G. Shankar

Physiology · 2005–2011

A researcher in the Science corpus: 6 papers; trusts 5 researchers and is trusted by 8 researchers here, as inferred from the citation graph.

Subfields

• Physiology — 44 citations into it; #302 of 2,276 by trust here, #273 by citations
• Cellular and Molecular Neuroscience — 35 citations into it; #879 of 2,998 by trust here, #334 by citations
• Molecular Biology — 21 citations into it; #16,480 of 17,773 by trust here, #9,136 by citations
• Computational Theory and Mathematics — 9 citations into it; #11,782 of 12,182 by trust here, #2,689 by citations
• Cognitive Neuroscience — 8 citations into it; #7,433 of 10,852 by trust here, #3,597 by citations

Whom G. Shankar trusts overall

Their strongest outbound trust, strongest first, inferred from their citations.

1. D. Selkoe
2. D. Walsh
3. Matthew Townsend
4. Michael D. Ehlers

Who trusts G. Shankar overall

1. D. Selkoe
2. J. Long
3. D. Holtzman
4. Shaomin Li
5. J. Palop
6. Rui Wang
7. L. Mucke
8. M. Jin
9. Binggui Sun
10. M. Busche

Papers from G. Shankar's perspective

Ordered by how strongly the researchers G. Shankar trusts endorse each paper. Same corpus, a different order for every researcher.

1. Alzheimer's Disease Is a Synaptic Failure (Science)
2. Common Structure of Soluble Amyloid Oligomers Implies Common Mechanism of Pathogenesis (Science)
3. Activation of synaptic NMDA receptors induces membrane insertion of new AMPA receptors and LTP in cultured hippocampal neurons. (Neuron)
4. Activity level controls postsynaptic composition and signaling via the ubiquitin-proteasome system (Nature Neuroscience)
5. Structural basis of long-term potentiation in single dendritic spines (Nature)
6. Altered expression of synaptic proteins occurs early during progression of Alzheimer’s disease (Neurology)
7. Short-term synaptic plasticity.
8. RAGE mediates amyloid-β peptide transport across the blood-brain barrier and accumulation in brain (Nature Medicine)
9. Bidirectional activity-dependent morphological plasticity in hippocampal neurons. (Neuron)
10. Intraneuronal Aβ Causes the Onset of Early Alzheimer’s Disease-Related Cognitive Deficits in Transgenic Mice

Their papers

• Natural oligomers of the amyloid-β protein specifically disrupt cognitive function (2005) — 1,747 citations
• Soluble Aβ oligomers inhibit long-term potentiation through a mechanism involving excessive activation of extrasynaptic NR2B-containing NMDA receptors (2011) — 644 citations
• Soluble oligomers of amyloid β-protein facilitate hippocampal long-term depression by disrupting neuronal glutamate uptake (2009) — 909 citations
• Amyloid-β protein dimers isolated directly from Alzheimer's brains impair synaptic plasticity and memory (2008) — 2,572 citations
• Natural Oligomers of the Alzheimer Amyloid-β Protein Induce Reversible Synapse Loss by Modulating an NMDA-Type Glutamate Receptor-Dependent Signaling Pathway (2007) — 1,641 citations
• Effects of secreted oligomers of amyloid β‐protein on hippocampal synaptic plasticity: a potent role for trimers (2006) — 645 citations