W. Klein

Physiology · 2001–2018

A researcher in the Science corpus: 11 papers; trusts 3 researchers and is trusted by 8 researchers here, as inferred from the citation graph.

Subfields

• Physiology — 107 citations into it; #521 of 2,276 by trust here, #264 by citations
• Cellular and Molecular Neuroscience — 59 citations into it

Whom W. Klein trusts overall

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

1. D. Selkoe
2. D. Walsh
3. G. Krafft

Who trusts W. Klein overall

1. M. Kirkitadze
2. P. Lacor
3. D. Selkoe
4. Christopher A. Ross
5. G. Bitan
6. Leslie A. Crews
7. David B. Teplow
8. J. Palop

Papers from W. Klein's perspective

Ordered by how strongly the researchers W. Klein 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. Naturally secreted oligomers of amyloid β protein potently inhibit hippocampal long-term potentiation in vivo (Nature)
3. Altered expression of synaptic proteins occurs early during progression of Alzheimer’s disease (Neurology)
4. 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)
5. A specific amyloid-beta protein assembly in the brain impairs memory. (Nature)
6. Pathways towards and away from Alzheimer's disease (Nature)
7. Immunization reverses memory deficits without reducing brain Aβ burden in Alzheimer's disease model (Nature Neuroscience)
8. Regulation of NMDA receptor trafficking by amyloid-β (Nature Neuroscience)
9. Effects of secreted oligomers of amyloid β‐protein on hippocampal synaptic plasticity: a potent role for trimers (Journal of Physiology)
10. Intraneuronal Aβ42 Accumulation in Human Brain

Their papers

• Alzheimer's disease-affected brain: Presence of oligomeric Aβ ligands (ADDLs) suggests a molecular basis for reversible memory loss (2003) — 1,118 citations
• Detection of a biomarker for Alzheimer's disease from synthetic and clinical samples using a nanoscale optical biosensor. (2005) — 802 citations
• The Amyloid-β Oligomer Hypothesis: Beginning of the Third Decade (2018) — 659 citations
• Modeling Alzheimer's disease with iPSCs reveals stress phenotypes associated with intracellular Aβ and differential drug responsiveness. (2013) — 728 citations
• An anti-diabetes agent protects the mouse brain from defective insulin signaling caused by Alzheimer's disease- associated Aβ oligomers. (2012) — 813 citations
• Protection of synapses against Alzheimer's-linked toxins: Insulin signaling prevents the pathogenic binding of Aβ oligomers (2009) — 616 citations
• Aβ Oligomers Induce Neuronal Oxidative Stress through an N-Methyl-D-aspartate Receptor-dependent Mechanism That Is Blocked by the Alzheimer Drug Memantine* (2007) — 904 citations
• Aβ Oligomer-Induced Aberrations in Synapse Composition, Shape, and Density Provide a Molecular Basis for Loss of Connectivity in Alzheimer's Disease (2007) — 1,061 citations
• Synaptic Targeting by Alzheimer's-Related Amyloid β Oligomers (2004) — 861 citations
• A Localized Surface Plasmon Resonance Biosensor: First Steps toward an Assay for Alzheimer's Disease (2004) — 645 citations
• Targeting small Aβ oligomers: the solution to an Alzheimer's disease conundrum? (2001) — 1,021 citations