulation, and Function (2010, neutral): “7) contains a prominent src target very near the C terminus on HVY1472EK, which may regulate endocytosis in some conditions (Cheung and Gurd, 2001; Nakazawa et al., 2001; Snyder et al., 2005).”
• Apolipoprotein E and apolipoprotein E receptors: normal biology and roles in Alzheimer disease. (2012, background): “Ab oligomers interfere with NMDAR tyrosine phosphorylation by activating tyrosine phosphatases (Snyder et al. 2005).”
• The cell biology of synaptic plasticity: AMPA receptor trafficking. (2007, neutral): “Aβ secretion in vivo is modulated by neuronal activity and depresses both AMPA and NMDA currents in slices (Cirrito et al. 2005, Kamenetz et al. 2003, Snyder et al. 2005).”
• Cellular and synaptic mechanisms of anti-NMDA receptor encephalitis (2010, neutral): “, NMDA receptor (NMDAR) antagonists causing psychosis] (GunduzBruce, 2009), and analysis of brain tissue from patients with Alzheimer’s disease or schizophrenia in which several molecular pathways causing a downstream alteration of glutamate receptors are affected (Snyder et al., 2005; Hahn et al., ”
• Oligomeric amyloid β associates with postsynaptic densities and correlates with excitatory synapse loss near senile plaques (2009, methodology): “In the APP/PS1 mice, shrinkage could result from interaction of oligomeric A with the PSD, causing internalization of receptors, as seen in vitro (5, 6).”
• apoE isoform-specific disruption of amyloid beta peptide clearance from mouse brain. (2008, background): “Clearance of Alzheimer’s amyloid β(1-40)-peptide from brain by LDL receptor-related protein-1 at the blood-brain barrier.”
• Aβ plaques lead to aberrant regulation of calcium homeostasis in vivo resulting in structural and functional disruption of neuronal networks (2008, neutral): “, 2007) and that local application of Aβ can induce LTD-like mechanisms in vitro (Snyder et al., 2005).”
• Imbalance between GABAergic and Glutamatergic Transmission Impairs Adult Neurogenesis in an Animal Model of Alzheimer’s Disease (2009, positive): “Our results also agree with the requirement of calcineurin for Ab-induced reduction in spines and in NMDA and AMPA receptors observed in cell or tissue cultures (Hsieh et al., 2006; Snyder et al., 2005a).”
• Soluble oligomers of the amyloid beta-protein impair synaptic plasticity and behavior. (2008, neutral): “Acute application of synthetic Aβ can trigger a rapid reduction of NMDARdependent currents in dissociated cortical neurons that is thought to result from Aβmediated activation of nicotinic acetylcholine receptors (nAchRs; Snyder et al. 2005).”