AD patients are characterized by an impairment of Long Term Potentiation (LTP)-like cortical plasticity. AD patients have a weakened Short Latency Afferent Inhibition (SLAI), a neurophysiological measure under cholinergic control. It’s been proposed that high levels of T-tau in AD patients CSF are related to a faster cognitive decline and more malignant form of dementia. Aim of this study is to investigate the relation between CSF values of beta-amyloid, T-tau and P-tau and cortical plasticity in a sample of AD patients. By means of repetitive transcranial magnetic stimulation we tested in 55 AD patients the LTP/LTD-like effects induced by the intermittent TBS (iTBS) and continuous TBS (cTBS) protocols, and the efficacy of SLAI circuits. K-means cluster analysis including the 3 CSF biomarkers was performed.The three resulting clusters differed by the value of T-tau: cluster 1 (low levels); cluster 2 (intermediate levels); cluster 3 (high levels). Cluster 2 showed more impaired LTP-like cortical plasticity and SLAI efficiency, while cluster 1 and cluster 3 have surprisingly the same pathological trends. Our results shed light on the role of tau protein in the physiopathology of AD, showing a similar U shaped-curve related to the level of LTP impairment and SLAI deficiency.