Overview
- A peer-reviewed Cell paper reports that the neuronal protein Arc packages into extracellular vesicles (EVs) and helps phosphorylated, disease-associated tau move from sick to healthy neurons in mouse models.
- In Alzheimer’s model mice that lacked Arc, brain EVs contained very little tau and intercellular tau transfer and seeding activity were sharply reduced, showing a causal role for Arc in tau spread.
- Removing Arc caused tau to build up inside neurons and produced early signs of cell toxicity in mice, indicating Arc both clears tau from damaged cells and enables its harmful spread to others.
- The authors found EVs from human postmortem brain tissue that contained both Arc and phosphorylated tau and reported a positive correlation between their levels, but they stress this human data are correlative and limited.
- Researchers propose targeting tau-containing EVs after they leave diseased neurons as a testable therapeutic idea, while warning that any intervention must preserve Arc’s normal role in synaptic plasticity and will require extensive safety and human validation.