Tau pathology is a hallmark of Alzheimer’s disease and other tauopathies, but the mechanisms of tau spread throughout the brain remain poorly understood. This study demonstrates that brain-derived extracellular vesicles from Alzheimer’s disease patients can spread tau pathology to interneurons, a critical cell type for maintaining neural network function. Using advanced imaging and biochemical techniques, we show that extracellular vesicles serve as vehicles for tau propagation and that interneurons are particularly vulnerable to tau-mediated dysfunction. These findings provide new insights into the mechanisms of disease progression and suggest potential therapeutic targets for preventing tau spread.
This research provides critical insights into the mechanisms of tau pathology spread in Alzheimer’s disease, highlighting the role of extracellular vesicles and the vulnerability of interneurons. The findings have important implications for understanding disease progression and developing therapeutic interventions.