This evidence suggests that toxic Aβ species (e.g., oligomers, protofibrils, and fibrils) trigger pathologic tau (tau hyperphosphorylation, fragmentation, and NFTs), which is associated with synapse and neuron loss (reviewed in [66] Although the mechanism linking Aβ and tau in AD is a profound mystery, disrupting the link between amyloid and tau pathologies, especially before cognitive impairment, may represent an effective therapeutic strategy for preventing AD. Here, MAPT is linked to Cognitive impairment.