Oligomeric, soluble Aβ exerts toxic effects, which are at least partially mediated through tau protein by inducing the neurodegenerative triad of synapse loss, dendritic simplification and cell death in Alzheimer’s disease.

Decreasing tau aggregation or lowering the level of potentially toxic tau species may be a promising therapeutic approach.

Most drugs that are currently in clinical trials do not qualify as primarily tau-targeting agents since they have pleiotropic actions and evidence that they exhibit their main biological function on tau is weak.