Tau load in select brainstem neurons predicts the severity and nature of balance deficits in the absence of cell death.

Patients with tauopathies present with profoundly different clinical symptoms , even within the same disorder . A central hypothesis in the field, well-supported by biomarker studies and post-mortem pathology , is that clinical heterogeneity reflects differential degeneration of vulnerable neuronal populations responsible for specific neurological functions. Recent work has revealed mechanisms underlying susceptibility of particular cell types , but relating tau load to disrupted behavior - es- pecially before cell death - requires a targeted circuit-level approach.