A key characteristic of many neurodegenerative diseases is the slow accumulation of misfolded protein deposits in the neurons of the brain. In particular, the accumulation and spread of a protein known as tau is a feature of several forms of dementia, ranging from the most common form, Alzheimer’s disease, to chronic traumatic encephalopathy, a dementia associated with repetitive head injuries. Writing in Nature, Rauch et al.1 provide a clue to how this harmful protein spreads: they identify a cell-surface receptor that enables tau to move between neurons.
In tau-associated forms of dementia, or tauopathies, disease progression correlates with the spread of tau deposits throughout the brain. This is thought to occur because of misfolded, disease-associated (pathological) tau entering healthy neurons. Pathological tau interacts with normal (physiological)…
