Soluble amyloid β-protein dimers isolated from Alzheimer cortex directly induce Tau hyperphosphorylation and neuritic degeneration

By M. Jin, Nina E. Shepardson, Ting Yang, Gang Chen, D. Walsh, D. Selkoe. Proceedings of the National Academy of Sciences of the United States of America, 2011

926 citations recorded by the source corpus.

Subfields: Cellular and Molecular Neuroscience, Molecular Biology, Physiology

View Paper: https://www.semanticscholar.org/paper/96d97409b73f59c9bd961b5f1c118ee9cbe02302

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. Lary C. Walker
2. Mathias Jucker

In Molecular Biology

1. Lary C. Walker
2. John Hardy
3. Mathias Jucker

In Physiology

1. C. Lane
2. Lary C. Walker
3. John Hardy
4. Jonathan M. Schott
5. Mathias Jucker

Citations in the corpus

• Pathogenic Protein Seeding in Alzheimer’s Disease and Other Neurodegenerative Disorders (2011, background): “…aggregates impair neuronal function remains uncertain, but evidence is growing that oligomeric forms of the protein, which can range in size from dimers to dodecamers or larger 14-18 , are more deleterious to brain function than are histologically obvious A β lesions such as senile plaques and CAA.”
• Alzheimer's disease (2018, background): “Human oligomers also induce hyperphosphorylation of tau at AD-relevant epitopes and cause neuritic dystrophy in cultured neurons [27].”