D. Walsh

Physiology · Neuron · 2002–2011

A researcher in the Science corpus: 10 papers; trusts 5 researchers and is trusted by 20 researchers here, as inferred from the citation graph.

Subfields

• Physiology — 99 citations into it; #80 of 2,276 by trust here, #70 by citations
• Molecular Biology — 53 citations into it; #15,518 of 17,773 by trust here, #5,320 by citations
• Cellular and Molecular Neuroscience — 44 citations into it; #394 of 2,998 by trust here, #93 by citations
• Pharmacology — 26 citations into it; #237 of 1,112 by trust here, #33 by citations
• Computational Theory and Mathematics — 16 citations into it; #9,788 of 12,182 by trust here, #1,437 by citations

Whom D. Walsh trusts overall

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

1. D. Selkoe
2. R. Kayed
3. L. Mucke
4. E. Masliah
5. Matthew Townsend
6. J. Götz
7. S. Oddo
8. J. Nicoll
9. Michael D. Ehlers

Who trusts D. Walsh overall

1. D. Selkoe
2. J. Palop
3. Michael T. Heneka
4. Randy L. Buckner
5. M. O’Banion
6. L. Mucke
7. R. Swerdlow
8. G. Shankar
9. Shaomin Li
10. Jeannie Chin

Papers from D. Walsh's perspective

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

1. Common Structure of Soluble Amyloid Oligomers Implies Common Mechanism of Pathogenesis (Science)
2. Alzheimer's Disease Is a Synaptic Failure (Science)
3. Tau Suppression in a Neurodegenerative Mouse Model Improves Memory Function (Science)
4. Altered expression of synaptic proteins occurs early during progression of Alzheimer’s disease (Neurology)
5. Alzheimer's disease: genes, proteins, and therapy. (Physiological Reviews)
6. Aberrant excitatory neuronal activity and compensatory remodeling of inhibitory hippocampal circuits in mouse models of Alzheimer's disease. (Neuron)
7. Activity level controls postsynaptic composition and signaling via the ubiquitin-proteasome system (Nature Neuroscience)
8. Early-onset behavioral and synaptic deficits in a mouse model of Alzheimer's disease. (Proceedings of the National Academy of Sciences of the United States of America)
9. A specific amyloid-beta protein assembly in the brain impairs memory. (Nature)
10. Enhanced Neurofibrillary Degeneration in Transgenic Mice Expressing Mutant Tau and APP (Science)

Their papers

• Natural oligomers of the amyloid-β protein specifically disrupt cognitive function (2005) — 1,747 citations
• Exogenous Induction of Cerebral ß-Amyloidogenesis Is Governed by Agent and Host (2006) — 983 citations
• Aβ Oligomers – a decade of discovery (2007) — 2,034 citations
• Soluble amyloid β-protein dimers isolated from Alzheimer cortex directly induce Tau hyperphosphorylation and neuritic degeneration (2011) — 926 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
• Deciphering the molecular basis of memory failure in Alzheimer's disease. (2004) — 1,244 citations
• Naturally secreted oligomers of amyloid β protein potently inhibit hippocampal long-term potentiation in vivo (2002) — 4,448 citations