R. Kayed

Physiology · 2003–2021

A researcher in the Science corpus: 13 papers; trusts 3 researchers and is trusted by 7 researchers here, as inferred from the citation graph.

Subfields

• Physiology — 95 citations into it; #474 of 2,276 by trust here, #111 by citations
• Molecular Biology — 61 citations into it; #9,540 of 17,773 by trust here, #3,659 by citations
• Neurology — 53 citations into it

Whom R. Kayed trusts overall

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

1. C. Glabe

Who trusts R. Kayed overall

1. M. Mańczak
2. M. Murphy
3. D. Selkoe
4. C. Glabe
5. J. Götz
6. Christopher M. Dobson
7. D. Walsh
8. S. Oddo
9. I. Hamley
10. L. Breydo

Papers from R. Kayed's perspective

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

1. Neuropathological stageing of Alzheimer-related changes
2. S3‐03‐05: Transmission and Spreading of Tauopathy in Transgenic Mouse Brain
3. Staging of Alzheimer disease-associated neurofibrillary pathology using paraffin sections and immunocytochemistry (Acta Neuropathologica)
4. A mutation in APP protects against Alzheimer’s disease and age-related cognitive decline (Nature)
5. Proliferation of amyloid-β42 aggregates occurs through a secondary nucleation mechanism (Proceedings of the National Academy of Sciences of the United States of America)
6. Cellular Prion Protein Mediates Impairment of Synaptic Plasticity by Amyloid-β Oligomers (Nature)
7. Propagation of Tau Misfolding from the Outside to the Inside of a Cell* (Journal of Biological Chemistry)
8. Protein misfolding, functional amyloid, and human disease. (Annual Review of Biochemistry)
9. A specific amyloid-beta protein assembly in the brain impairs memory. (Nature)
10. Tau-mediated neurodegeneration in Alzheimer's disease and related disorders (Nature Reviews Neuroscience)

Their papers

• Common Structure of Soluble Amyloid Oligomers Implies Common Mechanism of Pathogenesis (2003) — 4,109 citations
• Small Molecule Inhibitors of Aggregation Indicate That Amyloid β Oligomerization and Fibrillization Pathways Are Independent and Distinct* (2007) — 697 citations
• Permeabilization of Lipid Bilayers Is a Common Conformation-dependent Activity of Soluble Amyloid Oligomers in Protein Misfolding Diseases* (2004) — 871 citations
• Calcium Dysregulation and Membrane Disruption as a Ubiquitous Neurotoxic Mechanism of Soluble Amyloid Oligomers*♦ (2005) — 1,034 citations
• NLRP3 inflammasome activation drives tau pathology (2019) — 1,207 citations
• Amyloid Oligomers: A Joint Experimental/Computational Perspective on Alzheimer’s Disease, Parkinson’s Disease, Type II Diabetes, and Amyotrophic Lateral Sclerosis (2021) — 544 citations
• iPSC-derived human microglia-like cells to study neurological diseases (2017) — 989 citations
• The Role of Amyloid-β Oligomers in Toxicity, Propagation, and Immunotherapy (2016) — 668 citations
• Tau oligomers impair memory and induce synaptic and mitochondrial dysfunction in wild-type mice (2011) — 597 citations
• A specific amyloid-beta protein assembly in the brain impairs memory. (2006) — 1,267 citations
• A specific amyloid-β protein assembly in the brain impairs memory (2006) — 2,628 citations
• Curcumin Inhibits Formation of Amyloid β Oligomers and Fibrils, Binds Plaques, and Reduces Amyloid in Vivo* (2005) — 2,215 citations
• Triple-transgenic model of Alzheimer's disease with plaques and tangles: intracellular Abeta and synaptic dysfunction. (2003) — 4,164 citations