Nature Communications (May 2022)
Hyperphosphorylated tau self-assembles into amorphous aggregates eliciting TLR4-dependent responses
- Jonathan X. Meng,
- Yu Zhang,
- Dominik Saman,
- Arshad M. Haider,
- Suman De,
- Jason C. Sang,
- Karen Brown,
- Kun Jiang,
- Jane Humphrey,
- Linda Julian,
- Eric Hidari,
- Steven F. Lee,
- Gabriel Balmus,
- R. Andres Floto,
- Clare E. Bryant,
- Justin L. P. Benesch,
- Yu Ye,
- David Klenerman
Affiliations
- Jonathan X. Meng
- Department of Chemistry, University of Cambridge
- Yu Zhang
- Department of Chemistry, University of Cambridge
- Dominik Saman
- Department of Chemistry, University of Oxford
- Arshad M. Haider
- UK Dementia Research Institute at Cambridge
- Suman De
- Department of Chemistry, University of Cambridge
- Jason C. Sang
- Department of Chemistry, University of Cambridge
- Karen Brown
- Molecular Immunity Unit, Department of Medicine, MRC Laboratory of Molecular Biology, University of Cambridge
- Kun Jiang
- Department of Chemistry, University of Cambridge
- Jane Humphrey
- Department of Chemistry, University of Cambridge
- Linda Julian
- Department of Chemistry, University of Cambridge
- Eric Hidari
- UK Dementia Research Institute at Cambridge
- Steven F. Lee
- Department of Chemistry, University of Cambridge
- Gabriel Balmus
- UK Dementia Research Institute at Cambridge
- R. Andres Floto
- Molecular Immunity Unit, Department of Medicine, MRC Laboratory of Molecular Biology, University of Cambridge
- Clare E. Bryant
- Medicine and Veterinary Medicine, University of Cambridge
- Justin L. P. Benesch
- Department of Chemistry, University of Oxford
- Yu Ye
- Department of Chemistry, University of Cambridge
- David Klenerman
- Department of Chemistry, University of Cambridge
- DOI
- https://doi.org/10.1038/s41467-022-30461-x
- Journal volume & issue
-
Vol. 13,
no. 1
pp. 1 – 16
Abstract
In this work, the authors report that hyperphosphorylated recombinant tau spontaneously assembles into small, amorphous aggregates, which disrupt membranes and induce Toll-like receptor 4-dependent responses in human macrophages.
