Brian C. Kraemer

This study shows TMEM106B C-terminal fragment aggregation synergizes with α-synuclein and TDP-43 to worsen neurodegeneration in C. elegans, but not with tau.

The paper designs and validates protein readers that specifically detect disease-related modifications in Tau and Abeta in Alzheimer's disease models and human samples.

This study identifies tubulin gene mutations that rescue tauopathy phenotypes in C. elegans by altering microtubule properties rather than directly affecting tau protein levels or aggregation.

The paper identifies citrullination of tau as a novel posttranslational modification in Alzheimer's disease and tauopathy models, showing its association with disease progression.

This study identifies TMEM106B C-terminal fragments as aggregating proteins linked to neurodegenerative diseases and shows their toxic effects in a C. elegans model.