The synaptic interplay of Tau and Aβ oligomeric species in Alzheimer’s disease and related tauopathies.

Alzheimer’s Disease (AD) is characterized by gradual cognitive decline driven by the targeting of synapses by small oligomers of both Aβ (AβO) and tau (TauO), which results in synaptic dysfunction that ultimately underscores disease progression. Preventing the interaction of these oligomers with synapses might be effective to treat AD. However, clinical trial failures suggest low effectiveness of targeting Aβ in late‐stage AD thus redirecting the attention onto TauO whose levels increase later in the disease timeline. Here we show that TauO and AβO target synapses with different dynamics.