Studies have shown that tau can interact with postsynaptic proteins, such as the NMDA receptor, potentially altering synaptic plasticity.[69] These effects may contribute to the cognitive deficits observed in tauopathies, particularly Alzheimer's disease, where tau pathology spreads from the entorhinal cortex to other brain regions involved in memory and learning. This evidence concerns the gene MAPT and early-onset autosomal dominant Alzheimer disease.