By injecting tau-enriched extracts derived from AD brains into transgenic mice, researchers dissect how Aβ plaques fuel tau pathology.
Slow vital capacity, a measure of respiratory function, predicted the rate of disease progression in ALS patients, suggesting the test could be used as a primary endpoint in clinical trials.
Small molecules that stabilize G-quadruplexes cut C9ORF72 RNA and protein deposits in half.
A segment of tau forms a tight molecular zipper that promotes fibrillogenesis. Zipper inhibitors blocked aggregation of full-length tau in cells.